Neuroscience
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Review of the normally occurring neuronal patterns of the hippocampus suggests that the two principal cell types of the hippocampus, the pyramidal neurons and granule cells, are maximally active during different behaviors. Granule cells reach their highest discharge rates during theta-concurrent exploratory activities, while population synchrony of pyramidal cells is maximum during immobility, consummatory behaviors, and slow wave sleep associated with field sharp waves. Sharp waves reflect the summed postsynaptic depolarization of large numbers of pyramidal cells in the CA1 and subiculum as a consequence of synchronous discharge of bursting CA3 pyramidal neurons. ⋯ It is assumed that recurrent excitation during the population burst is strongest on those cells which initiated the population event. It is suggested that the strong excitatory drive brought about by the sharp wave-concurrent population bursts during consummatory behaviors, immobility, and slow wave sleep may be sufficient for the induction of long-term synaptic modification in the initiator neurons of the CA3 region and in their targets in CA1. In this two-stage model both exploratory (theta) and sharp wave states of the hippocampus are essential and any interference that might modify the structure of the population bursts (e.g. epileptic spikes) is detrimental to memory trace formation.
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The isolated Muller glial cell of the neotenous tiger salamander retina is used as an experimental model for studying the effects of non-uniform membrane conductance on the shape of charging curves in response to step current inputs. A simple cable model of the Muller cell is formulated and used to interpret the experimental data. The Muller cell model is completely described by three parameters: (a) electrotonic length L; (b) the membrane time constant tau m; and (c) the percentage of the total membrane conductance accounted for by the endfoot S. ⋯ The error that results from misinterpreting the first equalizing time constant tau l as the membrane time constant tau m can have a significant effect on estimates of specific membrane resistance and capacitance. The algorithm described in this paper provides a means for obtaining direct estimates of the membrane time constant and will make possible more accurate estimates of specific membrane resistance and capacitance in Muller glial cells. The fact that the estimation procedure is based on a simple electrophysiological measurement suggests that it may be useful for studying asymmetry of membrane conductance in glial and neural elements of the intact nervous system.
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[125I]Iodosulpride, a highly selective and sensitive probe for dopamine D-2 receptors, was used to study the expression of these receptors in binding studies performed on membranes and serial autoradiographic sections, throughout pre- and postnatal developmental periods. D-2 receptors were first detected autoradiographically in sensory and sympathetic ganglia at the embryonic age of 12 days, i.e. much earlier than in previous studies. In membrane binding studies, D-2 receptors were found to be modulated by guanylnucleotides as early as at embryonic day 15, suggesting that they were already functionally coupled to a regulatory G protein. ⋯ In areas of dopaminergic perikarya, e.g. substantia nigra and ventral tegmental area, where they largely correspond to somatodendritic autoreceptors, D-2 receptors appeared at embryonic days 17 and 21 respectively, i.e. 3-8 days after tyrosine hydroxylase immunoreactivity, suggesting that dopamine synthesis and release is not feedback regulated by autoreceptors at initial developmental stages. In areas where D-2 receptors are present in the absence of any established dopaminergic innervation (e.g. discrete layers of the hippocampus, cerebellum, parietal cortex or in cranial nerve nuclei), they generally appeared at a late stage, i.e. during the second or even the third postnatal week. Finally, there was transient and roughly concomitant expression of both D-2 receptors and tyrosine hydroxylase immunoreactivity in some areas such as spinal ganglia or the lateral ventricle floor, consistent with a possible development function of dopamine mediated by D-2 receptors.
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Angiotensin II-(3-8)-hexapeptide, at the dose of 1 nmol given intracerebroventricularly, only slightly less than angiotensin II (the same dose and route) stimulated exploratory locomotor behaviour in an open field and electromagnetic motimeter. Both peptides considerably enhanced stereotyped behaviour produced by apomorphine and amphetamine. ⋯ The results indicate that the effectiveness of equimolar doses of angiotensin II-(3-8)-hexapeptide and angiotensin II in improving processes related to learning and memory in rats is almost identical and thus must be independent of specific angiotensin receptors in brain to which the hexapeptide binds with about 1000 times lower affinity than angiotensin II. The stimulation of stereotypy, a dopamine-controlled behaviour, by the peptides points to the possibility of dopaminergic mediation of their psychotropic effects.
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Ablation of capsaicin-sensitive afferent neurons enhances experimentally induced ulceration in the rat gastric mucosa, which suggests that these neurons are involved in gastric mucosal protection. To provide direct evidence for such a function it was investigated whether stimulation of afferent nerve endings by the intragastric administration of capsaicin could counteract the ulcerogenic effect of 25% ethanol. Capsaicin (3.2-640 microM), administered together with ethanol, inhibited the development of haemorrhagic lesions in a concentration-dependent fashion but did not alter the ethanol-induced fall in the gastric potential difference. ⋯ The protective effect of intragastric capsaicin was not altered following acute subdiaphragmatic vagotomy, acute removal of the coeliac-superior mesenteric ganglion complex, acute bilateral ligation of the adrenal glands, or pretreatment of the rats with atropine or guanethidine. These findings indicate that stimulation of afferent neurons by intragastric capsaicin affords protection of the rat gastric mucosa against ethanol-induced damage. As the autonomic nervous system is not involved gastroprotection appears to represent a local effector function of sensory nerve endings in the stomach.