Cholinergic enzymes in neocortex, hippocampus and basal forebrain of non-neurological and senile dementia of alzheimer-type patients

Henke, H.; Lang, W.

doi:10.1016/0006-8993(83)90880-6

Cited by 169 publications

(46 citation statements)

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“…These neurons have been electrophysiologically subdivided into several discrete categories: slow firing-firing neurons expressing wide action potentials and pronounced sAHP; fast-spiking neurons also expressing pronounced fast duration action potentials and fast AHP; regular firing neurons and burst firing neurons which were further classified as type I and II (Henderson et al, 2001). Immunohistochemical characterization revealed that slow firing neurons express markers of cholinergic neurons such as the acetylcholine (Ach) degradation enzyme acetylcholinesterase, Ach synthesizing enzyme choline acetyl transferase (ChAT) (Henke and Lang, 1983, Brashear et al, 1986, Griffith and Matthews, 1986, Gaykema et al, 1991 and p75, a specific growth factor receptor which is selectively expressed in basal forebrain cholinergic neurons (Hartig et al, 2002). In a recent study, whole-cell patch clamp combined with retrograde reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the correlation of specific firing phenotypes with the expression of different mRNAs of enzymes synthesizing neurotransmitters (Sotty et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Garrido-Sanabria¹,

Perez²,

Bañuelos³

et al. 2007

Neuroscience

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Slow firing septal neurons modulate hippocampal and neocortical functions. Electrophysiologically, it is unclear whether slow firing neurons belong to a homogeneous neuronal population. To address this issue, whole-cell patch recordings and neuronal reconstructions were performed on rat brain slices containing the medial septum/diagonal band complex (MS/DB). Slow firing neurons were identified by their low firing rate at threshold (< 5Hz) and lack of time-dependent inward rectification (I h ). Unsupervised cluster analysis was used to investigate whether slow firing neurons could be further classified into different subtypes. The parameters used for the cluster analysis included latency for first spike, slow afterhyperpolarizing potential, maximal frequency and action potential (AP) decay slope. Neurons were grouped into three major subtypes. The majority of neurons (55%) were grouped as cluster I. Cluster II (17% of neurons) exhibited longer latency for generation of the first action potential (246.5±20.1 ms). Cluster III (28% of neurons) exhibited higher maximal firing frequency (25.3±1.7 Hz) when compared to cluster I (12.3±0.9 Hz) and cluster II (11.8±1.1 Hz) neurons. Additionally, cluster III neurons exhibited faster action potentials at suprathreshold. Interestingly, cluster II neurons were frequently located in the medial septum whereas neurons in cluster I and III appeared scattered throughout all MS/DB regions. Sholl's analysis revealed a more complex dendritic arborization in cluster III neurons. Cluster I and II neurons exhibited characteristics of "true" slow firing neurons whereas cluster III neurons exhibited higher frequency firing patterns. Several neurons were labeled with a cholinergic marker, , and cholinergic neurons were found to be distributed among the three clusters. Our findings indicate that slow firing medial septal neurons are heterogeneous and that soma location is an important determinant of their electrophysiological properties. Thus, slow firing neurons from different septal regions have distinct functional properties, most likely related to their diverse connectivity. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 January 22. Published in final edited form as:Neuroscience. (Griffith et al., 1991, Matthews and Lee, 1991, Jones et al., 1999, Morris et al., 1999, Knapp et al., 2000, Henderson et al., 2001, Sotty et al., 2003. Slow firing neurons are characterized by slow firing rates and pronounced slow post-spike afterhyperpolarization potenti...

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Section: Discussionmentioning

confidence: 99%

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Garrido-Sanabria¹,

Perez²,

Bañuelos³

et al. 2007

Neuroscience

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“…The administration of scopola mine, a muscarinic acetylcholine receptor antagonist, produces amnesic effects (21 23), while cholinergic drugs, including muscarinic agonists and acetylcholinesterase inhibitors, accelerate learning and memory in both hu mans and animals (22,24,25). The most strik ing and consistent change in AD and SDAT is in the cholinergic system, as measured by a marked decrease in choline acetyltransferase activity in the hippocampus and cerebral cor tex (8,9). These findings have drawn atten tion to the cholinergic system as a possible site for therapy of the dementing disorders.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, neuronal loss and a great number of neuro fibrillary tangles and senile plaques have been found in the hippocampus of patients with Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT) (6,7). In the hippocampal formation, there are also marked reductions in the activity of choline acetyl transferase, the enzyme that synthesizes acetyl choline, in these pathological states (8,9). In light of the role of the hippocampus in mem ory, these changes are likely to contribute to the memory deficits seen in AD and SDAT patients.…”

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Working and Reference Memory in Rats in the Three-Panel Runway Task Following Dorsal Hippocampal Lesions.

et al. 1992

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Using a three-panel runway task, the influence of dorsal hippocampal lesions on working and reference memory in rats was investigated. Despite 20 postop erative training sessions, rats with hippocampal lesions were unable to perform the working memory task. In the acquisition process of the reference memory task, however, there was no significant difference between hippocampal and sham-lesioned rats. On the other hand, rats trained preoperatively with a working memory proce dure, and then subjected to hippocampal lesions, showed more errors (pushes made on the two incorrect panels of the three panel-gates located at four choice points) than did sham-lesioned rats. The increase in working errors induced by hippocampal lesions was not reduced during 10 subsequent re-training sessions. Hippocampal le sions had no effect on retention of the reference memory performance. The increase in working errors in hippocampal-lesioned rats was significantly reduced by treatment with the cholinesterase inhibitor physostigmine at 0. 1 mg/kg and the cholinergic acti vating drug minaprine at 10 mg/kg. These findings suggest that lesions of the dorsal hippocampus selectively impair the ability to carry out the working memory task whether rats are trained preoperatively or postoperatively, and that the working mem ory loss in hippocampal-lesioned rats is mediated by lowering of the cholinergic func tion.

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“…65 Rossor et al and Henke and Lang reported that the brains of patients with AD showed the degeneration of cholinergic neurons and a reduction in cholinergic markers, whereas the activities of choline acetyltransferase (ChAT) and AChE were reduced in the cerebral cortexes of patients with AD. 66,67 A study reported by Soininen et al showed that AD patients carrying the apolipoprotein E (APOE) ε4 allele have a more severe cholinergic deficit than the AD patients without the APOE ε4 allele. 68 Phospholipase A2 (PA2) is the enzyme responsible for the synthesis of chemical mediators of inflammation and is also responsible for the conversion of phosphatidylcholine to choline.…”

Section: Ad Pathophysiologymentioning

confidence: 99%

Nanotechnology-based drug delivery systems for the treatment of Alzheimer’s disease

Fonseca-Santos¹,

Chorilli²,

Gremião³

2015

IJN

248

160

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Alzheimer’s disease is a neurological disorder that results in cognitive and behavioral impairment. Conventional treatment strategies, such as acetylcholinesterase inhibitor drugs, often fail due to their poor solubility, lower bioavailability, and ineffective ability to cross the blood–brain barrier. Nanotechnological treatment methods, which involve the design, characterization, production, and application of nanoscale drug delivery systems, have been employed to optimize therapeutics. These nanotechnologies include polymeric nanoparticles, solid lipid nanoparticles, nanostructured lipid carriers, microemulsion, nanoemulsion, and liquid crystals. Each of these are promising tools for the delivery of therapeutic devices to the brain via various routes of administration, particularly the intranasal route. The objective of this study is to present a systematic review of nanotechnology-based drug delivery systems for the treatment of Alzheimer’s disease.

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Cholinergic enzymes in neocortex, hippocampus and basal forebrain of non-neurological and senile dementia of alzheimer-type patients

Cited by 169 publications

References 50 publications

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Working and Reference Memory in Rats in the Three-Panel Runway Task Following Dorsal Hippocampal Lesions.

Nanotechnology-based drug delivery systems for the treatment of Alzheimer’s disease

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Cholinergic enzymes in neocortex, hippocampus and basal forebrain of non-neurological and senile dementia of alzheimer-type patients

Cited by 169 publications

References 50 publications

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Working and Reference Memory in Rats in the Three-Panel Runway Task Following Dorsal Hippocampal Lesions.

Nanotechnology-based drug delivery systems for the treatment of Alzheimer&rsquo;s disease

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Product

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Nanotechnology-based drug delivery systems for the treatment of Alzheimer’s disease