scholarly journals Dissociated cell culture of cholinergic neurons from nucleus basalis of Meynert and other basal forebrain nuclei.

1985 ◽  
Vol 82 (18) ◽  
pp. 6325-6329 ◽  
Author(s):  
Y. Nakajima ◽  
S. Nakajima ◽  
K. Obata ◽  
C. G. Carlson ◽  
K. Yamaguchi
Keyword(s):  
Cell Culture ◽  
Basal Forebrain ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert ◽  
Dissociated Cell Culture

scholarly journals Atrophy of Basal Forebrain Initiates with Tau Pathology in Individuals at Risk for Alzheimer’s Disease

2019 ◽  
Vol 30 (4) ◽  
pp. 2083-2098
Author(s):  
Jose L Cantero ◽  
Mercedes Atienza ◽  
Carmen Lage ◽  
Laszlo Zaborszky ◽  
Eduard Vilaplana ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
At Risk ◽  
Basal Forebrain ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Tau Pathology ◽  
Projection System ◽  
Prodromal Ad

Abstract Evidence suggests that the basal forebrain (BF) cholinergic system degenerates early in the course of Alzheimer’s disease (AD), likely due to the vulnerability of BF cholinergic neurons to tau pathology. However, it remains unclear whether the presence of tauopathy is the only requirement for initiating the BF degeneration in asymptomatic subjects at risk for AD (AR-AD), and how BF structural deficits evolve from normal aging to preclinical and prodromal AD. Here, we provide human in vivo magnetic resonance imaging evidence supporting that abnormal cerebrospinal fluid levels of phosphorylated tau (T+) are selectively associated with bilateral volume loss of the nucleus basalis of Meynert (nbM, Ch4) in AR-AD individuals. Spreading of atrophy to medial septum and vertical limb of diagonal band Broca (Ch1–Ch2) occurred in both preclinical and prodromal AD. With the exception of A+, all groups revealed significant correlations between volume reduction of BF cholinergic compartments and atrophy of their innervated regions. Overall, these results support the central role played by tauopathy in instigating the nbM degeneration in AR-AD individuals and the necessary coexistence of both AD proteinopathies for spreading damage to larger BF territories, thus affecting the core of the BF cholinergic projection system.

Nucleus basalis neuronal loss and neuritic plaques in advanced Alzheimer's disease

1986 ◽  
Vol 64 (3) ◽  
pp. 318-324 ◽  
Author(s):  
Pierre Etienne ◽  
Yves Robitaille ◽  
Serge Gauthier ◽  
N. P. V. Nair
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Basal Forebrain ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert ◽  
Neuritic Plaques ◽  
Cholinergic Cell

All our advanced severe cases of Alzheimer's disease had dramatic cholinergic cell loss in the basal forebrain, even after correction for cell or nucleolus shrinkage. We examined the relation between cell loss in the various subdivisions of the nucleus basalis of Meynert and plaque counts in corresponding and noncorresponding projection areas. This relation was not interpretable because of the ambiguity in the data.

scholarly journals Basal forebrain cholinergic neurons are part of the threat memory engram

2021 ◽  
Author(s):  
Prithviraj Rajebhosale ◽  
Mala R Ananth ◽  
Richard B Crouse ◽  
Li Jiang ◽  
Gretchen López- Hernández ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Basolateral Amygdala ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Early Gene ◽  
Intrinsic Excitability ◽  
Cholinergic Basal Forebrain ◽  
Basal Forebrain Cholinergic Neurons ◽  
Cholinergic Signaling ◽  
Memory Engram

Although the engagement of cholinergic signaling in threat memory is well established (Knox, 2016a), our finding that specific cholinergic neurons are requisite partners in a threat memory engram is likely to surprise many. Neurons of the basal forebrain nucleus basalis and substantia innonimata (NBM/SIp) comprise the major source of cholinergic input to the basolateral amygdala (BLA), whose activation are required for both the acquisition and retrieval of cued threat memory and innate threat response behavior. The retrieval of threat memory by the presentation of the conditioning tone alone elicits acetylcholine (ACh) release in the BLA and the BLA-projecting cholinergic neurons manifest immediate early gene responses and display increased intrinsic excitability for 2-5 hours following the cue-elicited memory response to the conditioned stimulus. Silencing cue-associated engram-enrolled cholinergic neurons prevents the expression of the defensive response and the subset of cholinergic neurons activated by cue is distinct from those engaged by innate threat. Taken together we find that distinct populations of cholinergic neurons are recruited to signal distinct aversive stimuli via the BLA, demonstrating exquisite, functionally refined organization of specific types of memory within the cholinergic basal forebrain.

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