Disease relevance of Basal Nucleus of Meynert

• The present investigations of 12 patients with Parkinson disease demonstrates that the demented patients with this disease also show a selective loss of cells in the nucleus basalis of Meynert, thus providing an important link between the dementias of Alzheimer disease and Parkinson disease [1].
• In contrast, cortically lesioned monkeys treated with monosialoganglioside did not reveal a significant loss of choline acetyltransferase activity or shrinkage of nucleus basalis of Meynert cholinergic neurons, but rather a modest hypertrophy [2].
• Primate nucleus basalis of Meynert p75NGFR-containing cholinergic neurons are protected from retrograde degeneration by the ganglioside GM1 [2].
• Neocortical infarction induces biochemical and morphological retrograde degenerative changes in cholinergic neurons of the rat nucleus basalis magnocellularis [Sofroniew et al. (1983) Brain Res. 289, 370-374] [3].
• The effects of focal electrical stimulation of the nucleus basalis of Meynert (NBM) and hypercapnia on diameter of the pial artery and regional cerebral blood flow (CBF) in the parietal cortex were examined in urethane-anesthetized rats [4].

Psychiatry related information on Basal Nucleus of Meynert

• Levels of dopamine and serotonin, and of their precursors and metabolites, were measured in the nucleus basalis of Meynert (nbM) of patients with Alzheimer's disease and control patients [5].
• Tetrahydroaminoacridine facilitates passive avoidance learning in rats with nucleus basalis magnocellularis lesions [6].
• Since cholinergic neurons of the nucleus basalis magnocellularis are GABA-modulated, it may be postulated that these neurosteroids modify paradoxical sleep by acting on the cholinergic transmission [7].
• Multiple injections of thyrotropin releasing hormone fail to reverse learning and memory deficits in rats with lesions of the nucleus basalis of meynert [8].
• Simple and configural association learning in rats with bilateral quisqualic acid lesions of the nucleus basalis magnocellularis [9].

High impact information on Basal Nucleus of Meynert

• In the brain of 25 week-old fetuses, FMR-1 mRNAs are produced in all nearly differenciated structures, with the highest level in cholinergic neurons of the nucleus basalis magnocellularis and in pyramidal neurons of hippocampus [10].
• Relatively high NGF levels (0.4-1.4 ng NGF/g wet weight) were found both in the regions innervated by the magnocellular cholinergic neurons of the basal forebrain (hippocampus, olfactory bulb, neocortex) and in the regions containing the cell bodies of these neurons (septum, nucleus of the diagonal band of Broca, nucleus basalis of Meynert) [11].
• Lesions of the nucleus basalis magnocellularis induced by 192 IgG-saporin block memory enhancement with posttraining norepinephrine in the basolateral amygdala [12].
• Reversible inactivation of the nucleus basalis magnocellularis induces disruption of cortical acetylcholine release and acquisition, but not retrieval, of aversive memories [13].
• The basal forebrain complex, which includes the nucleus basalis magnocellularis (NBM), provides widespread cholinergic and gamma-aminobutyric acid-containing projections throughout the brain, including the insular and pyriform cortices [13].

Chemical compound and disease context of Basal Nucleus of Meynert

• As a further test of the hypothesis, we investigated the effect of dexefaroxan in a rat model of 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 magnocellularis [14].
• Glutamate may act via an N-methyl-D-Aspartate (NMDA)-sensitive receptor site to destroy cholinergic neurons within the nucleus basalis magnocellularis in age-associated neurodegenerative diseases [15].
• Effect of stimulation of the nucleus basalis of Meynert on blood flow and extracellular lactate in the cerebral cortex with special reference to the effect of noxious stimulation of skin and hypoxia [16].
• In this study, the action of several tryptophan metabolites, yielded by the kynurenine pathway, on cortical cholinergic toxicity was evaluated following focal injection into the rat nucleus basalis magnocellularis (nbM) [17].
• Locomotor activity (LMA) was assessed in rats given ibotenic acid lesions in the nucleus basalis magnocellularis (group NBM) or sham surgery (group OC) [18].

Biological context of Basal Nucleus of Meynert

• The distribution of specifically-labeled neurotensin binding sites was examined in relation to that of cholinergic neurons in the rat nucleus basalis magnocellularis at both light and electron microscopic levels [19].
• Nerve growth factor and glial cell line-derived neurotrophic factor restore the cholinergic neuronal phenotype in organotypic brain slices of the basal nucleus of Meynert [20].
• Direct application of SP (0.74 pmol) into the region of the nucleus basalis magnocellularis (NBM) was also memory-promoting and reinforcing, and again, these effects were differentially produced by the N-terminus and C-terminus, supporting the proposed structure-activity relationship for SP's effects on memory and reinfrocement [21].
• The aim of the present study was to observe, if transplanted primary monocytes secreting NGF may counteract N-methyl-D-aspartate (NMDA)-induced cell death of cholinergic neurons of the basal nucleus of Meynert (nBM) in vivo [22].
• There is a good correlation between choline acetyltransferase activity and "healthy" cell number in the nucleus basalis of Meynert [23].

Anatomical context of Basal Nucleus of Meynert

• Ten days of estrogen deprivation after ovx resulted in significant decreases in trkA mRNA levels in the horizontal limb of the diagonal band of Broca and the nucleus basalis of Meynert [24].
• Primary fibroblasts modified to secrete nerve growth factor (NGF) were implanted into the nucleus basalis magnocellularis (NBM) of aged memory impaired rats [25].
• The positivity of amyloid deposits in AD was 100% in the cerebral cortex, hippocampus, amygdala, thalamus, caudate nucleus, claustrum, hypothalamus, nucleus basalis of Meynert, and cerebellar cortex [26].
• Choline acetyltransferase activity in Alzheimer's brains was markedly reduced in various cortical areas, in the hippocampus, and in the nucleus basalis of Meynert [27].
• Choline acetyltransferase activity was decreased in the hypothalamus and nucleus basalis of Meynert, and acetylcholinesterase activity was decreased in the nucleus basalis of Meynert only [28].

Associations of Basal Nucleus of Meynert with chemical compounds

• This cholinergic component of Alzheimer disease can be modeled in the rat by ibotenic acid lesions of the cholinergic nucleus basalis magnocellularis [29].
• Infusion of lidocaine, a calcium antagonist that disrupts neurotransmitter release, into the nucleus basalis of Meynert leads to the temporary reduction of released acetylcholine in the cortex [30].
• Effects of unilateral lesion of the nucleus basalis of Meynert on brain glucose utilization in callosotomized baboons: a PET study [31].
• Effect of quinolinic acid in the nucleus basalis magnocellularis on cortical high-affinity choline uptake [32].
• The present study investigated the effects of nucleus basalis magnocellularis (NBM) lesions in young (3 months), adult (9 months), and aged (24 months) rats by injections of either NMDA or AMPA upon performance of a delayed alternation task on a T maze [33].

Gene context of Basal Nucleus of Meynert

• Since galanin inhibits acetylcholine release, and produces cognitive deficits in animals, increased galanin immunoreactivity in the nucleus basalis of Meynert in AD may contribute to the cognitive deficits that characterize the illness [34].
• In both species, many large GluR1-positive neuronal perikarya and aspiny dendrites are present within the medial septal nucleus, the nucleus of the diagonal band of Broca, and the nucleus basalis of Meynert [35].
• GABAB receptor transduction mechanisms, and cross-talk between protein kinases A and C, in GABAergic terminals synapsing onto neurons of the rat nucleus basalis of Meynert [36].
• Increased expression of estrogen receptor alpha and beta in the nucleus basalis of Meynert in Alzheimer's disease [37].
• The cells survived well in the host brain for long periods of time (up to 4 weeks), and induced a hypertrophic response of cholinergic neurons (positive for acetylcholinesterase, choline acetyltransferase or low-affinity nerve growth factor receptor) in the nucleus basalis magnocellularis and striatum [38].

Analytical, diagnostic and therapeutic context of Basal Nucleus of Meynert

• In a second group of rats, after microinjection of ibotenate or quisqualate to the nucleus basalis of Meynert, iron accumulated in the ipsilateral entopeduncular nucleus and pars reticulata of substantia nigra [39].
• We used [14C]-2-deoxyglucose autoradiography in conscious rats to map the effects of excitatory amino acid agonist infusions into the nucleus basalis magnocellularis (NBM) on cerebral functional activity, as reflected by local rates of glucose utilization [40].
• Perfusion of the nucleus basalis magnocellularis (NBM) with histamine agonists and antagonists modulates the spontaneous release of cortical acetylcholine (ACh) in freely moving rats [41].
• Perfusion of the region of cholinergic neurons believed to be responsible for the cortical release of acetylcholine, the nucleus basalis magnocellularis, was carried out using a second microdialysis probe [42].
• Effects of lesions of the nucleus basalis magnocellularis on the acquisition of cocaine self-administration in rats [43].

References