Effects of apomorphine on free-operant avoidance behavior in the rat.
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Animals↗
Biomedical subjects
L L Butcher
Publications and source records attributed to L L Butcher.
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↗
Involvement of free oxygen radicals in beta-amyloidosis: an hypothesis.
Compelling evidence suggests that cerebral deposition of aggregating beta-amyloid protein may trigger the neurodegenerative cascades of Alzheimer's disease, Down syndrome, and, to a lesser degree, normal aging. We propose further that free oxygen radicals are critically involved in beta-amyloidosis. Apart from the established role of free radicals in other amyloidoses, our proposal is consistent with a large number of findings. Among these are (a) the salient relationship of Alzheimer's disease with aging and the increase in free oxygen radical liberation with advancing age; (b) biochemical and analytic epidemiologic evidence that free radical formation is increased in the disorder; (c) preliminary evidence that quenching free radicals slows the clinical progression of Alzheimer's disease; (d) the early and invariable beta-amyloid accumulation in trisomy 21, a syndrome associated with elevated free radical activity and with concomitant high levels of beta-amyloid precursor protein; (e) other factors that may be associated with increased liberation of free oxygen radicals and deposition of beta-amyloid protein. Possible mechanisms by which free radicals might modulate beta-amyloidosis are discussed.
Aging↗
Acetylcholinesterase and catecholamine distribution in the locus ceruleus of the rat.
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Acetylcholinesterase↗
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↗
Afferent projections to the dorsal motor nucleus of the vagus.
The afferent projections to the dorsal motor nucleus of the vagus (DMN) were investigated by iontophoretically infusing horseradish peroxidase (HRP) into that neural region of the rat. After the tetramethylbenzidine histochemical procedure was performed on the HRP-injected brains, projections to the DMN from several areas were observed including the nucleus reticularis parvocellularis and gigantocellularis, the nucleus of the solitary tract, the nucleus raphe obscuris, the principal sensory trigeminal nucleus, and the paraventricular nucleus of the hypothalamus. The pathway originating in the paraventricular nucleus was the only forebrain projection to the DMN, a finding compatible with observation of other investigators.
Afferent Pathways↗