To study the temporal changes in the sensory contents of associative memory without motivational and emotional contents, we induced memory for acoustic frequency by pairing a tone with stimulation of the cholinergic Nucleus basalis. They next received three days of training consisting of a conditioned stimulus (CS) tone (8.00kHz, 70dB, 2s) either Paired (n=5) or Unpaired (n=5) with weak electrical stimulation ( approximately 48muA) of the Nucleus basalis (100Hz, 0.2s, co-terminating with CS offset). 
The present study examined the expression of the immediate-early gene c-fos in different brain regions following a single 20-min session of unilateral electrical stimulation of the Nucleus basalis magnocellularis (NBM).
Converging lines of evidence have supported a role for the Nucleus basalis magnocellularis (NB) in attentional mechanisms; however, debate continues regarding the role of the medial septum in behavior (MS).
Animals in pre-treatment groups received one of five types of diet during four weeks prior Nucleus basalis Magnocellularis (NBM) electrical lesion normal diet (0), 10 g soy with isoflavone (10), 20 g soy with isoflavone (20), 10 g soy without isoflavone (-10) and 20 g soy without isoflavone (-20) in 30 g daily diet.
Results: The highest levels of this splice form were found in the hypothalamic supraoptic nucleus (SON), pontine nuclei, medulla oblongata, gray matter of the spinal cord, the hippocampus, glomeruli of the cerebellum, the Nucleus basalis of Meynert (NBM), and the tuberomamillary nucleus (TMN).
Loss of cholinergic neurons in the Nucleus basalis of Meynert in Alzheimer's disease (AD) patients was one of the first discoveries of neuron loss in AD.
beta-AP(1-40) was injected into Nucleus basalis magnocellularis (NBM).
The present study addressed the question of whether inhibition of calpain can prevent neuronal cell death and associated behavioral deficits in a disease-relevant animal model, which is based on excitotoxic lesions of the cholinergic Nucleus basalis magnocellularis of Meynert. Excitotoxic lesions of the Nucleus basalis with NMDA induced a markedly impaired performance in the novel object recognition test.
Intense AdipoR1 immunostaining was observed in neurons of lateral hypothalamic area and of Nucleus basalis of Meynert (NBM).
The roles of the basolateral amygdala and Nucleus basalis magnocellularis in fear conditioning reconsolidation were investigated by means of tetrodotoxin bilateral inactivation performed 96 h after conditioning, immediately after reactivation training. Nucleus basalis magnocellularis functional inactivation does not affect memory post-reactivation phase of any of the three conditioned fear responses.
METHOD: Bilateral infusions of Ibotenic acid (IBO) into Nucleus basalis of Meynert (NBM) using hamilton syringe and stereotaxic apparatus were adopted to establish the rat model of AD.
Previous research has demonstrated that Nucleus basalis magnocellularis (nbm) corticopetal cholinergic neurons modulate anxiety-like states, but cortical modulation by these neurons during anxiety-like states has not been characterized.
Abeta in the anterior cingulate gyrus, entorhinal cortex, amygdaloid complex and Nucleus basalis of Meynert is also associated with dementia as is tau in the CA2 sector of the hippocampus.
Many studies from our laboratories have demonstrated that circuitry that includes the amygdala central nucleus (CeA), the cholinergic neurons in the substantia innominata/Nucleus basalis region and their innervation of the posterior parietal cortex is critical for this surprise-induced enhancement of attention in learning.
We have evaluated the "cholinergic-memory" hypothesis by pairing a tone with stimulation of the Nucleus basalis (NB), which provides acetylcholine to the cerebral cortex. These findings indicate that NB-induced specific associative behavioral memory requires the action of intrinsic acetylcholine at muscarinic receptors, and supports the hypothesis that natural memory formation engages the Nucleus basalis and muscarinic receptors..
A lesser density of hFF2 neurons was identified in the ventromedial hypothalamic nucleus, lateral and posterior hypothalamic areas whereas few cells were visualized in the paraventricular hypothalamic nucleus, perifornical nucleus, horizontal limb of the diagonal band, ventral division of the bed nucleus of the stria terminalis, Nucleus basalis of Meynert and ventral tegmental area.
Very high to high binding also occurs in brain regions associated with the development of Alzheimer's disease (Nucleus basalis of Meynert, substantia innominata).
To test this hypothesis, we compared the Na,K-ATPase activity (Vmax/Km parameters) in aged rats with those in young rats with brain cholinergic dysfunction induced by electrolytic-, kainic acid-lesioned Nucleus basalis magnocellularis (NBM) or by intracerebroventricular AlCl_{3} administration.
Previous studies have demonstrated that corticopetal cholinergic lesions applied to the Nucleus basalis magnocellularis and substantia innominata (NBM/SI) attenuate operant suppression induced by aversive events.
A main characteristic of emotion-related brain regions (orbitofrontal cortex, anterior cingulated cortex, amygdala, insula) is their reciprocal anatomical connectivity with each other as well as with neuromodulatory systems (e.g., serotonergic dorsal raphe, cholinergic Nucleus basalis of Meynert, and dopaminergic ventral tegmentum) and with other brain areas involved in sensory, motor, and cognitive functions.
Towards achieving this goal, we are currently developing CERE-110, an adeno-associated virus-based gene delivery vector that encodes for human NGF, for stereotactic surgical delivery to the human Nucleus basalis of Meynert.
METHODS: Cholinergic lesions were produced by administration of the selective immunotoxin 192 immunoglobulin G-saporin into the lateral ventricles, the medial septum, or the Nucleus basalis magnocellularis.
Lesion of the Nucleus basalis magnocellularis (nbm) is a suitable approach to study cognitive deficit and behavior alterations involving cholinergic dysfunction, which is associated with the major types of dementia.
A depletion of cholinergic interneurons in the dorsal and ventral striatum, and cholinergic projection neurons in the Nucleus basalis is observed and is ascribed to an early and persistent defect in cholinergic neuron differentiation.
The aim of present work was the evaluation of the effects on brain levels of nerve growth factor (NGF) and of its high-affinity tyrosine kinase A receptor (TrkA), induced in rats unilaterally lesioned at Nucleus basalis magnocellularis (NBM), by treatment with choline pivaloyl ester (CPE).
The Nucleus basalis (NB) provides acetylcholine (ACh) to the cerebral cortex. These results are concordant with a memory-promoting role for the Nucleus basalis that places it "downstream" of motivational systems, which activate it to initiate the storage of the current state of its cholinergic targets..
Selective immunotoxic cholinergic lesions in the Nucleus basalis magnocellularis (NBM) impair visuospatial attention performance in a 5-choice serial reaction time task (5-CSRT task).
BACKGROUND: Fibers containing galanin (GAL) enlarge and hyperinnervate cholinergic basal forebrain (CBF) Nucleus basalis (NB) neurons in late-stage Alzheimer's disease (AD), yet the physiological consequences of this phenomenon are unclear.
In animals treated with saline, IA acquisition increased CO activity in the medial prefrontal cortex, the prelimbic cortex, and the medial mammillary body, and diminished it in the medial septum and the Nucleus basalis of Meynert with respect to animals exposed only to the IA apparatus.
This immunotoxin induced a loss of choline acetyltransferase-positive neurons in the medial septum (-82%) and in the Nucleus basalis (-55%).
BACKGROUND: It is well established that Nucleus basalis magnocellularis (NbM) lesions impair performance on tests of sustained attention.
The Nucleus basalis magnocellularis (NBM) is known to be involved in the memorization of several conditioned responses.
NADPH-diaphorase positive neurons were registered in the basal forebrain-medial septal nucleus (MS), the nuclei of the diagonal band of Broca (VDB, HDB), substancia innominata (SI) and the Nucleus basalis of Meynert (B).
BACKGROUND: Dysfunction of basocortical cholinergic projection neurons of the Nucleus basalis (NB) correlates with cognitive deficits in Alzheimer disease (AD). Nucleus basalis neurons receive cholinergic inputs and express nicotinic acetylcholine receptors (nAChRs) and muscarinic AChRs (mAChRs), which may regulate NB neuron activity in AD.
RESULTS: The most affected regions were the substantia nigra (SN; in 100% of cases) followed by the Nucleus basalis of Meynert (NBM) in 98.5%.
Neuromodulation is required for cortical plasticity, but it is uncertain how subcortical neuromodulatory systems, such as the cholinergic Nucleus basalis, interact with and refine cortical circuits. Pairing sensory stimulation with Nucleus basalis activation shifted the preferred stimuli of cortical neurons by inducing a rapid reduction of synaptic inhibition within seconds, which was followed by a large increase in excitation, both specific to the paired stimulus. Although Nucleus basalis was stimulated only for a few minutes, reorganization of synaptic tuning curves progressed for hours thereafter: inhibition slowly increased in an activity-dependent manner to rebalance the persistent enhancement of excitation, leading to a retuned receptive field with new preference for the paired stimulus.
In this paper, we present fate-mapping data on Nkx2.1-lineage neurons throughout the telencephalon, including the cerebral cortex, amygdala, olfactory bulb, striatum, globus pallidus, septum, and Nucleus basalis..
In addition, an increase in Fos-positive cells was detected in the substantia innominata/Nucleus basalis and the CN at the time of surprise.
Of the labelled cell bodies in the subcortical structures, about 38.8% were located in the ipsilateral basal forebrain (10.6% in the lateral amygdala LA, 11.5% in the globus pallidus GP, 3.7% in the ventral pallidum VPa, 13.0% in the Nucleus basalis NB), 13.1% in the ipsi- and contralateral diencephalon (6.4% in the posterior paraventricular thalamic nuclei, 6.7% in the hypothalamic area), and 48.1% in the midbrain (20.0% in the ipsilateral substantia nigra, 9.8% in the ipsi- and contralateral ventral tegmental area, 5.0% in the ipsi- and contralateral locus coeruleus, 13.3% the ipsi- and contralateral dorsal raphe nuclei).
The role of cholinergic Nucleus basalis (of Meynert) and the reticular thalamic nucleus in mechanisms of the generation spontaneous spike-and-wave discharges (SWDs) was investigated in the WAG/Rij rat model of absence epilepsy. Selective lesions were affected by local unilateral intraparenchymal infusions of immunotoxin 192 IgG-saporin and cholinotoxin AF64A to the Nucleus basalis and the rostral pole of reticular thalamic nucleus. Injections of 192 IgG-saporin into the Nucleus basalis increased the number of spontaneous SWDs, while injections in the reticular thalamic nucleus were not effective. Thereby, a loss of cholinergic activity in the Nucleus basalis stimulates the appearance of SWDs. At the same time, AF64A infused into reticular thalamic nucleus, besides the reduction of choline acetyltransferase immunoreactive neurons within contralateral Nucleus basalis, produced some unspecified lesion of adjacent neuronal tissue, resulted in decrease of number and duration of SWDs as well as in spectral changes in EEG. Considering that the Nucleus basalis is an important source of cortical and thalamic cholinergic afferentation, we conclude that cholinergic excitatory input from this structure is important in the control of SWDs in the WAG/Rij rat model of absence epilepsy..
OBJECTIVES: We examined the influence of 5-HT6 receptor ligands upon social memory in rats by use of systemic or local administration into the frontal cortex (FCX), striatum, or Nucleus basalis magnocellularis (NBM).
We have established that in addition to "target-derived" NGF neurotrophic stimulation, cholinergic neurons also respond dose-dependently, to intra-parenchymal NGF administration in the somato-dendritic region of the Nucleus basalis, thus illustrating the potential of alternative reparative therapies which would by-pass the undesirable effects of diffuse neurotrophin application.
Cholinergic Nucleus basalis (NB) neurons provide the major cholinergic innervation to the cortical mantle, are selectively vulnerable in late stage Alzheimer's disease (AD) and require the neurotrophin, nerve growth factor (NGF) and its receptors (TrkA and p75(NTR)), for their survival.
The corticopetal cholinergic projections were lesioned by intraparenchymal infusion of 192 IgG-saporin into the Nucleus basalis magnocellularis of adult rats.
Initial studies to demonstrated that 4OH-GTS-21 is likely brain permeant based on its ability to improve passive avoidance and Morris water task behaviors in Nucleus basalis-lesioned rats.
(1) Huperzine A, a promising therapeutic agent for Alzheimer's disease (AD), was tested for its effects on cholinergic and monoaminergic dysfunction induced by injecting beta-amyloid peptide-(1-40) into Nucleus basalis magnocellularis of the rat. (2) Bilateral injection of 10 mug beta-amyloid peptide-(1-40) into Nucleus basalis magnocellularis produced local deposits of amyloid plaque and functional abnormalities detected by microdialysis.
Rats were submitted to injection of 192 IgG-saporin in the medial septum/diagonal band of Broca complex and the Nucleus basalis magnocellularis.
Aspiration lesion of the medial septal area (MS) including the vertical limb of the diagonal band nucleus (DBN) caused increased latency to the onset of convulsions, whereas damage to the Nucleus basalis magnocellularis (NBM), nucleus accumbens, or both MS and NBM did not cause anticonvulsant effects.
Moreover, the number of cholinergic neurons in the Nucleus basalis magnocellularis (NBM) was examined.
Previous research demonstrated that repeated pairing of Nucleus basalis (NB) stimulation with a tone results in plasticity in primary auditory cortex (A1), mimicking the changes observed after classical conditioning.
192IgG-saporin (SAP) was used to selectively destroy cholinergic neurons in the rostral basal forebrain (e.g., medial septum (MS) and vertical limb of the diagonal band of Broca (VDB)) and/or the caudal basal forebrain (e.g., Nucleus basalis magnocellularis (NBM)) of ovariectomized Sprague-Dawley rats.
We investigated the effect of the acetylcholinesterase inhibitor donepezil administered subcutaneously in a rat model of partial unilateral cortical devascularization that induces a loss of the cortical cholinergic terminal network and a retrograde degeneration of the cholinergic projections that originate in the Nucleus basalis.
The Nucleus basalis cholinergic system is sufficient both for the induction of ARP and for the induction of specific auditory memory, including control of the amount of remembered acoustic details.
In the present article, the effects of lesions that disconnected CeA from the cholinergic substantia innominata/Nucleus basalis magnocellularis (SI/nBM) on performance are examined in a modified 5-choice serial reaction time (5CSRT) task, thought to assess selective or sustained attention.
Previous studies showed that a circuit including the amygdala central nucleus (CEA) and the cholinergic substantia innominata/Nucleus basalis magnocellularis (SI/nBM) is important for both sustained attention guiding action in a five-choice serial reaction time (5CSRT) task and for enhanced new learning about less predictive cues in a serial conditioning task.
Neuronal degeneration of cholinergic Nucleus basalis Meynert (NBM) neurons promote rest-activity disturbance and Sundowning in Alzheimer's disease.
The six topics presented in this paper are: (i) unattached presynaptic terminals in cerebellar neuroblastoma; (ii) neurofibrillary tangle formation in the Nucleus basalis of Meynert ipsilateral to a massive cerebral infarct; (iii) orderly arrangement of tumor cells in leptomeningeal carcinomatosis; (iv) interface between craniopharyngioma and brain tissue; (v) neurofibrillary tangles and Lewy bodies in a single neuron; and (vi) Cu/Zn superoxide dismutase positive Lewy body-like hyaline inclusions in anterior horn cells in familial motor neuron diseases.
Here we demonstrate that increasing receptive field size in primary auditory cortex by repeatedly pairing a train of tones with Nucleus basalis (NB) stimulation increases synchronization, and decreasing receptive field size by pairing different tone frequencies with NB stimulation decreases synchronization.
Previous functional investigations in rats failed to demonstrate that the classical cholinesterase inhibitor, physostigmine, can compensate for cortical cholinergic deficit induced by deafferentation from the Nucleus basalis magnocellularis (NBM).
In addition, unbiased stereological estimates of the number of choline acetyltransferase (ChAT) immunopositive neurons in the medial septal/diagonal band (MS/DB) and Nucleus basalis of Meynert (NBM) also reveal a selective cholinergic dysfunction: In PTD-treated rats a significant loss of ChAT-immunopositive cells was found only in the MS/DB, but not in the NBM.
Following acquisition of ODLS, animals were lesioned bilaterally in the Nucleus basalis magnocellularis (nBM) using either quisqualic acid (QUIS) or 192 IgG-saporin (SAP).
The Nucleus basalis cholinergic system is sufficient both for the induction of ARPs and the induction of specific auditory memory.
Although cholinergic neurons in the Nucleus basalis of Meynert are a major source of cholinergic projections for the cerebral cortex, it is unclear whether cortical neurons exhibit intrinsic CHT1 activity that is altered in AD.
This firing behavior is linked to muscarinic activation of a calcium-sensitive non-specific cation current and can be mimicked by stimulation of cholinergic afferents that originate from the Nucleus basalis of Meynert (n.
METHODS: As a measure of cholinergic function, we assessed choline acetyltransferase (ChAT) activities in the frontal and temporal neocortices and the immunocytochemical distribution of ChAT and p75 neurotrophin receptor (P75(NTR)) by in vitro imaging in the Nucleus basalis of Meynert of CADASIL subjects. RESULTS: ChAT activities were significantly reduced by 60% to 70% in frontal and temporal cortices of CADASIL cases, as were ChAT and P75(NTR) immunoreactivities in the Nucleus basalis.
Experiment 1 examined the effects of electrical stimulation of Nucleus basalis magnocellularis (NBM) on a relational odor-association task--the social transmission of food preference (STFP).
We compared selective cholinergic denervation by administration of the immunotoxin 192 IgG-saporin in the Nucleus basalis of Meynert (NBM) with intracerebroventricular (ICV) lesions of the basal forebrain in male rats 7 days after lesioning.
In addition to the area of the suprachiasmatic nucleus (SCN), a number of novel sites, including the paraventricular nucleus (PVN), periventricular nucleus, supraoptic nucleus (SON), sexually dimorphic nucleus, the diagonal band of Broca, the Nucleus basalis of Meynert, infundibular nucleus, ventromedial and dorsomedial nucleus, tuberomamillary nucleus, mamillary body, and paraventricular thalamic nucleus were observed to have neuronal MT1 receptor expression.
However, degeneration of the cholinergic neurons in the Nucleus basalis of Meynert may have an important contribution to the cognitive decline.
In addition, neurofibrillary tangles (NFTs) were found in the frontal, temporal, insular, and cingulate cortices, Nucleus basalis of Meynert, and locus coeruleus, and to a lesser degree, in the dentate nucleus, cerebellum, hippocampus, and amygdala.
In rats with ibotenate-induced lesions of the Nucleus basalis magnocellularis (NBM) or prenatally exposed to methylazoxymethanol (MAM), SL65.0155 (1 mg/kg/day, i.p.) administered for 7 days, improved the learning and memory capacity in animals tested in shuttle-box active avoidance and radial maze tests.
The subunit composition of NMDA-R of cholinergic cells in the Nucleus basalis has not yet been investigated. Here, by means of choline acetyl transferase and NR2B or NR2C double staining, we demonstrate that mice express both the NR2C and NR2B subunits in Nucleus basalis cholinergic cells. Our results show that the NR2C by NR2B subunit exchange in mice affects ACh content in two target areas of the Nucleus basalis..
Local infusions of ACEA (150 nm) or R(+)-methanandamide (mAEA; 1 microm), another CB1-r agonist, in the TMN augmented histamine release from the TMN, as well as from two histaminergic projection areas, the Nucleus basalis magnocellularis and the dorsal striatum.
A selective cholinergic lesion, induced by injection of the immunotoxin 192-IgG-Saporin into the Nucleus basalis magnocellularis, failed to alter the density of 5-HT6 receptor mRNA or protein expression in the deafferentated frontal cortex, suggesting that 5-HT6 receptors are not located on cholinergic neurons.
The highest RAD irradiation (mSv x year(-1)) occurred in the decreasing order of magnitude: amygdala (Amy) >> hippocampus (Hip) > temporal lobe (Tem) approximately = frontal lobe (Fro) > occipital lobe (Occ) approximately = parietal lobe (Par) > substantia nigra (SN) >> locus ceruleus (LC) approximately = Nucleus basalis (NB); generally more RAD accumulated in the proteins than lipids of gray and white (gray > white) brain matter.
The aim of this study was to investigate the role of cholinergic pathways from the Nucleus basalis of Meynert in mediating MK-801-induced neurotoxicity. Cholinergic projections from the Nucleus basalis of Meynert were lesioned by focal injection of 192-IgG-saporin (80 ng), which after 7 days reduced the number of cholinergic cell bodies by 70% in the lesioned nucleus compared to the uninjected nucleus. These results demonstrate that cholinergic neurones in the Nucleus basalis of Meynert play an important role in the heat shock response to NMDA antagonist-induced neurotoxicity but also reveal an unexpected divergence between the heat shock response and the pathophysiological response.
Local infusion of DKK1 in rats caused neuronal cell death and astrocytosis in the CA1 region of the hippocampus and death of cholinergic neurons in the Nucleus basalis magnocellularis.
Our paper on loss of neurons in the Nucleus basalis of Meynert (now considered part of the cholinergic basal forebrain) in Alzheimer disease (AD) stimulated scientific interest in this little studied brain region.
We report that neonatal handling results in increased number of choline-acetyl transferase immunopositive cells in the septum/diagonal band, in both sexes, while no such effect was observed in the other cholinergic nuclei, such as the magnocellular preoptic nucleus and the Nucleus basalis of Meynert.
Here we microinjected into the Nucleus basalis magnocellularis of rat brains aggregates of an Src homology 3 domain and the N-terminal domain of the prokaryotic HypF, neither of which is associated with amyloid disease.
Aromatase activity is increased in the Nucleus basalis of Meynert during aging and in Alzheimer's disease (AD), making the gene (CYP19), at 15q21.1, a potential candidate risk factor.We examined 18 single nucleotide polymorphisms spanning the 5'-untranslated region and the entire coding region of CYP19 in 227 patients with AD and 131 control spouses.We found that the gene region could be divided into two haplotype blocks; a haplotype in block 1 and a haplotype in block 2 increased the risk of developing the disease by twofold in APOE 4 carriers.
McNaught and colleagues reported recently that systemic administration of proteasome inhibitors PSI (Z-Ileu-Glu(OtBu)-Ala-Leu-CHO) or epoxomicin recapitulated many of the degenerative changes seen in Parkinson's disease including loss of striatal dopamine and cell loss in the substantia nigra, locus ceruleus, dorsal motor nucleus of the X cranial nerve, and Nucleus basalis of Meynert.
The aim of the present work was the assessment of the effects produced on the electroencephalographic (EEG) activity and the cognitive and memory performances of Nucleus basalis magnocellularis (NBM)-lesioned or aged rats by the combined treatment with [ 2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium 2,2-dimethylpropionate (choline pivaloyl ester) (CPE) and the Cholinesterase inhibitors (ChEIs) Tacrine (THA) and Galantamine (GAL).
Behavioral and pharmacological challenges using methamphetamine (MAP-0.5 and 1.0 mg/kg, i.p.), haloperidol (HAL-0.12 mg/kg, i.p.), and sulfated cholecystokinin octapeptide (CCK-0.05 and 0.1 mg/kg, i.p.) were used to evaluate the effects of excitotoxic lesions of cholinergic cell bodies in the medial septal area and the Nucleus basalis magnocellularis, radiofrequency lesions of the fimbria-fornix, and aspiration lesions of the frontal cortex on interval timing in rats trained on a 40-s peak-interval procedure. Results demonstrated that lesions of the Nucleus basalis magnocellularis and frontal cortex selectively reduced the modulatory control of clock speed which is likely mediated by dopamine D(2) receptors located on cortico-striatal neurons..
In 7-month-old TgCRND8 mice, the extracellular cortical acetylcholine levels in vivo, the number and morphology of cholinergic neurons in the Nucleus basalis magnocellularis and the ability to acquire an inhibitory avoidance response in the step-down test were studied. Choline acetyltransferase immunoreactivity in the Nucleus basalis magnocellularis was significantly decreased.
This article reports here on the influence of the static magnetic fields (MFs), locally applied to the brain area, on Na, K-ATPase activity in the rat with lesioned Nucleus basalis magnocellularis (NBM) by intracerebral injection of 5 microl, 1% AlCl3 into the nucleus.
Stimulation of the cholinergic Nucleus basalis (NBs) paired with a preceding tone induces CS-specific associative memory. Thus, a low level of acetylcholine released by the Nucleus basalis during learning is sufficient to induce associativity whereas a higher level of release enables the storage of greater experiential detail.
Previous reports from our laboratories demonstrated that circuitry, including the amygdala central nucleus (CeA), the cholinergic neurons of the substantia innominata/Nucleus basalis region, and their innervation of the posterior parietal cortex, is critical to these surprise-induced enhancements of attention in associative learning.
Previous research has suggested that cholinergic neurons in the Nucleus basalis magnocellularis and substantia innominata (NBM/SI) may be important in mediating aversive states.
The authors tested the hypothesis that the cholinergic Nucleus basalis magnocellularis (NBM) is involved in solving problems requiring cognitive flexibility.
Cholinergic neurons were cultivated in organotypic brain slices of the Nucleus basalis of Meynert and treated with conditioned medium derived from BCEC, supplemented with different protective factors.
In this study, we examined the metabolic activity of Nucleus basalis of Meynert (NBM) neurons in individuals clinically diagnosed with no cognitive impairment (NCI, n = 8), mild cognitive impairment (MCI, n = 9), and subjects with moderate Alzheimer disease (AD, n = 7).
A series of reports from our laboratories demonstrated that these surprise-induced enhancements of stimulus associability depend on circuitry that includes the amygdala central nucleus (CeA), the cholinergic neurons in the sublenticular substantia innominata/Nucleus basalis magnocellularis (SI/nBM), as well as certain cortical projections of these latter neurons.
Neurofibrillary degeneration in the Nucleus basalis and a loss of its cortical cholinergic projections are prominent components of the neuropathology in Alzheimer's disease (AD).
Thus, because the dysfunction of cholinergic system that project to the cerebral cortex from Nucleus basalis of Meynert (nbM) would be implicated in the memory function deficits in Alzheimer's disease (AD), evaluating cholinergic function may be useful for the early detection of AD. In this study, because the Nucleus basalis magnocellularis (NBM) in rats is equivalent to nbM in human, we investigated the change in cholinergic receptors in the frontal cortex of rats with unilateral lesion to the NBM to find an appropriate index for the early detection of AD using techniques of nuclear medicine.
Dysfunction of cholinergic basal forebrain (CBF) neurons of the Nucleus basalis (NB) is a cardinal feature of Alzheimer's disease (AD) and correlates with cognitive decline.
OBJECTIVE: The goal of this study was to elucidate the effect of neurospheres (NS) on dementia in the mouse model of Nucleus basalis of Meynert (NBM) lesion.
Cholinergic projections from the Nucleus basalis play a critical role in cortical plasticity. To assess whether N-methyl-d-aspartate receptors mediate the increase in GluR1 and spine density resulting from cholinergic deafferentation, we examined the effect of N-methyl-d-aspartate receptor blockade on Nucleus basalis lesion-induced upregulation of GluR1 and dendritic spines. Rats received unilateral sham or 192 IgG saporin lesions of the Nucleus basalis. GluR1 expression was increased after Nucleus basalis lesion, but this increase was prevented with MK-801. Similarly, Nucleus basalis-lesioned animals had significantly higher spine densities, and this effect was also prevented by treatment with MK-801.
In addition, a population of mixed large and small nNOS positive cells was found in the medial septum, diagonal band and Nucleus basalis overlapping the distribution of the magnocellular cholinergic system of the basal forebrain. However, a considerable number of large perikarya in the diagonal band and Nucleus basalis appeared to be single labeled for nNOS.
Results revealed a shift in the ratio of three-repeat tau (3Rtau) to four-repeat tau (4Rtau) mRNAs within individual human cholinergic basal forebrain (CBF) neurons within Nucleus basalis (NB) and CA1 hippocampal neurons during the progression of AD, but not during normal aging.
Neuromodulation via the cortical release of acetylcholine by the Nucleus basalis (NB) is hypothesized to be sufficient to induce specific, associative behavioral memory. Previously, we found that tone paired with stimulation of the Nucleus basalis (NBs) for 3000 trials over 15 days induced such memory, supporting the hypothesis.
The cholinergic basal forebrain is divided into four subregions (Ch1-4), and cholinergic neuronal loss in the Nucleus basalis of Meynert (Ch4) has been correlated with cognitive impairments in both Alzheimer's disease (AD) and dementia with Lewy bodies (DLB).
Galanin (GAL)-containing fibers enlarge and hyperinnervate remaining cholinergic basal forebrain (CBF) neurons within the anterior Nucleus basalis (NB) in late-stage Alzheimer's disease (AD).
Brain lesions (electrolitically, by kainic acid, with AlCl, and with 6-OHDA); stimulations (electrical, magnetic, or pharmacological); or restoration of some neurological functions (thermoregulatory and behavioral) by fetal graft allotransplantations in bilaterally lesioned anterior hypothalamic area (AHA-immune regulation) and Nucleus basalis magnocellularis (NBM-experimental AD) in our studies were designed to reproduce immune and cognitive deficits induced by lesions of these brain structures.
In the present study we analysed the neuroprotective effect of the L-type voltage-dependent calcium channel antagonist verapamil on cholineacetyltransferase (ChAT)-immunoreactive neurons in the cerebral cortex of rats with bilateral electrolytic lesions of the Nucleus basalis magnocellularis (NBM).
Furthermore, administration of FK962 (0.032-3.2 mg/kg, i.p.) significantly ameliorated memory deficits in passive avoidance task in animal models: scopolamine-treated rats, Nucleus basalis magnocellularis-lesioned rats and aged rats. FK962 (0.01- 1) mg/kg, i.p.) significantly improved spatial memory deficits induced by Nucleus basalis magnocellularis-lesion in water maze task.
The cholinergic neurons of the basal forebrain, including those in the medial septum, and in the vertical limbs of the diagonal band of Broca and the Nucleus basalis of Meynert, provide a major source of cholinergic enervation of the cortex and hippocampus.
Therefore, we lesioned the cholinergic corticopetal projections by local infusion of 192 IgG-saporin into the Nucleus basalis magnocellularis of rats.
The purpose of this paper is to study the basic pharmacological action of sarsasapogenin, a sapogenin from the Chinese medicinal herb Rhizoma Anemarrhenae, (abbreviated as ZMS in this paper), on learning ability and memory of three animal models: aged rats and two neurodegeneration models produced either by single unilateral injection of beta-amyloid 1-40 (Abeta1-40) plus ibotenic acid (Ibot A) or by bilateral injection of Ibot A alone into Nucleus basalis magnocellularis.
Quantitative and qualitative measurements of TrkA protein levels in the cortex and Nucleus basalis of aged rats that had been well-characterized behaviorally as 'unimpaired', 'mildly impaired' or 'fully impaired' demonstrated significant changes in TrkA expression.
Limited data indicate that the numbers of Nucleus basalis, locus coeruleus, and dorsal raphé neurons and the density of neurotransmitter receptors are not reduced in the majority of cases.
Rats were lesioned at either 3 or 17 months of age by injection of 192 IgG-saporin immunotoxin into the medial septum and the Nucleus basalis magnocellularis, and they were then tested on a range of behavioral tasks: a nonmatching-to-position task in a T-maze, an object-recognition task, an object-location task, and an open-field activity test.
Ibotenic acid was injected bilaterally into the Nucleus basalis of rats, which were distributed into three groups.
The auditory cortex (AC) is the major origin of descending auditory projections and is one of the targets of the cholinergic basal forebrain, Nucleus basalis (NB).
BACKGROUND: Alzheimer's disease (AD) leads to a degeneration of the Nucleus basalis of Meynert and thus to decreased cholinergic tonus in the brain.
Under anesthesia, cortical activation was elicited with electric stimulation of cholinergic nuclei (pedunculopontine tegmental in the brainstem and/or Nucleus basalis in the basal forebrain).
In the present series of experiments, we determined the possible contribution of apoptotic processes and other pathologic cascades to the degeneration of the cholinergic neurons of the Nucleus basalis of Meynert (NBM) in AD.
Alzheimer's disease is characterized by the degeneration and loss of cholinergic neurones in the Nucleus basalis Meynert, located within the substantia innominata at the ventral surface of the basal forebrain. An in vivo measure of morphological changes in the Nucleus basalis Meynert would be of high relevance to better understand the structural correlate of cholinergic dysfunction in Alzheimer's disease. When matching the locations of signal reductions in the in vivo MRI to the template of basal nuclei based on the postmortem brain, signal intensity was decreased in areas corresponding to anterior lateral and anterior medial Nucleus basalis Meynert and increased in the third ventricle, the transverse fissure and the optic tract in patients with Alzheimer's disease compared with controls. The reduction of the signal intensity in an area corresponding to the anterior lateral Nucleus basalis Meynert was significantly correlated with reduced grey matter concentration in the bilateral prefrontal cortex, inferior parietal lobule and cingulate gyrus.
In controls NFT were confined to the entorhinal cortex whereas in drug users they were also found in the subiculum, temporal neocortex, Nucleus basalis of Meynert and the locus coeruleus.
Nerve cell loss was most extensive in dorsal motor nucleus of the vagus nerve, substantia nigra and Nucleus basalis of Meynert.
It has long been recognised that Alzheimer's disease (AD) patients present an irreversible decline of cognitive functions as consequence of cell deterioration in the forebrain cholinergic projection system (FCPS), particularly, in a structure called Nucleus basalis of Meynert (nbM).
The lesion of the cholinergic neurons of the basal forebrain, especially of the Nucleus basalis magnocellularis (nbm) of rodents, has been the most utilized method for obtaining these models.
lesions of the Nucleus basalis of Meynert, the origin of cholinergic projections to the cortex underlying memory processes); and transgenic models, which are intended to reproduce some of the neuropathological hallmarks of Alzheimer's disease.
Choline-acetyl transferase-immunoreactive neurons were found in a position corresponding to the mammalian cholinergic cell-group (Ch4-group), which therefore may be homologous to the Nucleus basalis of Meynert.
Guanosine 5'-(gamma-[ 35S]thio)triphosphate basal binding in Nucleus basalis of Meynert and thalamic nuclei was increased in the vehicle treated group.
In the present study, we explore the issue of the primary site of action of estrogens by studying the regulation of expression of genes that characterize mature cholinergic neurons, i.e., choline acetyltransferase, trkA, and p75(NTR) in the medial septum and the Nucleus basalis complex.
After one month of separately pairing Nucleus basalis stimulation with 2 and 14 kHz tones, a greater proportion of A1 neurons responded to frequencies below 2 kHz and above 14 kHz. Neural response latencies were increased across the frequency map when Nucleus basalis stimulation was associated with asynchronous activation of the high and low frequency regions of A1. This set of changes did not occur when pulsed noise bursts were paired with Nucleus basalis stimulation.
Dysfunction of nerve growth factor (NGF) and its high (TrkA) and low (p75NTR) affinity receptors has been suggested to underlie the selective degeneration of the Nucleus basalis (NB) cholinergic cortical projection neurons in end stage Alzheimer disease (AD).
The 2 patients' brains revealed abundant tau pathology in the hippocampus and basal ganglia, whereas tau and alpha-synuclein aggregates coexisted only in the Nucleus basalis of Meynert, the only region where alpha-synuclein was present.
In this study, we used proteomic techniques to examine the regional in vivo protein oxidation induced by Abeta(1-42) injected into the Nucleus basalis magnocellularis (NBM) of rat brain compared with saline-injected control at 7 days post-injection.
We sought to determine the changes in the cholinergic pathways, which project from the Nucleus basalis of Meynert (nBM) and travel in the subinsular region, in vascular dementia of the Binswanger type (VDBT) and Alzheimer's disease (AD).
Rats were lesioned at 3 months of age by injection of the 192 IgG-saporin immunotoxin into the medial septum area and the Nucleus basalis magnocellularis, and then tested at different times after surgery (from days 7-500) on a range of behavioral tests, administered in the following order: a nonmatching-to-position task in a T-maze, an object-recognition task, an object-location task, and an open-field activity test.
Previously, we demonstrated that plasticity of frontal cortex is altered in aging rats: lesions of the Nucleus basalis magnocellularis (NBM) produce larger declines in dendritic morphology in frontal cortex of aged rats compared to young adults.
In cholinergic perikarya and dendrites of the Nucleus basalis magnocellularis (NBM), aging is associated with a decrease of the density of m2R at the plasma membrane and in the cytoplasm, suggesting a decrease of the total number of m2R in the somato-dendritic field.
We tested the hypothesis that activation of Nucleus basalis magnocellularis (NBM), which provides cholinergic input to cortex, facilitates motor control.
Compared to sham-operated controls at 19 days after injury, injured rats given either progesterone or any of three doses of allopregnanolone had equivalent numbers of ChAT-positive cells in the Nucleus basalis magnocellularis.
Cholinergic dysfunction is related to loss of cholinergic interneurons in the striatum, compounded by reduced inputs into the circuits from other cholinergic nuclei, such as the pedunculopontine nucleus and Nucleus basalis of Meynert.
In the present study we aimed at determining for the first time whether metabolic changes would also occur in vascular dementia (VD) patients in the supraoptic (SON), infundibular (INF), tuberomamillary (TMN), medial mamillary nuclei, vertical limb of the diagonal band of Broca (VDB), and Nucleus basalis of Meynert.
Electrical stimulation of the cholinergic Nucleus basalis (NB) enables plasticity in A1 that parallels natural learning and is specific to acoustic features associated with NB activity.
Magnetic resonance imaging (MRI) showed hemorrhagic infarcts in the head of the right caudate nucleus and the right basal forebrain of the medial septal nucleus, diagonal band of Broca and Nucleus basalis of Meynert.
Many regions contained equivalent amounts of both the VDR and 1alpha-OHase, however the macrocellular cells within the Nucleus basalis of Meynert (NBM) and the Purkinje cells in the cerebellum expressed 1alpha-OHase in the absence of VDR.
the vertical limb of the diagonal band of Broca (VDB) and the Nucleus basalis of Meynert (NBM), and in a number of hypothalamic nuclei, i.e.
Donepezil, a primarily central acetylcholinesterase inhibitor, could potentiate learning in subjects with stroke by amplifying cholinergic input to the cerebral cortex from the Nucleus basalis of Meynert.
The present work aimed 1) to evaluate whether an increase in galanin or galanin receptors could be induced in the Nucleus basalis magnocellularis (nbm) by degeneration of the basalocortical neurons from the cortex and 2) to analyze the consequences of such an increase on cortical activity.
In situ hybridization histochemical studies with human and rat brain sections revealed the presence of this mRNA in discrete neuronal (and possibly glial) cells of the substantia nigra, locus coeruleus, cortex, hippocampus, hypothalamus, thalamus, motor nuclei, Nucleus basalis, raphe nucleus, and other brain regions.
Alzheimer's disease (AD) is associated to a gradual loss of attention and memory that have been associated to impairment of brain cholinergic neurotransmission, particularly a deficit of cholinergic neurons in the Nucleus basalis of Meynert.
In the present study, adult male rats were subjected to bilateral injections of 192 IgG-saporin either into the septum (Sp), the Nucleus basalis magnocellularis (Nbm), both structures (SpNbm) or i.c.v.
We have previously reported that the alpha2-adrenoceptor antagonist dexefaroxan protects against the degeneration of Nucleus basalis magnocellularis (NbM) cholinergic neurons following cortical devascularization in the adult rat.
Because SCN neurons do not express TrkA, NGF might have exerted its effects either through direct signalling of the neurons via p75NTR or by enhancing the activity of the cholinergic afferents to the SCN, which arise from the Nucleus basalis magnocellularis (NBM).
Carbachol significantly increased [ (35)S]GTPgammaS binding in the vertical and horizontal limbs of the diagonal band of Broca, medial and lateral septum, and Nucleus basalis (B)/substantia innominata (SI).
Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder mainly characterized by degeneration of dopaminergic neurons in the substantia nigra and the ventral tegmental area, in combination with a varying loss of central noradrenergic (locus coeruleus), cholinergic (Nucleus basalis of Meynert) and serotonergic (dorsal raphe nuclei) integrity, leading to a multitude of motor and non-motor behavioral disturbances. PD-related dopaminergic deficiency in the nucleus caudatus and mesocortical areas (due to degeneration of projections from the substantia nigra and ventral tegmental area) and cholinergic deficiency in the cortex (due to degeneration of ascending projections from the Nucleus basalis of Meynert), combined with additional Alzheimer-pathology and cortical Lewy bodies, may greatly contribute to dementia.Current treatment of dementia in PD is based on compensation of the profound cholinergic deficiency.
All PD-brains showed AS-positive lesions in medullary, pontine and mesencephalic nuclei, with involvement of the Nucleus basalis (90.1%), limbic cortex (58.9%), cingulate cortex (46%), amygdala, CA 2/3 hippocampal region (36.2%), neocortex (28.8%), and striatum (11%). AS-positive lesions in AD showed decreasing incidence from midbrain (24-28%), limbic cortex and amygdala (17-18%), Nucleus basalis and medullary nuclei (13-17%), cingulate cortex (12%), CA 2/3 region (8%) to neocortex (2%), without gender differences or relationship to the severity of AD pathology (mean Braak stage 5.1).
In adult rats injected into the Nucleus basalis with preaggregated Abeta(1-42) we investigated glia reaction, the induction of inducible nitric oxide synthase (iNOS), the activation of p38 mitogen-activated protein kinase (p38MAPK) pathway and the number of choline acetyltransferase (ChAT)-positive neurons and, in naive rats we investigated, by microdialysis, cortical extracellular levels of nitrite.
Degeneration of cholinergic Nucleus basalis (NB) cortical projection neurons is associated with cognitive decline in late-stage Alzheimer's disease (AD).
In the present study, we compared the effects of these antipsychotic drugs on the expression of nerve growth factor (NGF) as well ChAT the in the rat cortex and Nucleus basalis of Meynert (NBM) in an effort to determine the underlying mechanism for the differential drug effects observed previously.
Histological examination disclosed neuronal loss with astrocytosis and the appearance of the Lewy bodies in the Nucleus basalis of Meynert, substantia nigra, locus ceruleus, and dorsal vagal nucleus.
We investigated whether an aqueous extract of Polygala tenuifolia Willd (PTW) could improve the rats' memory and behavioral disorders produced by lesioning Nucleus basalis magnocellularis (NBM) in rats. Two 0.5 microL injections were made in the vicinity of the bilateral side of the Nucleus basalis magnocellularis (NBM).
We show that in vivo D3 binds to TrkA receptors and affords a significant and long-lived phenotypic rescue of the cholinergic phenotype both in the cortex and in the Nucleus basalis.
At this age, the animals were subjected to a neurotoxic challenge by unilateral infusion of 60 mM of the glutamate analogue N-methyl-D-aspartate (NMDA) into the Nucleus basalis magnocellularis (NBM).
This study assessed the role of the Nucleus basalis magnocellularis (NBM) in specific memory phases of two-way active avoidance conditioning.
The electroencephalographic (EEG) effects of two choline pivaloyl esters, [ 2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium iodide (1) and [ 2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium 2,2-dimethylpropionate (2), were evaluated in scopolamine-treated or Nucleus basalis magnocellularis (NBM) lesioned rats.
Cortex cerebri and hippocampus were selectively cholinergically denervated by intraparenchymal injections of 192 IgG-saporin into Nucleus basalis magnocellularis and the medial septum/diagonal band of Broca, respectively.
Other work in our laboratory revealed the existence of a novel inward rectifier K+ channel (KirNB), which is located in cholinergic neurons of the Nucleus basalis (NB) and possesses unique single-channel characteristics.
This plasticity depends on the integrity of the cortical cholinergic innervation, which originates at the Nucleus basalis magnocellularis (NBM).
In addition, neurodegeneration occurred in the locus coeruleus, dorsal motor nucleus of the vagus, and the Nucleus basalis of Meynert.
Lesions were performed by microinjection of the cholinergic toxin 192 IgG-saporin into the Nucleus basalis magnocellularis.
Previously, we demonstrated that plasticity of frontal cortex is altered in aging rats: 3 months after surgery, excitotoxic lesions of the Nucleus basalis magnocellularis (NBM) produce larger declines in dendritic morphology in frontal cortex of aged rats relative to young adults.
In this study, we selectively inhibited PP2A by injection of okadaic acid (OA) into the Meynert Nucleus basalis of rats. We found that injection of OA induced hyperphosphorylation of tau and NF and decreased acetylcholine (ACh) level in the Nucleus basalis of Meynert.
In our present studies, we confirmed our previous results where change the levels of neuropeptides and peptidases in ibotenic acid (IBO) infusion into the rat Nucleus basalis magnocellularis, an animal model of AD.
The present study was performed to explore the role of oxytocin (OT) in spatial learning and memory in the Nucleus basalis of Meynert (NBM) of rats.
This question was addressed with thioflavin-S histofluorescence to identify neurofibrillary tangles (NFT) and two tau antibodies (AT8, Alz-50) to identify pre-tangle cytopathology in the Nucleus basalis, the source of cortical cholinergic innervation. NFT and AT8 (or Alz-50) immunostaining in cholinergic Nucleus basalis neurons existed even in the cognitively normal subjects. The percentage of tauopathy-containing Nucleus basalis neurons was greater in the cognitively impaired and showed a significant correlation with memory scores obtained 1-18 months prior to death.
Furthermore, the number of immunolabeled cholinergic neurons projecting to this region of cortex from the Nucleus basalis was also reduced by 50 +/- 6%. In contrast, neuronal number was strikingly preserved in an adjoining prefrontal cortical region also associated with working memory, area 46, and in the component of the Nucleus basalis projecting to this region.
We tested the hypothesis that efferents from the Nucleus basalis magnocellularis (NBM) play a direct role in the regulation of neuropeptide synthesis and expression by neurons of the rat suprachiasmatic nucleus (SCN).
Rats with selective lesions of the Nucleus basalis magnocellularis (NBM) and sham-lesion control animals were tested in an operant appetitive-to-aversive transfer task.
The cholinergic hypothesis states that cholinergic neurons of the basal forebrain Nucleus basalis magnocellularis (nbm) that project to cortical and amygdalar targets play an important role in memory.
Subsequent histological analyses of brain tissue were conducted to determine quantitatively the neuronal losses in both the mediodorsal nucleus of the thalamus (MDN) and the Nucleus basalis magnocellularis (NBM).
Quantitative immunofluorescence for either ChAT or the low-affinity p75 neurotrophin receptor in the Nucleus basalis Meynert failed to reveal differences between vehicle and estrogen treatment in either age group.
The effects of two choline pivaloyl esters, [ 2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium iodide (1) and [ 2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium 2,2-dimethylpropionate (2), on learning and memory impairments induced in rats by scopolamine or lesions of Nucleus basalis magnocellularis (NBM) have been evaluated by object recognition and Morris water maze tests in comparison with Tacrine (THA).
To verify the hypothesis that stimulation of the Nucleus basalis of Meynert (NBM) induces vasodilation in the cerebral cortical parenchyma, we investigated whether the diameter of parenchymal blood vessels of rat parietal cortex is increased during stimulation of NBM using histological techniques.
Subsequent to bilateral ibotenic acid lesions of the Nucleus basalis magnocellularis (NBM), NGF was delivered into the lateral ventricle or adjacent to the NBM for 11 weeks.
We have been investigating physiological properties of GIRKs in cultured noradrenergic neurons from the locus coeruleus (LC) and cholinergic neurons from the Nucleus basalis (NB).
We previously found apolipoprotein (apoE) epsilon4-dependent lower metabolic activity in Nucleus basalis of Meynert (NBM) neurons in Alzheimer disease (AD).
In addition to the SNc there is neurodegeneration in other areas including cerebral cortex, raphe nuclei, locus ceruleus, Nucleus basalis of meynert, cranial nerves and autonomic nervous system.
AIM: To investigate the primary electrophysiological and pharmacological properties of the Nucleus basalis magnocellularis (nbM) neurons.
The present study examined the long-term (2 years) effects of estrogen loss or estrogen replacement therapy (ERT) on cholinergic neurons in the Nucleus basalis of Meynert and on cholinergic fibers in the prefrontal and parietal cortex of adult female cynomolgus monkeys. No differences in parietal cholinergic fiber density or Nucleus basalis cholinergic neuron number or volume were found among intact, ovariectomized, or ERT monkeys.
A recent study suggests that lesions to all major areas of the cholinergic basal forebrain in the rat (medial septum, horizontal limb of the diagonal band of Broca, and Nucleus basalis magnocellularis) impair a spatial working memory task.
In the second experiment, another group of animals with selective 192 IgG-saporin lesions of the Nucleus basalis magnocellularis (nBM) were not impaired under conditions of low-attentional demand.
It is currently unclear whether impairment of the cholinergic system is present in Alzheimer disease (AD) already at an early stage and to what extent it depends on degeneration of the Nucleus basalis of Meynert (nbM).
The human cholinergic basal forebrain (CBF) is comprised of magnocellular hyperchromic neurons within the septal/diagonal band complex and Nucleus basalis (NB) of Meynert.
The present experiment examined whether p-chloroamphetamine (PCA), a serotonergic releasing/depleting agent, would block the memory-enhancing effect of physostigmine in rats with N-methyl-D-aspartic acid (NMDA)-induced unilateral lesions of the Nucleus basalis of Meynert (uni-nbM).
Ethanol (50-300 mM) applied in the Nucleus basalis through a second dialysis probe caused concentration-dependent biphasic changes in prefrontocortical ACh release.
Previous experiments have shown that infusions of ibotenic acid in the Nucleus basalis magnocellularis (NBM) induce a strong impairment in spatial navigation for a hidden platform in the Morris water maze.
We reported previously that the glycosaminoglycan heparin (HP) has the facility to improve learning in adult rodents when administered into the Nucleus basalis of the ventral pallidum.
Low-frequency (< 15 Hz) oscillations during slow-wave sleep, characterized by rhythmic and prolonged hyperpolarizations, are suppressed by brainstem cholinergic neurons and Nucleus basalis cholinergic and GABAergic neurons projecting to thalamic reticular neurons.
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