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At least 19 recordsLinked to original sources
PubMed1999

Parabrachial origin of calcitonin gene-related peptide-immunoreactive axons innervating Meynert's basal nucleus.

Meynert's basal nucleus is innervated by calcitonin gene-related peptide (CGRP)-immunoreactive axons synapsing with cholinergic principal cells. Origin of CGRP-immunopositive axons was studied in the albino rat. Since beaded axons containing the nicotinic acetylcholine receptor (nAChR) are also present in the basal nucleus, the microstructural arrangement raises the question whether or not an interaction between CGRP and nAChR exists like in the neuromuscular junction. We found that electrolytic lesion of the parabrachial nucleus results in degeneration of CGRP-immunoreactive axons in the ipsilateral nucleus basalis and induces shrinkage of principal cholinergic neurons while the contralateral nucleus basalis remains intact. Electrolytic lesions in the thalamus, caudate-putamen, and hippocampus did not induce alterations in Meynert's basal nucleus. Disappearance of CGRP after lesions of the parabrachial nucleus does not impair presynaptic nAChR in the basal nucleus, suggesting that, unlike in the neuromuscular junction, CGRP is not involved in the maintenance of nAChR in the basal forebrain. It is concluded that the parabrachial nucleus is involved in the activation of the nucleus basalis-prefrontal cortex system, essential in gnostic and mnemonic functions.

Animals↗
PubMed1989

Altered lipofuscin pigmentation in the basal nucleus (Meynert) in Parkinson's disease.

The basal nucleus (Meynert) and the horizontal limb nucleus of the diagonal band are composed of 3 types of neurons that can be differentiated with the use of Nissl preparations counterstained for the demonstration of lipofuscin pigment. The pattern of pigmentation of these neurons has been investigated in parkinsonian cases and compared with controls. In the parkinsonian cases the number of large multipolar neurons showing pigment granules in a dendritic stem is significantly higher than in controls. Moreover, the degree of pigment penetration is more pronounced in parkinsonian cases. The results show that staining of lipofuscin granules offers an approach to detecting further details of the changes in the basal nucleus in Parkinson's disease.

Aged↗
PubMed1998

Lectin staining in the basal nucleus (Meynert) and the hypothalamic tuberomamillary nucleus of the developing human prosencephalon.

Previous studies have demonstrated that extracellular matrix glycoconjugates, shown by lectin-histochemistry with Vicia villosa agglutinin (VVA) and peanut agglutinin (PNA) as so-called perineuronal nets, play an important role in brain maturation. Concanavalin A (ConA) binding to neuronal surface glycoconjugates may be a marker of synaptic junctions. The present study was done to demonstrate the binding sites of these lectins in two functionally related nuclei of the prosencephalon, the basal nucleus (Meynert) and the hypothalamic tuberomamillary nucleus. Fetal brains of 16-36 weeks of gestation were examined by using VVA, PNA, and ConA to determine appearance and distribution patterns of specific lectin-binding sites on glycoconjugates during fetal brain development. The basal nucleus and the tuberomamillary nucleus showed a characteristic "cellular staining" that may have been due to cytoplasmatic labeling, surface labeling, or both. Lectin-staining occurred much earlier in the basal nucleus than in the tuberomamillary nucleus. Although all three lectins were bound to neurons of the basal nucleus, only ConA-positive neurons were observed in the tuberomamillary nucleus. In conclusion, lectin-labeled cells most probably represent projection neurons that are GABAergic (tuberomamillary nucleus) or cholinergic (basal nucleus). Labeling with the three lectins demonstrated nuclear-specific staining patterns that occur early in fetal development and gradually increase. Binding sites for lectins characterizing perineuronal nets (VVA, PNA) occurred only in the basal nucleus, whereas binding sites for ConA on neuronal-surface glycoconjugates, which seem to play a role in early synaptogenesis, were present in the basal and the tuberomamillary nucleus. The basal nucleus, however, expressed ConA binding sites distinctly earlier, probably indicating early arriving afferents.

Cell Nucleus↗
PubMed2002

Neuronal vacuolation in the basal nucleus of meynert caused by fetal hydrocephalus.

The basal nucleus of Meynert, which provides the major source of cholinergic input to the cerebral cortex, was investigated in fetal hydrocephalic brains (n = 5) in comparison to controls (n = 5). To detect alterations, the neurons of the basal nucleus were immunostained with an antibody against the calcium-binding protein calbindin. In the basal nucleus of hydrocephalic brains, a moderate number of vacuolated neurons were observed. Such vacuolation was not seen in control brains. Vacuolation is interpreted as a degenerative change after injury of basal nucleus axons in cases of fetal hydrocephalus. The neuronal alterations in the basal nucleus may account at least in part for residual deficits observed after shunt placement.

Basal Nucleus of Meynert↗
PubMed1984

The basal nucleus of Meynert in idiopathic Parkinson's disease.

The basal nucleus of Meynert (bnM) was examined in 6 patients with idiopathic Parkinson's disease and in 5 age-matched controls. The histopathological study was followed by a quantitative analysis of the magnocellular population of the nucleus, with the determination of the number of neurons and their nucleolar volume. In Parkinson's disease, there was a neuronal loss ranging from 29.9% to 68.3% (mean 45.8%) and numerous surviving cells containing Lewy inclusion bodies. The percentage loss of cells did not display a significant correlation with the age of the patients, the duration of the illness, the mental state or the drug regime. On the other hand, no significant differences in nucleolar volume of bnM neurons were detected between patients and controls. The damage of the basal nucleus of Meynert in Parkinson's disease is less severe than that generally observed in Alzheimer's disease, and is slightly more pronounced than that reported for progressive supranuclear palsy.

Aged↗
PubMed1983

Neuronal loss in the basal nucleus of Meynert in progressive supranuclear palsy.

A morphometric study of the basal nucleus of Meynert (bnM) has been performed in a 70-year-old man with a 4-year history of pathologically confirmed progressive supranuclear palsy (PSP). An important neuronal loss (52%) was demonstrated in the bnM. This finding has not been previously documented with morphometric methods in PSP, but the involvement of the bnM is well known in other related conditions, i.e., Parkinson's disease, Alzheimer's disease, and Parkinson-dementia complex of Guam. Our findings yield support to the view that the involvement of the bnM, a nucleus with complex connections with various subcortical structures and diffuse cholinergic projections on the neocortex, could play an important role in the physiopatholog of subcortical dementia.

Aged↗
PubMed1985

Neuronal loss in the basal nucleus of Meynert in a patient with olivopontocerebellar atrophy.

A morphometric study of the basal nucleus of Meynert has been performed in a case of familial olivopontocerebellar atrophy with mental deterioration. The magnocellular population of the basal nucleus was found to be substantially reduced in number (over 60%) as compared with that of three age-matched controls. This finding has not been reported previously and might represent one of the anatomic substrates of some of the cognitive disturbances exhibited by a considerable number of patients with olivopontocerebellar atrophy (OPCA).

Atrophy↗
PubMed1997

Learning impairments following injection of a selective cholinergic immunotoxin, ME20.4 IgG-saporin, into the basal nucleus of Meynert in monkeys.

Four groups of monkeys (Callithrix jacchus) were injected with saline or increasing amounts of the immunotoxin, ME20.4 IgG-saporin, directly into the basal nucleus of Meynert via a frontal trajectory which avoided damage to the overlying basal ganglia. ME20.4 IgG binds to the primate p75 low-affinity neurotrophin receptor, when the saporin derivitized antibody is injected into the basal forebrain, it selectively destroys the magnocellular neurons of the basal nucleus of Meynert which are the cells of origin of the cholinergic projection to the neocortex. The highest dose of ME20.4 IgG-saporin produced a significant impairment on acquisition of a perceptually difficult visual discrimination. There was no significant effect on retention of tasks learnt before or after surgery, nor on concurrent acquisition of several perceptually easy discriminations or serial reversal of an easy discrimination. These results suggest that the impairment is not due to visual, motor or motivational difficulties and does not consist of difficulties with the formation of reward associations. Rather the impairment is largely confined to acquisition of perceptual discriminations. There was a significant correlation between the density of ME20.4 immunostaining in the basal nucleus of Meynert and the density of acetylcholinesterase histochemical staining in the frontal and temporal cortex and an inverse correlation between both of these and the degree of learning impairment in the animals. Lesioned animals also showed significant impairment on acquisition and reversal of perceptually easy discriminations when treated with a dose of scopolamine which did not impair performance in control animals. These results provide further evidence that cortical cholinergic neurotransmission contributes to certain forms of learning. The availability of a selective cholinergic immunotoxin effective in primates provides an important new tool for the study of cholinergic function and its involvement in ageing, Alzheimer's disease and other pathological states.

Animals↗
PubMed1976

Midbrain, diencephalic and cortical relationships of the basal nucleus of Meynert and associated structures in primates.

The structure and connectivity of the basal nucleus of Meynert, the substantia innominata in which it lies, and certain related areas have been examined in New World and Old World Monkeys, using retrograde and anterograde axonal transport methods. Experiments using the retrograde, horseradish peroxidase method confirm the observations of Kievet and Kuypers ('75) that the basal nucleus and substantia innominata project directly, heavily and with a somewhat crude topography upon the neocortex. Experiments involving the anterograde, autoradiographic method show that the basal nucleus and substantia innominata form part of a complex pathway that links them together with the lateral hypothalamus, certain parts of the amygdala and the peripeduncular nucleus of the midbrain. The peripeduncular nucleus is often regarded as a part of the central auditory pathway; it gives rise to a fiber bundle of considerable size that ascends on the dorsal surface of the ipsilateral optic tract and terminates ultimately in the lateral hypothalamic area of both sides. As well as distributing fibers to the basal nucleus, substantia innominata and lateral hypothalamus, this pathway provides a heavy projection to a cytoarchitectonically distinct posterior part of the lateral nucleus of the amygdala, the medial and intercalated nuclei of the amygdala and a less dense projection to the bed nucleus of the stria terminalis. Certain parts of the hypothalamus and possibly the preoptic areas give rise to a complementary descending pathway that distributes fibers to the ipsilateral basal nucleus, substantia innominata and amygdala, and ends in the peripeduncular nuclei of both sides. Decussating fibers in both the ascending and descending pathways cross in the ventral supraoptic commissure. It is concluded that the basal nucleus should include most of the aggregated and unaggregated large cells that lie in the substantia innominata and which in places intrude upon the preoptic regions and the nucleus of the diagnonal band of Broca. Together, these may form a complex that receives inputs from a variety of brainstem sources, and projects widely and diffusely upon all cortical structures of the telencephalon.

Amygdala↗
PubMed2000

Evolution of Alzheimer's disease-related cytoskeletal changes in the basal nucleus of Meynert.

This study examines the evolution of Alzheimer's disease (AD)-related pathology in a subcortical predilection site, the basal nucleus of Meynert (bnM), which is a major source of cortical cholinergic innervation. Brains of 51 autopsy cases were studied using silver techniques and immunostaining for tau-associated neurofibrillary pathology and for amyloid beta protein (Abeta) deposits. All cases are classified according to a procedure permitting differentiation of six stages of AD-related neurofibrillary changes in the cerebral cortex. Initial cytoskeletal abnormalities in the bnM are already noted in stage I of cortical neurofibrillary changes. The gradual development of the neurofibrillary pathology in the bnM parallels the progression of the AD-related stages in the cerebral cortex. A variety of morphologically distinguishable cytoskeletal alterations are observed in large nerve cells which predominate in the bnM. Based on these cellular alterations, a sequence of cytoskeletal deterioration is proposed. Initially, the abnormal tau protein is distributed diffusely throughout the cell body and the neuronal processes. Subsequently, it aggregates to form a neurofibrillary tangle, which appears as a spherical somatic inclusion. The cell processes gradually become fragmented. Finally the parent cell dies, leaving behind an extraneuronal "ghost tangle". With regard to the cortical stages of AD-related neurofibrillary changes, the initial forms of cytoskeletal changes in the bnM predominate in the transentorhinal AD stages (I and II), while "ghost tangles" preferentially occur in the neocortical stages (V and VI). The considerable morphological diversity of cytoskeletal alterations is typical of stages III and IV. These results indicate that individual neurons of the bnM enter the sequence of cytoskeletal deterioration at different times.

Aged↗
PubMed1994

Restoration of cognitive abilities by cholinergic grafts in cortex of monkeys with lesions of the basal nucleus of Meynert.

Three groups of marmosets were trained to perform a series of visual discrimination tasks in a Wisconsin General Test Apparatus. Two groups then received bilateral lesions of the basal nucleus of Meynert using the excitotoxin N-methyl-D-aspartate and were found to be severely impaired on relearning a visual discrimination first learnt prior to surgery. One lesioned group then received grafts of acetylcholine-rich tissue dissected from the basal forebrain of fetal marmosets. Three months later the marmosets with lesion alone remained impaired on a number of retention and reversal tasks whereas the transplanted animals were no longer significantly impaired. Histological examination of the brains indicated that all lesioned animals had sustained substantial loss of the cholinergic neurons of the basal nucleus of Meynert (assessed by nerve growth factor receptor immunoreactivity) and that the lesion-alone animals showed marked loss of the cholinergic marker acetylcholinesterase in the dorsolateral frontal and parietal cortex. All transplanted animals had surviving graft tissue (visualized by Cresyl Violet staining, dense acetylcholinesterase staining and the presence of a limited number of nerve growth factor receptor-immunoreactive neurons) in the neocortex and 5/6 transplanted animals showed near complete restitution of acetylcholinesterase staining in frontal and parietal cortex. Examination of individual animal data showed that the animal without this restitution performed very poorly. The performance of the remaining transplanted animals was significantly better than that of the animals with lesion alone. There was a significant positive correlation between the degree of acetylcholinesterase staining and good performance on tasks sensitive to frontal lobe damage. These results demonstrate that acetylcholine-rich tissue transplanted into the neocortex of primates with damage to the cholinergic projections to the neocortex can produce substantial restitution of function provided that an appropriate level of interaction between graft and host tissue is achieved.

Acetylcholine↗
PubMed1989

Correlative decrease of large neurons in the neostriatum and basal nucleus of Meynert in Alzheimer's disease.

A quantitative investigation was performed on the large neurons in the neostriatum and basal nucleus of Meynert (bnM) in patients with Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). The degree of decrease of the large neurons in the neostriatum was quite similar to that in the bnM; these decreases were significantly correlative in AD, but not in PSP. These findings indicate that the large neurons in the neostriatum and bnM, which are considered to be cholinergic and to exclusively possess nerve growth factor receptors in the cerebrum, degenerate simultaneously in an equal ratio in AD.

Aged↗
PubMed1986

Early cytoarchitectonic development of the anlage of the basal nucleus of Meynert in the human fetus.

The present study describes a short period of cytoarchitectonic development of the anlage of the basal nucleus of Meynert between 9 and 15 weeks of gestation (crown-rump length 42-120 mm). On the basis of temporo-spatial reconstruction of the cytoarchitectonic pattern within the basal telencephalon it was evident that magnocellular aggregations of the basal telencephalon contain the most differentiated cells in the whole prosencephalon of the 15-week-old human fetus. At this stage development many magnocellular islands can be observed in the sublenticular region. However, it seems that they are in antero-posterioral continuation and the real number of magnocellular islands is much smaller than observed in a single section. The most voluminous magnocellular aggregations are situated around the temporal limb of the anterior commissure and below the ventral pallidal surface in the 15th week of gestation. Between 12 and 15 weeks of gestation, at the most rostral levels, the distinct cell group appeared with unique cytoarchitectonic properties ('albino cell group'). This cell group is situated close to the ventral putaminal surface within the capsula externa fibres and it corresponds to the subputaminal nucleus of Ayala.

Basal Ganglia↗
PubMed1984

The basal nucleus of Meynert in patients with progressive supranuclear palsy.

The neuronal number and nucleolar volume of the magnocellular population of the basal nucleus of Meynert in 6 patients with progressive supranuclear palsy (PSP) - one associated with Alzheimer's disease - were compared with those of 5 controls. In the 5 typical PSP cases, an age-dependent neuronal loss was demonstrated ranging from 12.6% to 54.1%. In the PSP-Alzheimer patient, the loss of cells amounted to 73.8% and the surviving neurons exhibited a reduction in the nucleolar volume, suggesting a reduced protein synthetic capability. The involvement of the basal nucleus is therefore a usual anatomical feature of PSP. The damage is less severe than generally observed in Alzheimer's disease and biochemical studies are required to state whether this is accompanied by a substantial cholinergic deficit.

Aged↗
PubMed1998

[Changes in acetylcholine level and its related enzyme activities in rat brain following focal ischemia].

At 1 to 4 weeks following middle cerebral artery occlusion in Wistar rats, levels of acetylcholine, which is neuro-transmitter, were measured. In the hippocampus, which plays an important role in memory, levels of acetylcholine in the ischemic group could not be detected the significant difference compared with those in the sham-operated group. But in the anterior cortex and the caudate-putamen, levels of acetylcholine in the ischemic group were recognized the significant difference compared with those in the sham operated group. Moreover activities of choline acetyltransferase, which is the synthetic enzyme of acetylcholine, and activities of acetylcholinesterase, which is the degradative enzyme of acetylcholine, were measured in the anterior cortex which was recognized decrease of the acetylcholine level and the hippocampus which could not be detected the difference of the acetylcholine level. Activities of both enzymes in the hippocampus could not be recognized the significant difference between the ischemic group and the normal group. But in the anterior cortex activities of both enzymes in the ischemic group were significantly decreased compared with those in the normal group. These results suggest that these decreases in the ischemic group were due to damage of injection of cholinergic neuron from Meynert nucleus (basal nucleus of Meynert) to anterior cortex.

Acetylcholine↗
PubMed1983

Basal nucleus of Meynert. A neuropathological study in Alzheimer's disease, simple senile dementia, Pick's disease and Huntington's chorea.

The basal nucleus of Meynert (bnM) was examined in 9 patients with Alzheimer's disease--4 presenile and 5 senile cases--in 3 patients with simple senile dementia, 5 with Pick's disease, 5 with Huntington's chorea and 5 non-demented controls. The histopathological study was followed by a quantitative analysis of the magnocellular population of neurons and by the determination of their nucleolar volume. In Alzheimer's disease there was a neuronal loss ranging from 44 to 76%, which was negatively correlated with both the age at onset and age at death of the patients. Numerous surviving cells showed neurofibrillary tangles, and in 3 cases senile plaques were present. The nucleolar volume of the large neurons was significantly reduced and the percentage reduction correlated with the percentage loss of cells. In contrast, the bnM was relatively unaffected in the other disorders considered. The involvement of bnM in Alzheimer's disease confirms the previous neuropathological observations, providing further evidence that it constitutes a constant anatomical feature of this disorder. The extent of the damage is age-dependent. The sparing of the bnM in simple senile dementia suggests that it may be a different nosological entity from late onset Alzheimer's disease and this may constitute a simple criterion for distinguishing between the two forms of dementia on an anatomical basis.

Age Factors↗
PubMed1986

Learning impairment following lesion of the basal nucleus of Meynert in the marmoset: modification by cholinergic drugs.

Five common marmosets (Callithrix jacchus) received unilateral ibotenic acid lesions of the basal nucleus of Meynert (nBM). Seven days later, choline acetyltransferase activity was significantly reduced by 50% in the frontal and temporal neocortex, 40% in the amygdala, and approximately 30% in the motor, parietal and occipital cortex in the ipsilateral hemisphere. Four marmosets receiving equivalent bilateral ibotenic acid lesions were severely impaired on new visual object discrimination learning and on relearning an object discrimination learnt prior to surgery when compared with operated controls. New learning in lesioned animals was substantially improved by i.m. administration of the cholinergic agonist arecoline. Lesioned animals' learning ability improved with time but these animals were then differentially sensitive to the disruptive effect of scopolamine on discrimination learning. These results show that lesions of the nBM which destroy the rising cholinergic pathways impair learning ability but that this ability can be substantially restored by administration of a cholinergic agonist.

Acetylcholine↗
PubMed2005

Vascular endothelial growth factor counteracts NMDA-induced cell death of adult cholinergic neurons in rat basal nucleus of Meynert.

Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis in the brain and has recently been shown to possess neuroprotective activity. The aim of the present study was to observe if VEGF can counteract the excitotoxic N-methyl-D-aspartate (NMDA)-induced cell death of cholinergic neurons of the basal nucleus of Meynert in vivo in adult rats. Immunohistochemistry was used to detect vascular structures (RECA-1 or laminin staining) and cholinergic neurons (choline-acetyltransferase). To compare the in vivo VEGF effects also in vitro, VEGF was applied to axotomized cholinergic neurons in organotypic brain slices with or without NMDA. Our data provide evidence that VEGF counteracted cell death in vivo in adult rats but did not protect cholinergic neurons in developing brain slices. Nerve growth factor protected cholinergic neurons in vivo as well as in vitro. In conclusion, VEGF exhibits neuroprotective activity on adult cholinergic neurons of the basal nucleus of Meynert.

Age Factors↗