High densities were detected in the parafascicular nucleus (Pf), the dorsolateral, ventrolateral and posterior thalamic nuclei, and in the medial habenula. 
Frizzled5 (Fz5), a putative Wnt receptor, is expressed in the retina, hypothalamus, and the parafascicular nucleus (PFN) of the thalamus.
The posterior parafascicular nucleus (Pf) was heterogeneous with the lateral part having little DBH activity, while its medial division had most DBH-ir axons and its multiformis part had only a small number.
BACKGROUND AND OBJECTIVES: This study was designed to investigate the potential existence of the response of neurons in the parafascicular nucleus of the thalamus to acute myocardial ischaemia induced by selective coronary artery occlusion and the effects of midazolam on the response in rats. A single-barrel glass microelectrode was used for recording the unit discharges of the neuron in the parafascicular nucleus. CONCLUSIONS: The parafascicular nucleus is involved in the modulation of cardiac nociception and midazolam possesses antinociceptive property in modulating cardiac pain..
Experiments in the 6-hydroxydopamine rat model have shown that the parafascicular nucleus is overactive and its lesion alleviates basal ganglia neurochemical abnormalities associated with dopamine depletion.
METHOD: This study included 11 patients with non-tremulous Parkinson's disease (PD), who had DBS leads implanted in a range of targets, including the cZI, STN, VL nucleus, globus pallidus internus (GPi), centromedian and parafascicular nucleus (CM/Pf), and the pedunculopontine nucleus (PPN).
We recently reported that the thalamic parafascicular nucleus (Pf) in monkeys is strongly activated by vagus nerve afferents.
The present study investigated electrophysiologically the effect of Cro on pain-evoked unit discharge of neurons in thalamic parafascicular nucleus (Pf) and underlying mechanisms of its effect.
The present study was designed to investigate the function and mechanism of high-frequency stimulation (HFS) of the parafascicular nucleus (PF) used as a therapeutic approach for Parkinsonos disease (PD).
In the paraventricular thalamic nucleus and parafascicular nucleus, most of the calretinin-immunopositive interneurons expressed ERbeta.
Approximately 95% of PHA-L-labeled terminals from the central lateral, midline, mediodorsal, lateral dorsal, anteroventral, and ventral anterior/ventral lateral nuclei formed axospinous synapses, a pattern reminiscent of corticostriatal afferents but strikingly different from thalamostriatal projections arising from the parafascicular nucleus (PF), which terminated onto dendritic shafts.
Visualization of slices from animals previously injected with BDA into the parafascicular nucleus revealed the presence of axons of thalamic origin in the slice.
Then the parafascicular nucleus was examined. Some anterogradely labeled axon terminals originating in the spinal cord were observed to synapse with retrogradely labeled dendrites of parafascicular nucleus neurons which sent axons to the striatum. We concluded that information from the spinal cord was transmitted to the striatum, being relayed by parafascicular nucleus neurons..
During the past few years, there has been a growing body of evidence suggesting that the thalamic parafascicular nucleus in rodents (PF) exerts a multifaceted modulation of basal ganglia nuclei, at different levels.
We also recorded from cells in the parafascicular nucleus, a nucleus of the posterior intralaminar nuclear group, because they have unusual anatomical features that are similar to those of some of our paralaminar cells.
We identified (1) retrogradely labeled neurons in the parafascicular nucleus projecting to the anteromedial, limbic part of the external and internal pallidum, the substantia nigra and the subthalamic nucleus, (2) labeled terminals scattered in all these structures after anterograde tracer injection into the medial part of the parafascicular nucleus and (3) individual parafascicular terminals that arborized rather poorly in a large portion of each basal ganglia structure. Our study provides evidence that the parafascicular nucleus, and especially its medial part, can relay emotional and motivational information back to all basal ganglia components in primates..
Results revealed a distinct distribution of LGR8 in forebrain, with transcripts principally restricted to the posterior thalamus and highest densities detected in the parafascicular nucleus of both adult and developing rats.
In addition to the anticipated activation in the gustatory/visceral thalamic relay nucleus, we found an unexpectedly larger and earlier response focus with multi-unit discharges in the adjacent parafascicular nucleus.
Specific 5-HT(1F) receptor binding in rat brain was found in layers 4-5 of all cortical regions examined, as well as olfactory bulb and tubercle, nucleus accumbens, caudate putamen, parafascicular nucleus of the thalamus, medial mammillary nucleus, the CA3 region of the hippocampus, subiculum, and several amygdaloid nuclei.
It is highly expressed in the parafascicular nucleus of the thalamus, tuberomammillary nucleus of the hypothalamus and the mitral cell layer of the olfactory bulb.
The major excitatory input to these interneurons arises from glutamatergic neurons of the parafascicular nucleus of the thalamus (Pf).
The present study describes the thalamic innervation coming from the rat parafascicular nucleus (PF) onto striatal and subthalamic efferent neurons projecting either to the globus pallidus (GP) or to the substantia nigra pars reticulata (SNr) by using a protocol for multiple neuroanatomical tracing.
In the thalamus, [ (125)I]alpha-conotoxinMII binding was significantly reduced in the centromedian nucleus in both DLB groups, and also in the parafascicular nucleus in the DLB - EPF group.
The majority of the reports, however, showed that mainly the mediodorsal (MD) nucleus and the centromedian-parafascicular nucleus (Cm-Pf complex) are involved in penile erection.
BDA injection in the lateral part of the lateral parafascicular nucleus and the caudal part of the central lateral nucleus labeled fibers and boutons mainly in the dorsolateral sensorimotor territory of the Str and the middle territories of the GP. BDA injection in the medial part of the lateral parafascicular nucleus and the central lateral nucleus labeled mainly the middle association territory of the Str and the border and the caudomedial territories of the GP. BDA injection in the medial parafascicular nucleus and the central medial nucleus labeled mainly the medial limbic territory of the Str. The medial parafascicular nucleus projected to the medial-most region of the GP, while the central medial nucleus projection to the GP was very sparse.
In cases with spinal lamina I injections, terminations were also consistently found in the lateral habenula, the parafascicular nucleus, and the nucleus reuniens.
Previous experiments from our laboratory showed that retention of two-way active avoidance learning is improved by post-training intracranial electrical stimulation (ICS) of the parafascicular nucleus (PF) and impaired by pre-training electrolytic lesions of the nucleus basalis magnocellularis (NBM).
The parafascicular nucleus (PFN) of the rat, homologous to the human centre médian, is an intralaminar nucleus of the thalamus, classically considered as part of the ascending activating system.
The synaptic organization of afferents to the parafascicular nucleus (Pf) of the thalamus was studied in rats.
Extracellular electrophysiological recordings of neurons of the parafascicular nucleus of the thalamus were done in normal rats and in rats bearing lesions of either the cerebellar nuclei or the entopeduncular nucleus to investigate the functional control of the pedunculopontine nucleus on the parafascicular nucleus. A total of 97 neurons were recorded in the parafascicular nucleus in intact rats, 83 in rats bearing a chronic electrolytic lesion of the ipsilateral deep cerebellar nuclei, and 69 in rats bearing an ibotenate lesion of the ipsilateral entopeduncular nucleus. Two types of excitation and one type of inhibition were the main responses observed in neurons of the parafascicular nucleus following stimulation of the pedunculopontine nucleus. These results show that an excitatory influence on the parafascicular nucleus is exerted by the pedunculopontine nucleus irrespectively of the presence of cerebellofugal fibers. However, the variety of responses recorded suggests that the influences of the pedunculopontine nucleus on the parafascicular nucleus are by far more complex than those exerted on its basal ganglia targets such as the substantia nigra.
To evaluate whether intracranial self-stimulation (SS) ameliorates conditioning deficits induced by parafascicular nucleus (PF) damage in young and aged rats, the authors gave rats a daily session of 2-way active avoidance until a fixed criterion was achieved.
Contrary to the latter group, however, loss of intrastriatal and striatal-crossing fibre bundles was observed in the MPP(+) group as there was also some retrograde degeneration in the ipsilateral thalamic parafascicular nucleus.
We examined the occurrence and severity of the Alzheimer's disease (AD)-related cytoskeletal pathology and beta-amyloidosis in the seven intralaminar nuclei (central lateral nucleus, CL; central medial nucleus, CEM; centromedian nucleus, CM; cucullar nucleus, CU; paracentral nucleus, PC; parafascicular nucleus, PF; subparafascicular nucleus, SPF) in 27 autopsy cases at different stages of the cortical neurofibrillary pathology (cortical NFT/NT-stages I-VI) and beta-amyloidosis (cortical phases 1-4).
The present experiments aimed to investigate whether the caudate nucleus (Cd) was involved in cortical sensorimotor area I (Sm I) generating descending modulation of the parafascicular nucleus (Pf) in acupuncture analgesia (AA), and what type of opiate receptors in Cd were involved.
In rats, ErbB4 expression was observed in the habenular nuclei, the paraventricular nucleus, intermediodorsal nucleus, the central medial thalamic nucleus, the posterior nucleus, the parafascicular nucleus, the subparafascicular nucleus, the suprageniculate nucleus, the posterior limitans nucleus, the medial part of the medial geniculate nucleus, the peripeduncular nucleus, the posterior intralaminar nucleus, the lateral subparafascicular nucleus, the lateral posterior nucleus, and all ventral thalamic nuclei.
One group projects directly onto the VM and VL, and the other projects to the VM/VL and to the parafascicular nucleus.
The results revealed a wide but discrete distribution of the transcript with strongly JP05 mRNA expressing cells, presumably neurons, present in the cerebral cortex (layer II), hippocampus (pyramidal CA3 neurons and granule cells), amygdala (basal and periamygdaloid cortical nuclei), in the endopiriform nucleus, diagonal band of Broca, thalamus (nucleus reuniens, parafascicular nucleus) and hypothalamus (posterior, dorsal, and around the medial mammillary).
The antidromic activation foci were localized to these sites (and occasional projections to other sites were also observed, such as the parafascicular nucleus and zona incerta).
Positive neurons, stained very intensely as in adult rats, were seen in the pedunculopontine tegmental nucleus, laterodorsal tegmental nucleus and parafascicular nucleus.
Seven adult Sprague-Dawley rats, chronically implanted with standard electrodes to monitor frontoparietal electroencephalographic (EEG) and nuchal electromyographic (EMG) activity, received, under deep anesthesia, unilateral or bilateral microinjections of ibotenic acid in the lateral part of the parafascicular nucleus of the thalamus.
The frequency distribution of c-fos labeling per neuron in dorsal striata of lesioned rats treated with SKF-82958 was shifted to the left, and its median was lower than in the sham-operated striata treated with the D-1 receptor agonist.The results provide evidence that the excitatory projections from the parafascicular nucleus of the thalamus, thought to operate primarily through the N-methyl-D-aspartate receptors, exert a facilitatory control over D-1 receptor-induced c-fos gene expression specifically in the dorsal striatum..
We have examined the patterns of Fos-like immunoreactivity in the ventral thalamus (thalamic reticular nucleus (Rt), zona incerta (ZI) and ventral lateral geniculate nucleus (LGv)) after electrical or chemical stimulation of nuclei in either the brainstem (midbrain reticular nucleus), basal forebrain (substantia innominata) or dorsal thalamus (parafascicular nucleus).
MRI scan revealed infarction affecting part of the dorsomedian, lateral posterior, ventral lateral, ventral posterior lateral nuclei, and centromedian-parafascicular nucleus of the contralateral thalamus.
Electrophysiological recordings of thalamic parafascicular nucleus neurons were done in normal rats and in three groups of rats at different time intervals after injection of 6-hydroxydopamine into the pars compacta of substantia nigra.
In addition, this technique has provided evidence that the change in STN activity is owing not only to decreased inhibition from the GPe but to hyperactivity of excitatory inputs from the parafascicular nucleus of the thalamus and the pedunculopontine nucleus in the brainstem..
A model of a Skinner box food-procuring reflex in rats was used to study the relationship between the strength applied to a pedal and disruption of the parafascicular nucleus of the thalamus and microinjections of the cholinolytic scopolamine and the cholinomimetic carbachol into the neostriatum at different stages of learning. In untrained rats at the stage of learning to press strongly on the pedal without the conditioned signal being switched on (i.e., every strong press was rewarded) showed (a) a decrease in the rate of learning to press strongly and an increase in the number of weak pedal presses after bilateral lesioning of the parafascicular nucleus of the thalamus; (b) that rats with bilateral lesions of this nucleus responded to microinjections of scopolamine into the neostriatum with increases in the number of strong presses, with no change in the number of weak pedal presses, while microinjections of carbachol decreased the number of strong and increased the number of weak presses as compared with the pre-microinjection baseline. In trained rats at the stage of recovery the reflex (i.e., strong pedal presses were reinforced only during exposure to the conditioned signal), lesioning of the parafascicular nucleus of the thalamus had the effect that the time required for recovery of the reflex became dependent on the level of pre-operative training; scopolamine microinjections into the neostriatum of rats achieving high levels of correct performances of the reflex only after surgery led to sharp degradation in performance of the reflex on the day of microinjections; microinjection of carbachol into the neostriatum of rats with low post-operative levels of performance of the reflex had no effect on this measure..
To evaluate whether electrical stimulation of the parafascicular nucleus of the thalamus can improve short-term (24 h) and/or long-term (11 days) retention of two-way active avoidance, rats were implanted with an electrode at this nucleus (experimental groups with stimulation in the parafascicular, and control groups without stimulation) or above it (other control groups without stimulation).
Using a combination of metabolic measurement and retrograde tracing, we show that the neurons in the pedunculopontine nucleus and parafascicular nucleus of the thalamus that project to the subthalamic nucleus are hyperactive after nigrostriatal dopaminergic denervation in rats.
To evaluate whether electrical stimulation of the parafascicular nucleus (PF) can improve short-term (24 h) and/or long-term (21 days) retention of two-way active avoidance, rats were implanted with an electrode at this nucleus (experimental groups) or above it (control groups).
Expression of alpha1 and beta2 subunit genes was altered in a parallel manner following a 6-hydroxydopamine lesion; messenger RNA levels for both were significantly increased in the substantia nigra pars reticulata (11 +/- 4% and 17 +/- 1%, respectively), and significantly reduced in the globus pallidus (18 +/- 3% and 16 +/- 3%, respectively) and parafascicular nucleus (19 +/- 3% and 16 +/- 5%, respectively).
The organization of the descending projections from the intralaminar parafascicular nucleus was studied using biocytin as an anterograde tracer in rats. After biocytin injection into the lateral parafascicular nucleus, three bundles of fibers descending throughout the brainstem were seen. The organization of these extensive descending connections to both motor and sensory structures does not allow functions to be conclusively attributed to the parafascicular nucleus neurons.
Effects of bilateral lesions of the thalamic parafascicular nucleus (Pf) and bilateral microinjections of scopolamine (cholinolytic) and carbacholine (cholinomimetic) into rat neostriatum on the strength of pressing the bar at different stages of acquisition of food-procuring reflex were studied in 51 rats.
A behavioral analysis of intracranial self-stimulation was provided for parafascicular nucleus. To evaluate whether intracranial self-stimulation in this nucleus could be site-specific and to determine if the positive sites are the same parafascicular areas that facilitate learning when stimulated, rats were tested via monopolar electrodes situated throughout the parafascicular nucleus. Twenty-two of the 42 animals included in the study, had the electrode at the parafascicular nucleus.
The anterograde tracer biotinylated dextranamine was injected into the parafascicular nucleus of adult rats. Of 311 synaptic boutons originating from the parafascicular nucleus, 75.9% synapsed with unlabeled dendrites, 22.5% with unlabeled spines, and 1.3% had parvalbumin-immunoreactive dendrites as a postsynaptic target. Only 4% of all asymmetric synapses on parvalbumin-immunoreactive dendrites were derived from the parafascicular nucleus. A separate group of animals underwent bilateral neocortical deafferentation on the third postnatal day, prior to injection of anterograde tracer into the parafascicular nucleus of adult animals. In decorticates, 219 striatal synaptic contacts derived from the parafascicular nucleus, out of which 77.2% were on unlabeled dendrites, 20.9% were upon unlabeled spines, and 0.9% targeted parvalbumin-immunoreactive dendrites. We conclude that the thalamic parafascicular nucleus indeed sends synaptic input to parvalbumin-immunoreactive striatal neurons. parafascicular nucleus inputs to striatal parvalbumin-immunoreactive interneurons are sparse in comparison to other asymmetric inputs, most of which are likely to be of cortical origin.
By contrast, the posterior group of intralaminar nuclei (centre median nucleus and parafascicular nucleus) showed a complementary pattern of staining; the centre median nucleus showed immunoreactivity only for one calcium-binding protein, parvalbumin, while the parafascicular nucleus showed immunoreactivity for both calbindin-D28k and calretinin.
Acute high-frequency (60/s) high-intensity (2,100-2,300 microA) stimulation of the mesial, caudal and inferior portion of the centromedian thalamic region within or close to the parafascicular nucleus produced a sharp, intense, cramp-like painful response localized to the face and shoulder (medial stimulation) or arm and hand (lateral stimulation) contralateral to the stimulation site in 4 intractable epileptic patients in whom depth electrodes had been implanted as a part of a neuroaugmentive procedure for seizure control.
In the present study, we tested the effects of (i) blocking its excitatory inputs (originating mainly in the cerebral cortex and the parafascicular nucleus of the thalamus) via the NMDA receptors and (ii) stimulating its GABA receptors to mimick the influence of its inhibitory inputs (mainly from the globus pallidus).
Results indicated that rats stimulated at the posterior region of the parafascicular nucleus (PF) showed a better acquisition than those stimulated at the central one.
In the thalamus, gamma1 subunit messenger RNA was detected only in the parafascicular nucleus.
Anterograde tract-tracing by means of biotinylated dextran amine injection in the frontoparietal cerebral cortex or the parafascicular nucleus of the thalamus was combined with immunogold detection of striatin.
In the dorsal thalamus, highest mRNA levels were found in the anteroventral nucleus and in the parafascicular nucleus.
The paraventricular nucleus is densely innervated by adrenergic axons throughout, while the densest innervation of the parafascicular nucleus is located in its medial part and the strongest mediodorsal nuclear immunolabelling is found in its most posterior and medial region.
At the level of the posterior intralaminar nuclei, the central median nucleus was virtually free of immunostaining whereas the parafascicular nucleus was moderately labelled.
Only the medial part of the parafascicular nucleus expressed moderate levels of CR mRNA.
Electrophysiological studies using chloral hydrate-anesthetized rats were performed to elucidate the role of serotonin1A (5-HT1A) receptors in the regulation of neuronal activity of nucleus accumbens (Acc) neurons receiving input from the parafascicular nucleus of the thalamus (Pf).
In the thalamus, labeled fibers and terminals were observed in the avian thalamic reticular nucleus, the proposed motor part of the avian ventral tier (ventrointermediate area), the avian parafascicular nucleus (nucleus dorsointermedius posterior), as well as in the avian nucleus subrotundus (which may be comparable to the posterior intralaminar nuclei of mammals).
Acute (one day) and chronic (14 days) electrolytic lesions of the parafascicular nucleus resulted in 58% and 23% decreases in glutamate decarboxylase 67 messenger RNA expression, respectively, as determined by northern blot analysis.
Pharmacological stimulation of the parafascicular nucleus with carbachol increased tonically the pallidal discharge rate by 142%. Our results demonstrate the complex role of the parafascicular nucleus in activating both the globus pallidus and the subthalamic nucleus, two closely related structures.
Similarly, (1DMe)Y8Fa (5 nmol) inhibited morphine effects in the hot-plate test after co-injection into the parafascicular nucleus. Furthermore, (1DMe)Y8Fa injected into the parafascicular nucleus attenuated analgesia induced by morphine injected into the nucleus raphe dorsalis and similarly, the neuropeptide FF analog in the nucleus raphe dorsalis decreased the effects of 27 nmol morphine injected in the parafascicular nucleus. Similarly, the serotonin (5-HT) depletion induced by a systemic administration of para-chlorophenylalanine did not modify morphine analgesia microinjected into the nucleus raphe dorsalis and the parafascicular nucleus but blocked the ability of (1DMe)Y8Fa to reverse morphine effects in both nuclei. These data show that neuropeptide FF exerts anti-opioid effects directly into both the nucleus raphe dorsalis and the parafascicular nucleus and acts also at distance on opioid functions.
After those injections, dense plexuses of anterogradely labelled varicosities were found in common thalamic nuclei, including the parvocellular ventral anterior nucleus (VApc), the dorsal VL (VLd), and the rostrodorsal part of the parafascicular nucleus (PF).
These characteristics indicate that: (1) SHL and medial and dorsal parts of DMA and DMP are comparable to mammalian midline thalamic nuclei, including the medial components of the intralaminar nuclei; (2) lateral parts of DMA and DMP are comparable to the mediodorsal nucleus in mammals; (3) DIP is comparable to the parafascicular nucleus in mammals; and (4) DLM and DLP are comparable to the laterally located intralaminar nuclei in mammals.
By contrast, DNQX or NBQX did not prevent the increase in striatal acetylcholine release evoked by parafascicular nucleus stimulation, but MK-801, in accordance with previous results, did so. The results provide in vivo evidence that the cerebral cortex facilitates cholinergic activity in the dorsal striatum apparently through the non-tonic activation of AMPA-type glutamatergic receptors while the parafascicular nucleus does this through tonic activation of NMDA receptors.
Drugs were microiontophoretically applied to the immediate vicinity of Acc neurons receiving inputs from the parafascicular nucleus (Pf) of thalamus.
This study examined at the ultrastructural level the putative relationships between afferent fibres coming from the parafascicular nucleus of the thalamus and neuropeptide Y (NPY)-containing neurones in the rat striatum.
Acute bilateral electrolytic lesions of the parafascicular nucleus of the thalamus prevented the stimulation of striatal acetylcholine output by SKF 82958 and d-amphetamine but only slightly reduced basal acetylcholine release.
Thalamostriatal projections arising from the posterior intralaminar nuclei (P1; the parafascicular nucleus and the adjacent caudalmost part of the posterior thalamic group) were studied in rats by tracing the axons of small pools of neurons labelled anterogradely with biocytin. Before entering the striatum some axons of the parafascicular nucleus give rise to descending collaterals that arborize in the entopeduncular nucleus, in the subthalamic nucleus and in the vicinity of the red nucleus.
Thalamocortical projections originating from the parafascicular nucleus were reinvestigated using biocytin or biotylinated dextran amine as anterograde tracers in the rat. After stereotaxic injection of the marker in the lateral part of the parafascicular nucleus, labelled ascending fibres were observed running ipsilaterally to the frontal motor and anterior cingulate areas.
To evaluate a possible role of the parafascicular nucleus (PF) in modulating distributed two-way active avoidance acquisition and long-term retention (LTR), we designed two experiments.
In order to understand better how the activity of subthalamic neurons and hence the output of the basal ganglia are controlled, we have reexamined the topography and examined in detail the synaptology and neurochemical nature of the two major excitatory projections to the subthalamic nucleus, that from the cortex and from the parafascicular nucleus of the thalamus.
Three different types of labeled terminals (numerous small boutons, less numerous large claw-like terminals, varicosities in close apposition to blood vessel walls) originating from the parafascicular nucleus were present in the raphe system. Based on previous retrograde data and our observations, we conclude that the relationship between the parafascicular nucleus and raphe system is reciprocal and concerns most of the raphe nuclei, suggesting that parafascicularis cell population may be involved in many of the functions ascribed to the raphe system..
The activity of subthalamic neurons was recorded extracellularly in anaesthetized rats after stimulation, inhibition or lesioning of the parafascicular nucleus. Electrical stimulation of the parafascicular nucleus evoked a complex response with two excitatory phases. Microinjection of carbachol into the parafascicular nucleus enhanced by 119% the discharge rate of the neurons in the ipsilateral subthalamic nucleus and that of muscimol decreased the discharge rate by 91%. In contrast to the above results, the unilateral excitotoxic lesion of the parafascicular nucleus, performed one week before recording, decreased the discharge rate by 69% of the ipsilateral subthalamic nucleus neurons and by 34% that of the contralateral neurons. The opposite changes recorded in the ipsi- and contralateral subthalamic nucleus during unilateral microinjection of excitatory or inhibitory drugs in the parafascicular nucleus emphasize the importance of this thalamic structure in the bilateral regulation of basal ganglia activity via the subthalamic nucleus..
In the present study we used retrograde cell labeling, multi-unit anterograde labeling and immunohistochemical methods to study both ipsi- and contralateral NRT projection to the parafascicular nucleus (Pf) in the rat.
The facilitatory effect of parafascicular nucleus stimulation does not appear to be associated with indirect action through the cerebral frontal cortex because acute lesion of the excitatory corticostriatal afferents, which by itself reduced basal ACh release by 40%, did not modify the effect of 10 Hz stimulation. The results provide in vivo evidence that the activity of the cholinergic neurons in the dorsal striatum is trans-synaptically modulated by parafascicular nucleus excitatory afferents through activation of the NMDA subtype of glutamate receptors that is probably located in the striatum..
Four major output pathways were identified: (i) an ipsilateral descending projection which had terminations in the microcellular tegmental nucleus, lateral and ventral pontine reticular nucleus pars oralis, ventrolateral tegmental nucleus, ventral and caudal pontine reticular nucleus pars caudalis, raphe magnus nucleus and the gigantocellular nucleus; (ii) a contralateral descending projection which for the most part targeted the same brainstem structures but with weaker terminal labelling; (iii) a projection to the contralateral dorsal midbrain with comparatively weak terminal label in the contralateral superior colliculus, intercollicular nucleus, periaqueductal gray, mesencephalic reticular formation and cuneiform area; (iv) ipsilateral ascending pathway with terminations in the red nucleus, zona incerta, peripeduncular area, parafascicular nucleus, lateral hypothalamus, parts of the pretectum and caudal thalamus.
All regions of the ventral striatum receive strong projections from the midline thalamic nuclei and from the parafascicular nucleus.
Spikes elicited by stimulation of the parafascicular nucleus (Pf) of the thalamus were extracellularly recorded in the Acc neuron of chloral hydrate-anesthetized adult Wistar rats using a glass microelectrode attached along a seven-barreled micropipette, each of which was filled with dopamine, OPC-14597, SKF 38393 (D1 receptor agonist), quinpirole (D2 receptor agonist) and 2M NaCl.
Rats with adjuvant arthritis were used as an animal model of pathological pain in this experiment and the nociceptive response of neurons in parafascicular nucleus (Pf) were recorded and intracerebroventricular (icv) injection of naloxone and atropine was adopted in order to investigate the effect of electroacupuncture (EA) and to analyze the neurotransmitters involved.
The True Blue- and Nuclear Yellow-labelled neurons wee located in different parts of the parafascicular nucleus ipsilateral to the injections. In the rostral part of the parafascicular nucleus, True Blue-labelled neurons were located ventral to the fasciculus retroflexus, and in the caudal part of the nucleus. Nuclear Yellow-labelled neurons were found mainly to encircle the fasciculus retroflexus in the rostral part of the parafascicular nucleus and in the dorsolateral sector of the caudal part of the parafascicular nucleus.
The spontaneous motor activity and locomotion initiated by electrical stimulation of the lateral hypothalamus were recorded after electrical stimulation (50-500 microA, 10-30 Hz, 0.1 ms pulses) of the frontoparietal cortex (FrPaM) and parafascicular nucleus of the thalamus (PF).
Diencephalic targets of ventral pallidal fibers are the lateral hypothalamus, the reticular nucleus of the thalamus, the mediodorsal thalamic nucleus, the dorsomedial part of the subthalamic nucleus, the medial part of the parafascicular nucleus and the lateral habenula.
The parafascicular nucleus projection to the subthalamic neurones has an excitatory synaptic effect.
This pattern was also observed in the caudal intralaminar nuclei where cerebellar label predominated in the centrum medianum (CM), while the parafascicular nucleus (Pf) primarily contained nigral label.
Rats received injections of the anterograde tracers Phaseolus vulgaris-leucoagglutinin or biocytin at multiple sites in the frontal cortex or parafascicular nucleus of the thalamus.
On the day of birth, expression of the transgene is observed in several discrete regions of the CNS; including the olfactory bulb, hippocampus, retrosplenial cortex, parafascicular nucleus of the thalamus, and several cranial nerve nuclei.
Using [ 35S]-labelled riboprobes to either the rat or human D5 receptor, this mRNA was localized to the hippocampus and the parafascicular nucleus of the thalamus.
A total of 166 neurons in parafascicular nucleus (PF) were studied, 85 from intact animals, 72 following dorsal spinal cord transection (D.Sp.C.X.), and 9 following complete transection of the spinal cord.
The inositol 1,4,5-trisphosphate receptor mRNA but not kinase mRNA was found in a majority of the neurons in the thalamus, especially in the parafascicular nucleus; hypothalamus, especially the medial hypothalamus; substantia nigra pars compacta and ventral tegmental area; superior colliculus; lateral interpeduncular nucleus and central gray.
The local glucose metabolic rate after noxious stimulation was increased in the somatosensory cortex, cingulate cortex, ventroposterior and parafascicular nucleus of the thalamus, septal area, habenular nucleus, head of caudate nucleus, periaqueductal gray (PAG) and dorsal raphe nucleus (P < 0.05). After stimulating the head of the caudate nucleus, the local glucose metabolic rate of nucleus raphe magnus (rm) and nucleus paragigantocellularis (pgcl) was increased significantly and that of the PAG and dorsal raphe nucleus had a tendency to increase, while stimulation of the head of caudate nucleus could partially abolish the increased glucose metabolic rate in the somatosensory cortex, cingulate cortex, ventroposterior and parafascicular nucleus of the thalamus, septal area and habenular nucleus as induced by noxious stimulation.
Finally, in caudal thalamus, the central portion of MD, as well as the parafascicular nucleus (Pf), contained autoradiographic label.
Ibotenic acid lesions in the parafascicular nucleus of the medial thalamus attenuated the analgesic effect of cocaine in the formalin test. These results suggest that both cocaine and the parafascicular nucleus interact with dopaminergic mechanisms that attenuate nociceptive spinal projections to the medial thalamus..
Study of the afferents of the rat globus pallidus (GP) with Fluoro-gold, a retrograde tracer, revealed retrogradely labeled neurons in the ipsilateral parafascicular nucleus of the thalamus (PF), a previously undescribed afferent of the rat GP.
Reconstruction of electrode trajectories indicated that recordings were made from the region corresponding to the lateral aspect of the mediodorsal thalamic nucleus, the central lateral nucleus, a small part of the central median nucleus, and the parafascicular nucleus.
In the host neostriatum, labeled fibers from the parafascicular nucleus (PF) arborized in a large region in the neostriatum, but avoided small patchlike areas.
The effects of PFC stimulation on spontaneous and evoked discharges of neurons of parafascicular nucleus of thalamus were observed in rats. The results suggest that PFC might have analgesia action which was accomplished by modulating electric activities of pain-related neurons of parafascicular nucleus in thalamus..
Spike generation by stimulation of the parafascicular nucleus of thalamus was extracellularly recorded in the nucleus accumbens of chloral hydrate-anesthetized adult Wistar rats using a silver-wire microelectrode attached along a seven-barreled micropipette, each of which was filled with dopamine, SKF 38393 (D-1 agonist), bromocriptine (D-2 agonist), haloperidol, SCH 23390 (D-1 antagonist) and domperidone (D-2 antagonist). Effects of dopamine receptor antagonists on the inhibition of the spike generation by conditioning stimuli applied to the ventral tegmental area preceding the test stimulus to the parafascicular nucleus and those of dopamine agonists on the test stimulus-induced spikes were examined. The parafascicular nucleus stimulation-induced spikes were inhibited by dopamine as well as D-1 and D-2 agonists and by the conditioning stimulation of the ventral tegmental area. Activation of D-1 receptors, which make probably synaptic contact with dopaminergic nerve terminals from the ventral tegmental area, is considered to result in inhibition of the neuronal activity of the nucleus accumbens neurons receiving input from the parafascicular nucleus of the thalamus.
The synaptic effect of the projection from an intralaminar thalamic structure, the parafascicular nucleus, to the subthalamic nucleus was investigated through extracellular recordings of subthalamic unit activities. Electrical stimulation of the parafascicular nucleus caused a complex response with two successive excitatory phases. These results suggest that the intralaminar parafascicular nucleus contributes to the activation of subthalamic neurons..
The lateral part of the parafascicular nucleus sends fibres predominantly to the lateral agranular field of the motor cortex and the rostral part of the parietal cortex. The medial part of the parafascicular nucleus projects rather sparsely to the dorsal part of the prelimbic cortex, the anterior cingular cortex and the medial agranular field of the motor cortex.
No analgesia was observed in other sites: centro-lateral nucleus of the thalamus, posterior thalamic nuclear group, parafascicular nucleus, bed nucleus of the stria terminalis, mesencephalic tegmentum, nucleus of the tractus solitarius, spinal trigeminal complex, and brainstem reticular formation.
We have observed the influences of opioid-like substances in preoptic area (POA) on the electric activities of pain response neurons in parafascicular nucleus of thalamus (Pf).
The lateral part of the parafascicular nucleus projects to the most lateral part of the caudate-putamen, whereas projections from the medial part of this nucleus terminate in the medial part of the caudate-putamen and in the dorsolateral part of the nucleus accumbens.
Lesions to 12 of the 37 brain sites investigated (anterior pretectal area, subthalamus, posterolateral hypothalamus, frontocingulate cortex, anterior thalamus, mediodorsal thalamus, ventromedial thalamus, parafascicular nucleus, mamillary bodies, cerebellum, olfactory bulb, and ventromedial hypothalamus) retarded puzzle-box learning.
Dense alpha-1 binding was detected in most thalamic nuclei: however, only 1 small area, the parafascicular nucleus, showed a significant increase in alpha-1 binding following repeated ECS.
They were identified by antidromic stimulation of the parafascicular nucleus and central lateral nucleus.
The results indicate that, besides a massive input from the dorsal pallidum, the STN receives substantial projections from several districts of the cerebral cortex (the medial division of the prefrontal cortex, the first motor and primary somatosensory areas, and the granular insular territory), the ventral pallidum, the parafascicular nucleus of the thalamus and the pedunculopontine tegmental nucleus, as well as a modest innervation from the dorsal raphe nucleus.
There were also smaller changes in portions of the thalamus (ventral anterior nucleus, parafascicular nucleus) and premotor cortex.
The pain-discharges of the pain-excitation neurons (PEN) in the parafascicular nucleus (Pf) were inhibited, ie, decreasing in frequency of pain-discharges and lengthening in latent period of pain-discharges.
The data showed that the pain threshold of animal was increased when septal area was stimulated by electro-acupuncture, and that electrical stimulation of septal area had a marked inhibitory effect on the pain discharges of cells in parafascicular nucleus of thalamus, lateral habenular nucleus, periaqueductal gray and dorsal raphe nucleus.
Microiontophoretic experiments were performed to determine whether inhibition mediated by the ventral tegmental area neurons of the nucleus accumbens, receiving input from the parafascicular nucleus of thalamus, is mediated by dopamine D1 or D2 receptors, using rats anesthetized with chloral hydrate. Spikes, elicited by test stimuli applied to the parafascicular nucleus were inhibited by conditioning stimuli to the ventral tegmental area, given 30 msec before the test stimuli. The reduction by conditioning stimulation of the ventral tegmental area of the mean number of spikes of the 25 neurons upon stimulation of the parafascicular nucleus, was abolished by SCH 23390. In contrast, domperidone did not affect the mean number of spikes of the 22 neurons upon stimulation of the parafascicular nucleus in the presence of conditioning stimulation of the ventral tegmental area. In addition, spikes elicited by stimulation of the parafascicular nucleus were dose-dependently inhibited by iontophoretic application of both SKF 38393, a D1 agonist and bromocriptine, a D2 agonist. These results suggest that inhibition by dopamine, derived from the ventral tegmental area of neurons of the nucleus accumbens, receiving input from the parafascicular nucleus, is mediated mainly by dopamine D1 receptors, although both D1 and D2 receptors are expressed on the same neuron of the nucleus accumbens, which is also inhibited by exogenously applied D2 agonists..
Of these, 13 were located in the ventrobasal complex (VB), 17 were located in the central lateral nucleus and the parafascicular nucleus of the intralaminar nuclei (ILN).
To investigate the mechanism of analgesia noted with electrical stimulation of the thalamic sensory relay nucleus and medial thalamus, modulations of neuronal activities in the periaqueductal gray matter (PAG) were studied in response to electrical stimulations of the ventroposterolateral nucleus (VPL) and parafascicular nucleus (Pf) and to peripheral noxious stimulations in rats.
The effect of LHb stimulation was completely abolished by a knife cut transecting the dorsal NA bundle either immediately rostral to the locus coeruleus or at the level of the parafascicular nucleus.
Thalamostriate fibers projecting to the caudate nucleus (CN) and the putamen (Put) originate from different neuronal populations; clusters of cells in the rostral ITN and in the parafascicular nucleus (PF) project to the CN, while cells in the centromedian nucleus (CM) project to the Put.
The centromedian nucleus receives more cortical projections than the parafascicular nucleus. These projections, however, are mainly directed to the centromedian nucleus and the lateral portions of the parafascicular nucleus.
The combination of autoradiographic and topographic methods in macaques reveals that nigral axons only cross through the medial part of the parafascicular nucleus and end more dorsally and anteriorly in the thalamus. Pallidal endings are scarce in the centre médian and essentially located in the lateral parafascicular nucleus.
After injection of the fluorescent dye, Fluorogold, into several areas of the cortex and corpus striatum, almost all retrogradely labeled cells in the thalamus (except in the parafascicular nucleus) expressed the CCK gene..
To investigate the mechanism of analgesic effect of electrical stimulation of the thalamic parafascicular nucleus (Pf), we studied modulations of neuronal activities in the periaqueductal gray (PAG) and the adjacent reticular formation (RF) in response to Pf electrical and peripheral noxious stimulations in the rat.
AADC-IR neurons were localized in the ventromedial part of the thalamus, lateral posterior complex, paracentral nucleus and lateral dorsal nucleus of the thalamus, medial habenula, parafascicular nucleus, subparafascicular nucleus, and periaqueductal gray.
Similar stimulation of the globus pallidus increased LGCU in the globus pallidus, substantia nigra pars reticulata and compacta, entopeduncular nucleus, subthalamic nucleus, lateral habenular nucleus, parafascicular nucleus of the thalamus, deep layers of the superior colliculus and pedunculopontine nucleus, exclusively on the ipsilateral side.
Afferent projections to the parafascicular nucleus of the rat have been mapped using the retrograde transport of unconjugated wheat germ agglutinin and immunohistochemistry using very short survival times. These results are discussed in the context of the connections of parafascicular nucleus with the motor system, particularly the basal ganglia. These indicate that the parafascicular nucleus lies at an interface between the reticular activating system on the one hand, and the motor system on the other. This result thus enlarges on present concepts of the parafascicular nucleus.
The area of the central neostriatum that receives input from both the parafascicular nucleus of the thalamus and the somatosensory cortex was identified by retrograde transport of a conjugate of horseradish peroxidase and wheat germ agglutinin (HRP-WGA). The same region of the neostriatum was studied in rats that had received multiple electrolytic lesions in the somatosensory cortex and also an injection of HRP-WGA in different parts of the parafascicular nucleus. However, even though numerous boutons labelled anterogradely by HRP-WGA from the parafascicular nucleus were found within the dendritic fields of neurons that received cortical input, none of the terminals from the thalamus made synaptic contact with these neurons. Two such neurons that received input from the parafascicular nucleus were Golgi-impregnated and appeared to be medium-size spiny neurons, but they had a lower density of spines than the typical very densely spiny neurons. An independent confirmation that the targets of thalamostriatal neurons originating in the parafascicular nucleus are dendritic shafts was provided by studying the boutons labelled following electrolytic lesioning or injection of the lectin Phaseolus vulgaris-leucoagglutinin (PHA-L) into this nucleus: these boutons were also found to form asymmetric synaptic contacts with dendritic shafts within the neostriatum. It is concluded that although afferents from the somatosensory cortex and from the parafascicular nucleus converge upon the same part of the neostriatum, they probably do not converge upon the same spiny neurons.(ABSTRACT TRUNCATED AT 400 WORDS).
The effects of thyrotropin-releasing hormone (TRH) were examined on neuronal activity in the nucleus accumbens, receiving an input from the parafascicular nucleus of the thalamus or the hippocampus, in chloral hydrate-anesthetized rats, using a microiontophoretic technique. The spikes produced by stimulation of the parafascicular nucleus were predominantly and dose-dependently inhibited during iontophoretic application of TRH. Both TRH- and dopamine-induced inhibition of the spikes induced by stimulation of the parafascicular nucleus was antagonized by simultaneous application of haloperidol. In animals treated with reserpine, inhibition of the generation of spikes upon stimulation of the parafascicular nucleus did not occur in any neurons in the nucleus accumbens during application of TRH, whereas the dopamine-induced inhibition was still observed. These results suggest that inhibitory effects of TRH on the neurons of the nucleus accumbens receiving an input from the parafascicular nucleus are mediated by dopamine released from the dopaminergic nerve terminals located in the nucleus accumbens..
Fast blue was injected into the substantia nigra (SN) while Nuclear yellow was delivered to one of the following nuclei: globus pallidus (GP), entopeduncular nucleus, subthalamic nucleus (STN) or parafascicular nucleus of the thalamus.
In the intralaminar nuclei, GABA-immunoreactive cells and terminals abounded in the dorsal portion of the paracentral and centrolateral nuclei, whereas more caudally, GABA-positive terminals pervaded the entire parafascicular nucleus.
Apomorphine 0.5 mg/kg decreased LCGU in the cingulate, parietal and occipital cortex, anteromedial and lateral thalamus and lateral habenula but increased it in laminae IV and VI of the sensorimotor cortex, in the parafascicular nucleus of the thalamus, and in some parts of the basal ganglia and related nuclei.
Alterations in local cerebral glucose utilization (LCGU) induced by electrical stimulation of the sensory relay nucleus (VPL) or parafascicular nucleus (Pf) of the thalamus in conscious rats were measured by the [ 14C]2-deoxyglucose method, the objective being to assess the mechanism of analgesia induced by electrical stimulations of these structures.
Microiontophoretic studies were performed to elucidate the acute effects of methamphetamine on the nucleus accumbens (Acc) neurons receiving input from the parafascicular nucleus (Pf) of the thalamus using rats anesthetized with chloral hydrate.
Here a distinct, varicose terminal network was seen extending caudally from an area lateral to the medial lemniscus, running medially over the medial lemniscus, traversing the parafascicular nucleus and running dorsal to the fasciculus retroflexus into the periventricular gray matter.
Electrical stimulation of one parafascicular nucleus produced further bilateral elevations of dopamine utilization in the caudate-putamen complex without altering these parameters in the substantia nigra.
Increased rates of glucose utilization were observed in the sensorimotor cortex, parafascicular nucleus, ventrolateral nucleus of the thalamus, substantia nigra, caudate nucleus, globus pallidus, red nucleus, subthalamic nucleus, cerebellar cortex and vermis.
Furthermore, in the centromedian/parafascicular complex retrograde cell labeling is seen exclusively in parafascicular nucleus on the caudate-injected side and only in the centromedian nucleus, except its lateralmost portion, on the putamen-injected side.
The parafascicular nucleus projects towards the striatum and premotor cortex.
Labelled fibres and "terminal-like" labelling were found in the anterior pretectal area, in the thalamic parafascicular nucleus, in the posterior nucleus and the ventroposterior complex, in the zona incerta and in the fields of Forel, but none were observed in the supraoptic or paraventricular nuclei.
Spike generation by hippocampal stimulation was inhibited by both LC conditioning stimulation and iontophoretic application of noradrenaline, but spikes elicited by stimulation of parafascicular nucleus of thalamus were rarely affected by LC conditioning stimulation or noradrenaline.
The contralateral anterograde labeling was less intense than the ipsilateral one and it was distributed in the anterior intralaminar structures, in the parafascicular nucleus, in the ventromedial, ventrolateral and ventrobasal nuclei and in the posterior complex, symmetrically to the labeling observed on the ipsilateral side.
In the thalamus only the parafascicular nucleus and the anterior parts of the rhomboid and reuniens nuclei were positive.
In 13 of 17 Acc neurons which failed to respond to hippocampal stimulation, the spike generation produced by stimulation of the parafascicular nucleus of thalamus was inhibited by both VTA conditioning stimulation and iontophoretically applied dopamine. These results strongly suggest that dopamine derived from VTA inhibits Acc neurons receiving input from the parafascicular nucleus of thalamus but not from the hippocampus..
The parafascicular nucleus contains two groups of large, radiate cells characterized by the presence or absence of somatic spines.
Efferent connections of the centrum medianum and parafascicular nucleus (CM-Pf complex) were investigated by the anterograde autoradiographic method in cat.
Both anatomical and physiological studies in cats substantiated the existence of a thalamus-cortex-thalamus neuronal circuit in which neurons in the centre median send fibers to wide areas of the cerebral cortex and the cerebral cortex, the motor cortex in particular, may send the fibers back to the parafascicular nucleus. On the basis of this observation it is assumed that constantly discharging corticothalamic neurons may exert a tonic excitatory influence on the pain-receiving center, parafascicular nucleus, so as to keep it in a state of constant alertness to the tissue-damaging danger signals and that the inhibitory action of the ascending fibers from centre median would serve to suspend the excitatory action of the cortex on the parafascicular nucleus, resulting in relief of pain.
Cells labeled from the striatal injections densely filled the thalamic parafascicular nucleus. Cells labeled from the medullary injections were seen ventrally to the fasciculus retroflexus in the subparafascicular nucleus.
In caudal intralaminar nuclei, caudate-labeled cells are strictly confined to parafascicular nucleus and putamen-labeled cells present only in centre median, without any overlap between the two neuronal populations.
parafascicular nucleus).
In this way, pedunculopontine projections were confirmed to the globus pallidus, entopeduncular nucleus, subthalamic nucleus, substantia nigra, parafascicular nucleus and pontine reticular formation.
On radiant heat stimulation of the sole of the hind foot of rat, the neurons in the parafascicular nucleus of thalamus would not respond until the skin temperature was raised to 45 degrees C.
Other structures, such as the parafascicular nucleus of the thalamus, were more resistant and exhibited degeneration only after four periods of thiamine deprivation.
Postmortem examination in these experimental animals showed neuronal degeneration in the basal ganglia, the parafascicular nucleus of the thalamus, and discrete nuclei of the brainstem and cerebellum.
We found that thalamic zones with multiple projections to the cerebral cortex, using the centromedian-parafascicular nucleus as a prototype, were mostly symmetric.
In addition to centromedian labeling in all animals, the parafascicular nucleus was also labeled when isotope was injected into dorsal GPi.
Also, the axospinous type IV striatal synapses, which originate in the center median or parafascicular nucleus of the the thalamus, react to interruption of their axons in the pallidum externum with the dark or crystalloid forms of degeneration.
Experiments utilizing the retrograde transport of horseradish peroxidase (HRP) were performed in order to locate the cells of origin of ascending projections to the parafascicular nucleus (Pf) of the cat.
In Acc neurons receiving input from parafascicular nucleus (Pf) of thalamus, VTA conditioning stimulation produced an inhibition of spike generation with Pf stimulation.
Among the heavily labeled nuclear groups were the the parvocellular red nucleus, the interstitial nucleus of Cajal, the nucleus of Darkschewitsch, and the caudomedial extremity of the subparafascicular nucleus. Occasional cells were also labeled in the reticular formation lateral to the interstitial nucleus of Cajal in the caudomedial parafascicular nucleus, in the nucleus of the fields of Forel, and in the central gray.
Single unit activity was recorded in 92 units in the parafascicular nucleus (PFN) of the rat.
The effects of stimulation of the sciatic nerve and ipsilateral thalamic parafascicular nucleus on the thalamic posterior nucleus have been investigated by recording both the evoked potentials (EP) and neuronal activity in guinea pigs under light chloralose or nembutal anaesthesia. Both the EP and neuronal responses to stimulation of the parafascicular nucleus had mainly short latencies (3-12 ms) and monophasic negative configuration. The inhibitory effect of conditioning stimulation of the parafascicular nucleus on somatically evoked responses was demonstrated as well..
Deep tectal input also has been shown to terminate quite extensively within the paralamellar region of the mediodorsal nucleus and in the parafascicular nucleus; very little input to the central lateral and centromedian nuclei was observed.
Male rats were subject to bilateral lesions in the parafascicular nucleus (PF) of the thalamus.
Following lesions in the lateral hypothalamic complex (LHC) which produce aphagia and adipsia as well as the injection of labeled proline into the LHC, projections were seen in the nucleus accumbens, the preoptic area, the lateral habenular nucleus, the ventromedial hypothalamic nucleus, the nucleus reuniens, the parafascicular nucleus, the posterior hypothalamus, the zona incerta, the central gray matter, the tegmentum, the substantia nigra (pars compacta), the ventral tegmental area of Tsai and the parabrachial area.
In animals with injections confined to the internal pallidal segment, retrograde label was seen in neurons of the pedunculopontine nucleus, dorsal raphe nucleus, substantia nigra, caudate, putamen, subthalamic nucleus, parafascicular nucleus, zona incerta, medial and lateral subthalamic tegmentum, parabrachial nuclei, and locus coeruleus.
Isotope injections confined to the pars reticulata (SNR) label sparse nigrostriatal fibers, and numerous nigrothalamic fibers ascending mainly to the nucleus ventromedialis and in lesser number to the parafascicular nucleus and the paralamellar zone of the nucleus mediodorsalis.
Following HRP injections confined to the areas of the VTA containing the dopamine cell groups, labelled neurons appeared in prefrontal cortex, dorsal bank of rhinal sulcus, nucleus accumbens, bed nucleus of stria terminalis, amygdala, diagonal band of Broca, substantis innominata, magnocellular preoptic area, medial and lateral preoptic areas, anterior, lateral and postero-dorsal hypothalamus, lateral habenular, nucleus parafascicular nucleus of thalamus, superior colliculus, nucleus raphe dorsalis, nucleus raphe nagnus and pontis, dorsal and ventral parabrachial nuclei, locus coeruleus and deep cerebellar nuclei.
An ipsilateral projection appears to exist to the anterior thalamic nuclei, lateral portion of the medial thalamic nucleus, parafascicular nucleus, pretectal nucleus, posterior thalamic nucleus, and deep layers of the superior colliculus.
The increase was not due to a behavioral deficiency per se as lesions in the parafascicular nucleus did impair acquisition behavior without affecting B receptors.
administration of antivasopressin serum the alpha-MPT-induced disappearance of noradrenaline was decreased in the dorsal septal nucleus, parafascicular nucleus and the rostral part of the nucleus tractus solitarii, whereas that of dopamine was lowered in the caudate nucleus and in the A2 region of the medulla oblongata.
Pain evoked unit discharges in the parafascicular nucleus could be inhibited by direct electrical stimulation of the centromedian nucleus of thalamus, with residual inhibitory effect lasting for several minutes after cessation of stimulation.
Placement of electrolytic lesions in the zona incerta or parafascicular nucleus of the rat forebrain resulted in a marked reduction of choline acetyltransferase (ChAc) activity in the head of the striatum 2-4 weeks later. Lesions of the habenula did not cause this effect implying that concomitant destruction of the fasciculus retroflexus with the parafascicular nucleus was not responsible for the effects observed. The data suggest that there is a cholinergic fiber tract connection between the parafascicular nucleus of the thalamus and the head of the striatum in the rat forebrain..
A positive correlation exists between the location and extent of the coagulation foci in the parafascicular nucleus and the appearance of degenerated boutons in the fundus striati.
After HRP injections in the medianus raphe nucleus labelled neurons appeared in the lateral habenular nucleus and parafascicular nucleus.
In addition, a smaller projection to the ipsilateral parafascicular nucleus was observed.
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