Cholinergic and serotonergic systems in the brain and spinal cord: anatomic organization, role in intercellular communication processes, and interactive mechanisms.
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Acetylcholine↗
Biomedical subjects
N J Woolf
Publications and source records attributed to N J Woolf.
Cholinergic neurons in the caudate-putamen complex proper are intrinsically organized: a combined Evans blue and acetylcholinesterase analysis.
In an attempt to determine whether or not acetylcholinesterase (AChE)-containing neurons of the caudate-putamen proper were the source of striatal efferent fibers, we infused Evans Blue, a retrogradely transported fluorescent label, into the globus pallidus, entopeduncular nucleus, substantia nigra, or retrorubral area. Following microscopic analysis of the striatum for Evans Blue-labelled somata, the same brain sections were processed for AChE according to the pharmacohistochemical regimen and, after additional microscopic evaluation, were counterstained with cresyl violet. Histology for Nissl substance revealed that the areal density of cell bodies in the caudate-putamen complex proper was about 1510 somata/mm2. Striatal neurons labelled with Evans Blue, those considered to be projection cells, were medium-sized (approximate minor and major dimensions: 11 X 14 microns), had a density of roughly 833 cells/mm2, and were predominantly oval with lesser proportions being fusiform, triangular, or round. Each of the target structures received input from approximately 55% (range = 26-78%) of the total population of striatal neurons in regions where the projection cellsions: 11 X 14 microns), had a density of roughly 833 cells/mm2, and were predominantly oval with lesser proportions being fusiform, triangular, or round. Each of the target structures received input from approximately 55% (range = 26-78%) of the total population of striatal neurons in regions where the projection cellsions: 11 X 14 microns), had a density of roughly 833 cells/mm2, and were predominantly oval with lesser proportions being fusiform, triangular, or round. Each of the target structures received input from approximately 55% (range = 26-78%) of the total population of striatal neurons in regions where the projection cells were located. The two types of AChE-containing somata in the caudate-putamen complex proper--the medium-sized, lightly staining Type A and the large, intensely staining Type B cell--had densities of 14 and 15 somata/mm2, respectively. None of the AChE neurons contained Evans Blue, indicating that they were not the source of striatal efferent fibers but rather interneurons that could be categorized best as the aspiny or sparsely spined cells described in Golgi studies.
Acetylcholinesterase↗
Interstellar silicate absorption bands.
Interstellar silicate absorption is observed in the direction of the galactic centre. Most interstellar silicon seems to be in silicate form.
Journal Article↗
Neurotrophic agents may exacerbate the pathologic cascade of Alzheimer's disease.
The thesis is advanced that Alzheimer's disease is triggered by alterations in the regulatory mechanisms governing the patterns of cytoskeletal protein expression in structurally plastic neurons in the mature nervous system. As a consequence, polypeptide species acting to stabilize the cytoskeleton are preferentially affected, and neuronal architecture becomes increasingly determined by proteins involved in labile structural states. A cascade of interdigitating pathologies is then postulated to develop characterized by nerve terminal aberrancies, subsequent extrusion of atypical polypeptide species and their conjugates, reactive gliosis, abnormal neuronal growth, and degeneration. Within this context, growth factors promote and accelerate the pathologic cascade. Based on this model, a treatment strategy is suggested that the most effective management of Alzheimer's disease, particularly during earlier stages, is to delay its projected normal onset and to control the aberrant neuronal growth that is a hallmark of the malady.
Alzheimer Disease↗
Monoaminergic-cholinergic relationships and the chemical communication matrix of the substantia nigra and neostriatum.
The historical development of histochemical methods for monoamines and chemicals involved with cholinergic function is reviewed. The use of these methods to elucidate neurochemical interactions in the substantia nigra and caudate-putamen complex is then discussed. Three hypotheses accounting for the localization of acetylcholinesterase within and/or on substantia nigra, pars compacta neurons are presented and evaluated: (a) to catabolize acetylcholine released from afferent cholinergic fibers, (b) to catabolize substance P released from some neostriato-nigral axon terminals, and/or (c) to serve as a communication link with nigral vasculature. Despite experimental evidence in favor of each of these possibilities, none have met with unqualified acceptance. Possible mechanisms and morphologic substrates accounting for dopaminergic-cholinergic, serotonergic-cholinergic, GABAergic-cholinergic, enkephalinergic-cholinergic, and cholinergic-cholinergic interactions in the caudate-putamen complex are discussed. These include synaptic and non-synaptic relationships, dendroaxonic information flow, and mutual regulatory processes.
Acetylcholinesterase↗
Cholinoceptive cells in rat cerebral cortex: somatodendritic immunoreactivity for muscarinic receptor and cytoskeletal proteins.
Adult rat telecephalon was surveyed for cells demonstrating immunopositivity for muscarinic receptor (M35 antibody), microtubule-associated proteins, neurofilaments, and brain-spectrin. Neurons immunostained for muscarinic receptor were found in frontal, parietal, temporal, and occipital isocortex where they accounted for approximately 15-16% of all neurons. This labeling involved a large proportion of layer V pyramidal cells, some layer III pyramidal cells and a small proportion of non-pyramidal cells in layers II-VI. In the hippocampus, pyramidal cells, non-pyramidal cells and granular cells were immunoreactive, as were many pyramidal cells in subicular and entorhinal cortices. In every cortical region examined, cells demonstrating muscarinic receptor were morphologically identical to cells stained lightly to moderately for acetylcholinesterase following pretreatment with diisopropylfluorophosphate, and they were found in similar numbers and in a similar laminar distribution. These characteristics further corresponded to those of cells whose somatodendritic compartments were intensely immunostained by antibodies to microtubule-associated proteins (MAP): MAP-1, MAP-2, MAP-5; neurofilament proteins (NF): NF-68kD, NF-160kD, NF-200kD; and brain-spectrin. Double immunostaining using a fluorescence method followed by an avidin-biotin staining procedure revealed that cortical cells which possessed immunoreactivity for muscarinic receptor demonstrated an 80-85% overlap with cells that were immunoreactive for MAP-2 (and tau) or NF-200kD. Following unilateral ibotenic acid lesions of the nucleus basalis, MAP-2 immunostaining was reduced in the ipsilateral isocortex. This significant reduction was most evident in the parietal cortex, exactly where maximal loss of acetylcholinesterase-containing fibers occurred. The same lesion produced no significant difference in immunodensity of muscarinic receptor, MAP-1, MAP-5 NF-68kD, NF-160kD and NF-200kD. Thus, cortical cholinoceptive cells are enriched with cytoskeletal components and cholinergic afferents modulate cortical MAP-2.
Acetylcholinesterase↗