Neuroscience
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Synaptosomal-associated protein, 25 kD, (SNAP-25) is a novel protein containing a possible transition metal binding site and encoded by a neuronal-specific mRNA. We examined the distribution of SNAP-25 mRNA and protein in the hippocampal formation of the adult rat following kainic acid, colchicine, and entorhinal lesions. The results show that destruction of granule cells of the dentate gyrus and CA3 pyramidal cells did not diminish SNAP-25 immunoreactivity in the dendritic fields of these cells. ⋯ These results support the identification of SNAP-25 as a novel presynaptic protein. In addition, SNAP-25 immunoreactivity was increased in afferent fibers which project to areas adjacent to the deafferented region, and expression of SNAP-25 mRNA was increased in neurons deafferented by the lesion. Examination of SNAP-25 immunoreactivity and mRNA expression may provide a useful marker of major hippocampal pathways and of axonal plasticity in neurological disorders such as Alzheimer's disease and temporal lobe epilepsy.
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The regional, cellular and subcellular distribution of GABA, GABA receptors and benzodiazepine receptors was investigated by light and electron microscopy in the human lumbar spinal cord taken post-mortem from eight cases aged 20-76 years. Firstly, the regional distribution of GABA receptors and benzodiazepine receptors was studied using autoradiography following in vitro labelling of cryostat sections with tritiated ligands. This was followed by a detailed study of the cellular and subcellular distribution and localization of GABA and benzodiazepine/GABAA receptors by light and electron microscopy using immunohistochemical techniques with monoclonal antibodies to GABA and to the alpha and beta subunits of the benzodiazepine/GABAA receptor complex. ⋯ Benzodiazepine/GABAA receptors were localized within the same types of synaptic complexes in which GABA-immunoreactive axon terminals were found. In these synaptic complexes, benzodiazepine/GABAA receptor immunoreactivity was associated with presynaptic and postsynaptic membranes and on apparent non-synaptic membranes. These results show a high concentration of GABA, GABA receptors and benzodiazepine receptors in lamina II of the dorsal horn of the human spinal cord and suggest a possible role for GABA in spinal sensory functions.
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We have examined the distribution of microglia in the normal adult mouse brain using immunocytochemical detection of the macrophage specific plasma membrane glycoprotein F4/80. We were interested to learn whether the distribution of microglia in the adult brain is related to regional variation in the magnitude of cell death during development and resulting monocyte recruitment, or whether the adult distribution is influenced by other local microenvironmental cues. We further investigated the possibility that microglia are sensitive to their microenvironment by studying their morphology in different brain regions. ⋯ They can be extremely elaborate and there is wide variation in the length and complexity of branching of the processes. There was no evidence of monocyte-like cells in the adult CNS. The systematic variation in microglial morphology provides further evidence that these cells are sensitive to their microenvironment.
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Local treatment of rat peripheral nerves with capsaicin induces permanent impairment of afferent C-fiber functions and changes in the response properties of spinal dorsal horn neurons. In this study a new experimental approach, the "capsaicin gap" technique, has been utilized in an attempt to unravel pathomorphological alterations which commence in the domain of primary sensory neurons as a consequence of perineural treatment with capsaicin. The technique relies on the facts that peripheral nerves in the spinal dorsal horn are represented in a strict somatotopic manner, and on the observation that in the adult rat systemic injection of appropriate doses of capsaicin results in a selective degeneration of primary afferent fibers within Rexed's laminae I and II of the spinal cord. ⋯ It is concluded that the central terminals of capsaicin-sensitive sciatic afferents underwent transganglionic degeneration as a result of prior perineural treatment with capsaicin, and a subsequent systemic injection of this neurotoxin therefore failed to cause axon terminal degeneration in somatotopic areas served by the treated nerve. Comparative quantitative morphometric analysis of cell populations of dorsal root ganglia related to capsaicin- or vehicle-treated nerves disclosed (1) a marked reduction in the proportion of small-sized neurons, (2) a fall of about 80% in the percentage of neurons which undergo degeneration after the systemic injection of capsaicin, and (3) a marked decrease in the total number of neurons in ganglia ipsilateral to the capsaicin-treated nerves. Quantitative electron microscopic studies on saphenous nerves treated perineurally with capsaicin revealed a 32% reduction in the number of unmyelinated axons as compared with the controls, whereas the number of myelinated fibers was unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)
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Dysfunction of subcortical serotoninergic neurons has been implicated in some behaviour disturbances. The serotoninergic neurons in the dorsal and median raphe project widely in the brain. They innervate the olfactory bulbs and can be targets for exogenous agents attacking the olfactory epithelium and bulbs. ⋯ In spite of this the animals, as adults, had a severe serotonin depletion in the cerebral cortex and hippocampus, and showed abnormal locomotor and explorative behaviour as well as learning deficits. The neocortex was histologically intact and parameters related to other neurotransmitters such as dopamine, noradrenaline, GABA and acetylcholine showed no marked changes. A relatively selective damage to serotoninergic nuclei as a result of virus neuroinvasion through a natural portal of entry, may constitute a new pathogenetic mechanism for cortical dysfunction and behavioural deficits.