One week later, ibotenic acid or sham lesions were made in the mPFC centered on the prelimbic region (Brodmann's area 32) or the cingulate cortex (Brodmann's area 24). Lesions of area 24 did not produce deficits at either retesting period. These findings were interpreted to indicate that area 32, but not area 24, is involved in retrieval processes, rather than consolidation or storage, in that the animals were impaired at both retesting times, but were able to relearn the task.. 
Of these 59 cells, 38% were located in area 24b, another 38% were located in area 8, and the remaining cells were located in areas 24a and 25. Nociceptive neurons in the ACC were distributed in area 24 and motor related regions.
Source localization analyses at the time of maximal N450 activity revealed that MDD subjects had significantly reduced dorsal anterior cingulate cortex (dACC; Brodmann area 24/32) and left dorsolateral prefrontal cortex (Brodmann area 10/46) activation to incongruent relative to congruent trials.
Group analysis found that various brain areas of patients with congenital scoliosis showed glucose hypometabolisms in the left prefrontal cortex (Brodmann area 10), right orbitofrontal cortex (Brodmann area 11), left dorsolateral prefrontal cortex (Brodmann area 9), left anterior cingulate gyrus (Brodmann area 24) and pulvinar of the left thalamus.
Cells projecting to the orofacial and forelimb areas of M1 were distributed in the anterior cingulate cortex (area 24) but not in the posterior cingulate cortex (retrosplenial cortex; area 29), according to topographical mapping.
Here, we report an analysis of the anatomical organization of projections from anterior cingulate area 24 and motor and prefrontal cortices to areas 29a-d in the rat, using the axonal transport of cholera toxin B subunit and biotinylated dextran amine. Area 29a receives projections from rostral area 24a, area 24b, the ventral orbital area, and the caudal secondary motor area. Rostral area 29b receives projections from caudal area 24a, whereas caudal area 29b receives projections from rostral area 24a. Area 29b also receives projections from area 24b and the ventral orbital area.
SPM99 analyses, using the ACC as a region of interest, revealed clusters of increased rCBF during medial frontal TMS in Brodmann area 24 and reduced rCBF in more ventral ACC, the latter occurring in both experiments.
METHODS AND RESULTS: To address this problem, the effects of chronic ethanol self-administration in male cynomolgus monkeys on GABA(A) receptor subunit mRNA expression was studied in 3 frontal cortical fields: orbitofrontal cortex (OFC; area 13), anterior cingulate cortex (ACC; area 24), and the dorsolateral prefrontal cortex (DLPFC; area 46).
In family-positive but not family-negative subjects, striatal D(2) receptors were associated with metabolism in anterior cingulate (Brodmann area 24/25) and orbitofrontal (Brodmann area 11) and prefrontal (Brodmann area 9/10) cortices, and with personality scores of positive emotionality.
The Anterior cingulate cortex (ACC, Brodmans area 24) is implicated in the pathogenesis of schizophrenia due to its normal functions and connectivity together with reports of structural, morphological and neurotransmitter aberrations within this brain area in the disease state.
As in the macaque monkey, we found that pyramidal cells in anterior cingulate gyrus (area 24) were more branched and more spinous than those in posterior cingulate gyrus (area 23).
Monetary reward blackjack was associated with significantly higher relative metabolic rate in the primary visual cortex (Brodmann area 17), the cingulate gryus (Brodmann area 24), the putamen and prefrontal areas 47 and 10, compared to blackjack playing for points only.
We found that pyramidal cells in anterior cingulate gyrus (area 24) were more branched and more spinous than those in posterior cingulate gyrus (area 23).
area 24 (cingulate gyrus).
To assess this possibility further, we investigated capillary length densities in prefrontal cortex area 9 and anterior cingulate cortex area 24 in postmortem brains from 13 schizophrenics and 13 age- and sex-matched controls. Mean cortical thickness was significantly reduced in area 24, but not in area 9, in schizophrenics.
RESULTS: Schizophrenia patients had significant gray matter reductions in the absolute (mm(3)) volume of Brodmann's area 24 in anterior cingulate and, when corrected for brain size, in the whole cingulate and retrosplenial (areas 29-30) cortex.
The reductions in opioid receptor binding within the medial system were observed mainly in the dorsolateral (Brodman area 10) and anterior cingulate (Brodman area 24 with some extension into area 23) and insula cortices and the thalamus.
The total number of neurons and glial cells in brains of 12 schizophrenia subjects and 14 comparison subjects were determined in two subdivisions of the prefrontal cortex: Brodmann's area 24, a part of the anterior cingulate cortex, and Brodmann's area 32 in the paracingulate cortex. RESULTS: The average total of bilateral glial cells in Brodmann's area 24 was 201 x 10(6 )in subjects with schizophrenia and 302 x 10(6 )in comparison subjects, a statistically significant difference of 33%, whereas there was a nonsignificant difference between the schizophrenia subjects and the comparison subjects in total number of glial cells in Brodmann's area 32. CONCLUSIONS: A selective reduction in glial cells in Brodmann's area 24 (but not in area 32) is seen in brains of subjects with schizophrenia relative to those of comparison subjects.
Here, we report an analysis of the anatomical organization of projections from areas 29a-29d to area 24 and motor and prefrontal cortices in the rat, using the axonal transport of biotinylated dextran amine (BDA) and cholera toxin B subunit (CTb). Area 29a projects to rostral area 24a, whereas area 29b projects to caudodorsal area 24a and ventral area 24b. Caudal area 29c projects to mid-rostrocaudal area 24b, whereas rostral area 29c projects to caudal areas 24a and 24b and caudal parts of primary and secondary motor areas.
Finally, a portion of the anterior cingulate cortex (area 24) and supplementary motor area 6 demonstrated a high pain-specific response (P3).
Activation is generally confined to area 24 in the caudal ACC, and has been confirmed by subdural and intracortical recordings.
RESULTS: When we compared (18)F-FDG brain PET images of postlingually deaf patients with those of age- and sex-matched healthy control subjects by performing a t test at every voxel, the glucose metabolism of deaf patients was significantly (P < 0.001) lower than that of the control subjects in both anterior cingulate gyri (Brodmann area 24 [ BA24]) and superior temporal cortices (BA41, BA42) and in the right parahippocampal gyrus.
Considering the physiologic characteristics and fiber connections, the SI and SII cortices appear to be involved in somatosensory-discriminative pain, and the anterior cingulate cortex (area 24) in the affective-cognitive aspect of pain.
In anterior cingulate area 24, [ (3)H]N/OFQ and N/OFQ-stimulated [ (35)S]GTPgammaS binding were highest in layers V and VI. The cellular localization of ORL-1 receptors and activated G-proteins in area 24 was examined using two strategies: ibotenic acid injection into the cortex or undercut lesions to remove afferent axons, followed by autoradiography.
There was a highly significant correlation between CDR scores and regional LB scores in the entorhinal cortex and area 24. LB densities in area 24 could explain 25.2% of this variability. These results imply that an assessment of LB pathology limited to the entorhinal cortex and area 24 may be sufficient to predict cognition in PD.
For four out of five subjects, it was located at the border of the caudal division of left anterior cingulate cortex (area 24/32') with left posterior cingulate cortex (area 23/31).
In subjects with schizophrenia, but not bipolar disorder, apoD levels were significantly elevated in the amygdala (42.8%) and thalamus (31.7%), while in bipolar disorder, but not schizophrenia, additional increases were detected in the parietal cortex (Brodmann Area 40; 123%) and the cingulate cortex (Brodmann area 24; 57.7%).
Subjects with short reaction times showed significantly more ACC activation (Brodmann area 24) and an increased error rate.
In separate experiments, pseudorabies virus (PRV) was injected into one of the three different cytoarchitectonic regions that comprise the medial prefrontal cortex: infralimbic (Brodmann area 25), prelimbic (Brodmann area 32), and cingulate (Brodmann area 24) cortical areas.
In cingulate cortex, the highest [ 3H]imipramine and [ 3H]paroxetine B(max) values were noted in Brodmann area 33 followed by area 24, while postsynaptic 5-HT(2A) receptors were mainly distributed through Brodmann areas 23 and 29.
RESULTS: Patients with depression had a statistically significant 32% smaller medial orbitofrontal (gyrus rectus) cortical volume, without smaller volumes of other frontal regions including anterior cingulate Brodmann's area 24 (subgenual gyrus), anterior cingulate Brodmann's area 32, subcallosal gyrus (Brodmann's area 25), or whole brain volume.
Lesions of the anterior cingulate cortex (area 24) did not affect EB conditioning in a trace paradigm.
Midcingulate area 24' and posterior cingulate area 29 had overall lower binding in each layer. In contrast, DAMGO-stimulated [ (35)S]guanosine-5'-O-(gamma-thio)-triphosphate (GTPgammaS) binding in area 24' was similar to that in area 24, whereas area 29 had low and homogeneous binding. Anti-DBH-saporin reduced [ (3)H]DAMGO binding in layer I of area 24; DAMGO-stimulated [ (35)S]GTPgammaS binding was unchanged in areas 24' and 29.
Patients with bipolar disorder showed a substantial decrease in laminar thickness and neuron densities in layers III, V, and VI of the subgenual part of area 24, whereas patients with major depression were comparable to controls.
In this paper we review the literature and present a new study investigating synaptic abnormalities in the anterior cingulate cortex (area 24) in the Stanley Foundation brain series.
RESULTS: The patients with better responses showed hyperactivity (higher theta activity) in the rostral anterior cingulate (Brodmann's area 24/32).
Significant elevations in SERT were measured in the orbitofrontal gyrus (Brodmann area 11), the anterior portion of the insular cortex and the cingulate gyrus (Brodmann area 24) in CO and ED victims.
Here are presented the results of a series of electrophysiological investigation of the focus of localization in the supracallosal (area 24) and infracallosal (area 25) part of the anterior cingulate gyrus of evoked potentials of maximal amplitude and minimal latent period to stimulation of pelvic, splanchnic and sciatic nerves. It was shown that evoked potentials of maximal amplitude and minimal latent periods to stimulation of viscero-somatic nerves are recorded in the supragenual area 24 in comparison with the infragenual area 25 of the anterior limbic cortex. In a series of microelectrophysiological studies of reactions of neurons of area 24 and 25 it was established that the reactivity of neurons of area 24 is higher than that of area 25. All these data indicate to the leading role of area 24 in reception and treatment of viscero-somatic afferent signals. Study of characteristics of influence of dorsal (area 24) and ventral (area 25) regions of rostral limbic cortex on bioelectrical activity of two postganglionic sympathetic nerves-inferior cardiac and vertebral branches of stellate ganglion, innervating coronary vessels and vessels of anterior extremities correspondingly, showed that stimulation of ventral area 25 evoked increase of electrical activity of the two sympathetic nerves and reliable increase of systemic arterial pressure, while stimulation of dorsal area 24 evoked decrease of tonic activity of the two sympathetic nerves and reliable decrease of systemic arterial pressure. In the paper are presented also the results of microelectrophysiological investigation of peculiarities of reactions of inspiratory and expiratory neurons of bulbar respiratory center to high frequency stimulation of area 24 and 25--in case of stimulation of dorsal area 24 the prevailing effect is suppression of spike activity of neurons, of stimulation of ventral, infragenual area 25 the prevailing influence is excitatory. In another series of microelectrophysiological experiments it was shown downward blocking inhibitory influence of dorsal supragenual area 24 of anterior limbic cortex on activity of vagal viscerosensory neurons of bulbar solitary tract nucleus. It is concluded that the strictly connected one another areas 24 and 25 of limbic cortex are functionally differentiated: the infra-limbic cortex is mainly a viscero-motor cortex, while the prelimbic area 24 plays a leading role in reception and treatment of viscero-somatic afferent information..
Many lines of evidence implicate the anterior cingulate cortex (ACC, Brodmann's area 24) and parasylvian cortex in pain perception.
Terminals of corticorubral axons originating from ipsilateral primary motor area 4 (the densest projection), the supplementary motor area, cingulate area 24, area 8, and posterior parietal area 5, were each mapped in the parvocellular red nucleus.
This study investigated whether chronic schizophrenia is associated with glial changes in 3 regions of the cerebral cortex: dorsolateral prefrontal cortex (Brodmann's area 9), the superior temporal gyrus (area 22), and the anterior cingulate gyrus (area 24). In area 24 the same trend was evident, but the results did not reach significance.
As for mPFC ablation, the lesioned area involved the agranular precentral region (Brodmann's area 8), the anterior cingulate cortex (Brodmann's area 24) and the prelimbic area (Brodmann's area 32).
In the patients, the greatest reductions in normalized, relative glucose metabolism after sleep deprivation were observed in the anterior cingulate cortex (Brodmann area 24), and they persisted after recovery sleep and antidepressant treatment.
Non-PTSD subjects activated anterior cingulate (area 24) to a greater degree than PTSD patients.
001) in Brodmann's area 24 of the anterior cingulate cortex (ACC).
The anterior cingulate cortex (area 24) is innervated by a group of DA neurons primarily located between these laterally and medially concentrated populations.
These results demonstrate that there is significant direct nociceptive input to the human anterior cingulate gyrus (Brodmann's area 24)..
The latter comparisons and correlation analysis indicated a wide range of active regions including bilateral prefrontal, inferior parietal and premotor cortices and thalamic responses, contralateral hippocampus, insula and primary somatosensory cortex and ipsilateral perigenual cingulate cortex (area 24) and medial frontal cortex (area 32).
For the nonspatial rule, performance of the evaluation task led to a learning-related increase in rCBF in a caudal and ventral part of the premotor cortex (PMvc, area 6), bilaterally, as well as in the putamen and a cingulate motor area (CM, area 24) of the left hemisphere.
The exact location of this activation varied from subject to subject, but was typically in the posterior part of area 24.
Specifically, neocortical activations were observed in the right anterior cingulate gyrus (Brodmann area 24), in the intraparietal sulcus of right posterior parietal cortex, and in the mesial and lateral premotor cortices (Brodmann area 6)..
This method has been applied to the anterior cingulate (ACCx; Brodmann area 24) and prefrontal (PFCx: Brodmann area 10) cortices from a cohort of 15 normal control and 10 schizophrenic cases.
All neurons were in area 24 of the ACCx.
In the present study, indirect immunocytochemistry with an antibody against PV was performed on serial sections of human anterior cingulate cortex (Brodmann's area 24), an important relay centre of the limbic system. area 24 contains two densely immunolabelled neuropil bands in layers III and Vb.
in some postmortem brain structures of the dopaminergic system: the substantia nigra, ventral tegmentum area, prefrontal cortex (area 10), anterior cingulate cortex (area 24), the head of the caudate nucleus in schizophrenia and age-matched controls without mental disorders.
The present studies employed experimental techniques to remove afferent axons or classes of projection neurons from rat ACC area 24 followed by coverslip autoradiography to localize changes in binding of [ 3H]Tyr-D-Ala-Gly-MePhe-Gly-ol (DAMGO) to mu receptors and 2-[ 3H]D-penicillamine-5-D-penicillamine-enkephalin (DPDPE) to delta receptors. Removal of all afferents to area 24 with undercut lesions did not alter DPDPE binding, but significantly reduced binding of DAMGO in layers I, III, and V. To explore the distribution of postsynaptic receptors, immunotoxin lesions were made in area 24 by injection of OX7-saporin into the caudate and/or thalamic nuclei. It is proposed that opioidergic circuits in area 24 are organized according to an input/output model for mu opioid regulation.
The present study compares the time-course and tempo of neurogenesis and synaptogenesis in the anterior cingulate cortex (area 24 of Brodmann) and in the primary visual cortex (area 17) in a series of pre- and postnatal rhesus monkeys. Autoradiographic analysis of animals fetally injected with 3H-thymidine showed that all neurons destined for area 24 are generated by embryonic day 70, which is 30 days earlier than in area 17. The rapid phase of synaptogenesis in area 24 starts during the third embryonic month and continues at the same rate through the remainder of gestation and the first 2 months after birth, as has been seen in neocortical areas examined previously. Statistical analysis of the linear portions of the rapid phase indicates that, although neurogenesis in area 24 is completed 1 month earlier than in area 17, the rapid phase of synaptogenesis occurs 41 days later. After the second postnatal month, synaptic density in area 24 remains at a high level until sexual maturity.
Areas 33 and 25 have poor laminar differentiation, and there are three parts of area 24: area 24a adjacent to area 33 and partially within the callosal sulcus has homogeneous layers II and III, area 24b on the gyral surface has the most prominent layer Va of any cingulate area and distinct layers IIIa-b and IIIc, and area 24c in the ventral bank of the CS has thin layers II-III and no differentiation of layer V. There are four caudal divisions of area 24. area 24c' is caudal to area 24c and has densely packed, large pyramids throughout layer V. area 24c' g is caudal to area 24c' and has the largest layer Vb pyramidal neurons in cingulate cortex.
For example, the premotor area 6 can be distinguished from prefrontal areas by its high concentration of adrenergic alpha 1 receptors as labelled with [ 3H] prazosin, with only the cingulate area 24 showing higher values.
Spindle neurons are restricted to the subfields of the anterior cingulate cortex (Brodmann's area 24), exhibiting a greater density in anterior portions of this area than in posterior portions, and tapering off in the transition zone between anterior and posterior cingulate cortex. Furthermore, a majority of the spindle cells at any level is located in subarea 24b on the gyral surface.
The affect division includes areas 25, 33 and rostral area 24, and has extensive connections with the amygdala and periaqueductal grey, and parts of it project to autonomic brainstem motor nuclei.
A recent positron emission tomography (PET) study demonstrated that the anterior cingulate cortex (area 24), in addition to SI and SII cortices, was activated by painful stimuli. In order to elucidate the participation of relay nuclei in the ascending pain pathway to area 24, we performed a regrograde labelling study with WGA-HRP injection into area 24 in cats. area 24 was found to receive pain-related thalamic inputs from the intralaminar nuclei including the central medial nucleus, midline nuclei, modiodorsal nucleus and possibly the submedial nucleus. Although more Fos positive cells were observed in area 24 in experimental than in control cats, the difference was not significant. Our findings suggest that the demonstrated response of area 24 on PET scan represents stress- and emotion-related events rather than pain.
The present study was attempted to study ipsilateral corticocortical connections of the anterior part (area 24) of the cingulate cortex of the macaque monkey by means of wheat germ agglutinin-conjugated peroxidase (WGA-HRP) method.
Both groups displayed highly significant differences in responses to painful heat compared with non-painful heat in the thalamus, anterior cingulate cortex (area 24), lentiform nucleus, insula, and prefrontal cortex.
Fibers from the anterior CiG (area 24) passed through the anterior portion of the CC while those from the posterior CiG (area 23) passed through the posterior portion of the CC..
These cell types are similar to those previously found in the more dorsal anterior cingulate cortex (area 24) and frontal eyefields (area 8).
The dorsal portions of area 32, and all of area 24 were, however, devoid of these projections.
The profile of cortical and subcortical activation during performance of freely selected joystick movements relative to stereotyped movements was abnormal in ALS patients: (i) ALS patients with a normal fluency score showed significantly (P < 0.01) attenuated rCBF responses in comparison with controls in the left medial prefrontal cortex (Brodmann area 10) and the right and left parahippocampal gyri; (ii) ALS patients with impaired verbal fluency showed significantly (P < 0.01) attenuated rCBF responses in comparison with controls in the right and left medial prefrontal cortex (areas 9 and 10), the rostral aspects of the right anterior cingulate cortex (areas 24 and 32), the right parahippocampal gyrus and the anterior thalamic nuclear complex; (iii) ALS patients with impaired verbal fluency showed significantly (P < 0.01) attenuated rCBF responses in comparison with patients with normal verbal fluency in the right parahippocampal gyrus, the anterior thalamic nuclear complex and the rostral anterior cingulate cortex (area 24).
Comparison of the increase in rCBF caused by freely selected joystick movements over the resting state between the two groups of subjects showed significantly (P < 0.001) greater activation in ALS patients in the ventral third (face area) of the contralateral primary sensorimotor cortex and in the adjacent contralateral ventral premotor and parietal association cortices; significantly (P < 0.01) greater activation of the contralateral anterior insula and the ipsilateral anterior cingulate cortex (dorso-caudal area 24) was also present in ALS patients.
Single-unit responses in area 24 of cingulate cortex were examined in halothane-anesthetized rabbits during stimulation of the skin with transcutaneous electrical (TCES, 3-10 mA), mechanical (smooth or serrated forceps to the dorsal body surface or graded pressures of 100-1,500 g to the stabilized ear) and thermal (> 25 degrees C) stimulation. Most nociceptive cingulate units were in dorsal area 24b in layers III (n = 35), II (n = 13), or V (n = 9). Cortical knifecut lesions were made in five rabbits to determine if the responses in area 24 were dependent on lateral or posterior cortical inputs.
An additional motor representation was found in the dorsocaudal part of area 24 (24d). The excitability threshold of area 24d is higher than that of F1 and F3. Evoked movements were occasionally observed also after stimulation of area 24c.
The present data showed also that area 24 is formed by four subareas: 24a, b, c and d. Areas 24a and b occupy the ventral part of area 24, whereas its dorsal part is formed by area 24c, located rostrally, and area 24d, located caudally. The following features distinguish area 24d from area 24c: (1) larger pyramidal cells in layer V, (2) presence of medium-size pyramidal cells in the lower part of layer III, (3) more prominent columnar pattern, (4) higher myelinization with the presence of an evident horizontal plexus.
Electrolytic lesions encompassing anterior and posterior cingulate cortex (area 24 and 29) or ibotenic acid lesions in area 24 only were made prior to avoidance conditioning wherein rabbits learned to step in response to a tone conditional stimulus (CS+) in order to avoid a brief, response-terminated 1.5 mA. Activity was also recorded in area 29 in the rabbits with area 24 lesions. Learning in rabbits with combined lesions was severely impaired and it was moderately retarded after lesions in area 24. Early-, but not late-developing training-induced unit activity in area 29c/d was absent in rabbits with area 24 lesions, indicating that area 24 is a source of early-developing area 29 plasticity. These results are consistent with hypotheses of a theoretical working model, stating that: a) learning depends on the integrity of two functional systems, a mnemonic recency system comprised by circuitry involving area 24 and the MD nucleus and a mnemonic primacy system comprised by circuitry involving area 29 and the anterior thalamic nuclei; b) corticothalamic information flow in these systems suppresses thalamic CS elicited activity in trained rabbits; c) corticostriatal information flow is involved in avoidance response initiation. An absence of rhythmic theta-like neuronal bursts in area 29b in rabbits with area 24 lesions is attributable to passing fiber damage..
On the basis of horseradish peroxidase and fluorescent dye injections, LM projects primarily to area 29 and posterior area 24. The midregion of LM also projects to caudal area 24.
The majority of cortical neurotensin fibers was observed in the anterior cingulate cortex (Walker's area 24) and adjacent medial prefrontal regions (areas 6 and 32). In area 24, the fiber density was similar to that in the nucleus accumbens.
Electron microscopic morphometric study of synaptic contacts on dendritic spines and shafts was performed in layer II of the anterior cingulate cortex (area 24) of autopsy brain of paranoid schizophrenics (n-5), manic-depressive patients (MDP) (n-2) and controls (n-7).
The most rostral portion of the medial subcallosal fasciculus, located in the lateral angle of the frontal horn (extremely deep to Broca's area), contains projections from the cingulate gyrus (area 24) and the supplementary motor area, to the caudate nucleus.
DA afferents were densest in the anterior cingulate (area 24) and the motor areas (areas 4, 6, and supplementary motor area [ SMA]).
The results revealed that the orbital frontal, medial prefrontal, and temporal polar proisocortices have substantial projections to both the dorsomedial and medial pulvinar nuclei, whereas the anterior cingulate proisocortex (area 24) projects exclusively to the dorsomedial nucleus.
In the cingulate cortex, labeled cells were observed in area 25, area 32, and rostral levels of area 24; fewer cells were observed at caudal levels of area 24 or in area 23.
Autoradiographic cases indicated that area 24c received input from the insula, parietal areas PG and PGm, area TG of the temporal pole, and frontal areas 12 and 46. Additionally, caudal area 24 was the recipient of area PG input but not amygdalar afferents.
area 24 has three divisions of which area 24a is adjacent to the callosal sulcus and has the least laminar differentiation. area 24b has more clearly defined layers II, III, and Va, and area 24c, which forms the lower bank of the anterior cingulate sulcus, has a particularly dense layer III. Most input to premotor cingulate area 24c appeared to originate in VA, MDdc, and Li.
The frequency of multi-unit neuronal firing in response to tonal conditional stimuli increases, and the neuronal responses become discriminative in character, in the anterior and posterior subfields of the cingulate cortex (Brodmann's area 24 and 29, respectively) during the course of discriminative avoidance conditioning in rabbits. Yet, available data indicate that the subicular projection reaches only Area 29, not area 24. Here we test the hypothesis that the subicular influence attains area 24 via a synaptic relay in Area 29. The results showed in keeping with the hypothesis, that bilateral aspirative or electrolytic lesions in Area 29 eliminated the training-induced neuronal responses in area 24. As in the case of subicular lesions, the Area 29 lesions increased the amplitude of the macropotentials in area 24.
The distribution of the prosomatostatin-derived peptides (PSDP), somatostatin-28 and somatostatin-28(1-12), in the cynomolgus monkey (Macaca fascicularis) neocortex was characterized in quantitative immunohistochemical studies of 3 visual areas (V1, primary visual cortex; V2, the adjacent visual association area; and AIT, a visual association area in anterior inferior temporal cortex), 2 auditory areas (AI, primary auditory cortex; and T1, an adjacent auditory association area) and anterior cingulate cortex (area 24). area 24, the most densely labeled area, had nearly 6 times as many PSDP-immunoreactive neurons as V1. Both auditory areas contained approximately two-thirds the number of PSDP-immunoreactive neurons found in area 24; however, both had nearly 4 times as many immunoreactive neurons as V1. Both the supra- and infragranular layers were densely labeled in area 24 and Area T1, however, in AI, V1, V2, and AIT the infragranular layers were relatively sparsely labeled.
The loss of nLC neurons was found to correlate significantly with norepinephrine concentration, choline acetyltransferase (ChAT) activity, and numbers of plaques and tangles on Brodmann area 24 (cingulate); ChAT and plaque counts in area 21 (temporal); and with ChAT activity in area 10 (frontal).
Two main dopaminergic (DA) subpopulations reach the medial cortex of the rat: 1) a deep one, first detected in the anterior frontal cortex on day 16 of embryonic life, was well developed at birth and extended caudally in layer V and/or layer VI toward the splenium of corpus callosum; 2) a superficial one was detected in layer I of the anterior cingulate cortex (area 24) on postnatal day 3 to 5 and invaded layer III from day 6 to 14.
Reciprocal corticocortical connections were observed primarily with the supplementary motor area (SMA) in medial premotor area 6 and dorsal bank of the cingulate sulcus, postarcuate area 6 cortex, dorsal cingulate cortex (area 24), superior parietal lobule (area 5, PE/PEa), and inferior parietal lobule (area 7b, PF/PFop, including the secondary somatosensory SII region).
Unique 'error' potentials were observed in the anterior cingulate cortical area 24 during a transitional learning-stage when the animals were uncertain about fulfilling the required task appropriately.
area 24 (anterior cingulate) had the greatest density of immunoreactive cell bodies (148 +/- 14/mm2), area 9 was of intermediate density (109 +/- 13/mm2), and area 46 was the least dense (83 +/- 12/mm2).
Field potentials in cingulate cortex (area 24) produced by electrical stimulation of the mediodorsal thalamic nucleus were diminished by iontophoretic ejection of the cholinergic agonist, carbachol.
Several characteristics of the dopaminergic innervation were similar to that of the superficial anterior cingulate cortex (area 24): the laminar distribution to the superficial I-III layers, the secondarily developed varicose aspect in catecholamine fluorescence histochemistry and the delayed postnatal ingrowth in contrast with the early prenatal dopaminergic input to the prefrontal cortex.
The postnatal development of the dopaminergic input to the rat anterior cingulate cortex (area 24) was followed using anti-tyrosine hydroxylase immunocytochemistry and catecholamine fluorescence histochemistry in control and noradrenaline-depleted rats. The superficial cingulate dopaminergic field extended into the pregenual part of area 24b.
In contrast, binding in area 24 was homogeneous, with only a 14% variation.
The projections from the medial parietal cortex (areas PEc and PGm) are similar to those of the superior parietal lobule but they tend to concentrate in the more rostral part of dorsal area 6, MII, and in the cingulate gyrus (area 24). The middle inferior parietal lobule (areas PFG and PG) projects to the ventral part of area 46 and area 8, whilst the posteriormost inferior parietal lobule (caudal PG and area Opt) is connected with both dorsal and ventral area 46, dorsal area 8, as well as the anteriormost dorsal area 6, and the cingulate gyrus (area 24)..
Those fibers from area 24 of the cingulate gyrus are directed to the premotor and prefrontal regions as well as area 23 and retrosplenial cortex.
area 24 connections: Afferents to area 24 originate primary from cingulate areas 25 and 29 and visual area 18b and medial area 17. Efferent projections of area 24a are distributed within cingulate cortex, while area 24b has more extensive projections to posterior cingulate and visual cortices. area 24b is the cingulate subdivision which is both the primary recipient of visual cortex afferents as well as the source of most of the projections of anterior cingulate cortex to visual areas.
Lesions were placed in the rat anterior thalamus (nucleus mediodorsalis and nucleus anteromedialis) known to project to the cingulate cortex (area 24). The results suggest that in the area 24 of the rat the thalamic afferent fibres terminate at both these pyramidal neurons.
Afferents from the mediodorsal thalamic nucleus terminate in area 24. Quantitative analysis of degenerating axon terminals in area 24 indicates that there may be as many as seven times more callosal than mediodorsal thalamic terminals in this cortex.
area 24, for example, projects to the premotor region (areas 6 and 8), the fronto-orbital cortex (area 12), the rostral part of the inferior parietal lobule, the anterior insular cortex, the perirhinal area and the laterobasal nucleus of amygdala.
The anterior cingulate gyrus (area 24) is related to the intralaminar, mediodorsal, and ventral anterior thalamic nuclei, the amygdala, and the nucleus accumbens septi.
The lateral segment projects to the anterior cingulate area (area 24) and the medial precentral area on the dorsomedial shoulder of the hemisphere, while the central segment projects to the ventral agranular insular area in the dorsal bank of the rhinal sulcus, and to a lateral part of the orbital cortex further rostrally.
Projections from this area were observed to terminate in the rostral portions of the temporal lobe (areas TA, TE and TG) and cingulate gyrus (area 24), the insular cortex, and some dorsolateral prefrontal areas.
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