摘要:

AbstractWe model a small system of hypothetical neurons having ongoing afferent input (“stimulus”) short‐term refraction/inhibition, and brief‐latency intercellular excitatory feedback loops. We incorporate postsynaptic plasticity: synapses onto a given cell are grouped into dendritic “neighborhoods” wherein sufficiently large local postsynaptic potentials sums cause proportional changes in local synaptic efficacy. The efficacies record multiple cell‐to‐cell and time‐to‐time correlations. The efficacy patterns fall into several classes, for each of which there is a stereotypical relationship leading from “steady‐state” stimuli to corresponding sets of possible “responses” (periodic firing patterns). We examine the system's ability to discriminate between stimuli via firing patterns and to retain information during change of efficacies. There is an optimal region for efficacy configurations inside of which discrimination is good and outside of which the system can be inactive, particularly forgetful, of perseverative. We find that stimulus discrimination is enhanced by divergence and convergence in the pattern of afferent input. Perseverative firing patterns, invoked or suppressed by cotransmitters, can play a role in associat

ISSN:0887-4476    

DOI:10.1002/syn.890030202

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractEthanol (ETH) and general anesthetics have been reported to facilitate the chloride channel opening, possibly, or at least partly, through an interaction with the GABA‐benzodiazepine (BZ) receptor‐gated chloride ionophore “supramolecular complex”. Recently Ro 15‐4513, a novel BZ ligand, has been indecated as a potent and selective antagonist of various ETH‐induced behavioral and biochemical effects. However, since its precise characterization is still a matter of debate, we have tested and compared the effect of Ro 15‐4513, as well as its antagonism against ETH, in two objective electrophysiological parameters, i.e., the electroencephalograph (EEG) pattern in freely moving rats and single unit activity of reticulata neurons.Ro 15‐4513 produced an EEG state of alertness and antagonized the behavioral impairment and the EEG deterioration by ETH. However, while its protective action was consistent against moderate doses (2 g/kg) of ETH, it was much less evident versus higher doses. (4 and 8 g/kg).On reticulata cells, Ro 15‐4513 potently stimulated their spontaneous firing and reversed the depression by both ETH and Na‐pentobarbital. Moreover, the ß‐carboline DMCM also had similar effects.The “pure” BZ antagonist Ro 15‐1788 was completely inefective against ETH, yet fully cancelled the reversing actions of Ro 15‐4513 and DMCM upon ETH or Na‐pentobarbital effects.It is concluded that Ro 15‐4513 behaves as a BZ inverse agonist, so that its opposition to ETH and Na‐pentobarbital is probably the result of its “negative” coupling with the BZ recognition site that triggers the closing of chloride channels. It suggests that BZ inverse agonists might constitute, in the nea

ISSN:0887-4476    

DOI:10.1002/syn.890030203

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractThe nicotinic agonists dimethylphenylpiperazinium iodide (DMPP) and carbachol (CARB) as well as (−)nicotine ((−)NIC) were tested alone and in combination with N‐methyl‐D‐aspartate (NMDA) for their abilities to enhance the efflux of3H‐norepinephrine (NE) from slices of rat hippocampus. CARB and (−)NIC produced small, transient increases in NE efflux, while DMPP produced larger, longlasting increases. Inasmuch as the nicotinic antagonists mecamylamine (MECA) and hexamethonium (C6) did not consistently inhibit the increases in NE efflux produced by these agonists, the role of a nicotinic receptor in mediating these responses is uncertain. CARB and DMPP enhanced the ability of NMDA to stimulate NE release, while (−)NIC did not. MECA, but not C6, was found to selectively antagonize NMDA‐stimulated NE release that did not appear to involve a nicotinic receptor. Binding studies indicated that MECA and the related nicotinic antagonist pempidine produced an inhibition of NMDA‐stimulated NE release by an action at the PCP receptor that is known to be linked to the NMDA receptor‐ionophore complex. These data suggest that the actions of these ganglionic blocking agents on excitatory responses in the hippocampus involve inhibition of excitatory amino acid as well a

ISSN:0887-4476    

DOI:10.1002/syn.890030204

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractThe time course of synaptogenesis in the visual part of the superior colliculus (SC) of pigmented rats has been studied. The number of synaptic profiles per unit area and volume of neuropil in the stratum griseum superficiale (SGS) was estimated in seven groups of animals at ages 3, 9, 15, 21, 30, 49 and 85 days after birth.At 3 days only 1.5 ± 0.06 synaptic contacts per unit area and 5.5 ± 0.18 per unit volume were found. Most of them were immature contacts between growing processes. The density of synaptic contacts increased slowly during the first week. By day 9, 4.1 ± 0.25 and 13.4 ± 0.66 synaptic contacts were counted per unit of area and volume, respectively. A rapid synaptic proliferation occurred during the next 3 weeks and there were 7.7 ± 0.27 and 25.5 ± 1.04 synaptic contacts per unit area and volume at 15 days, 21.1 ± 1.70 and 86.4 ± 5.11 at 21 days, and 25.9 ± 1.20 and 96.7 ± 3.48 at 30 days. At the same time, the synaptic population gradually acquired more mature morphological characteristics: the pre‐ and postsynaptic structures became more specialized, the number of synaptic vesicles within presynaptic structures increased, and the synaptic junctional apposition became defined. After 30 days, a decrease in the density of synaptic profiles was recorded: 23.9 ± 0.44 and 79.8 ± 1.43 per unit area and volume of neuropil at 49 days and 13.4 ± 0.53 and 49.7 ± 2.40 at 85 days, respectively. Thus, after the phase of synaptic proliferation, a significant reduction of synaptic density occurred in the SGS neuropil until it was stabilized at the adult level by the third month of life.Considering the data available on the development of the retinal and visual cortical projections to the SC, the process of synaptic elimination, which takes place after the first postnatal month, does not appear to be directly connected with segregation of these particu

ISSN:0887-4476    

DOI:10.1002/syn.890030205

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractIntracellular recordings were made from rat medial vestibular nucleus (MVN) neurons in transverse brain slices containing the root of the vestibular nerve (N. VIII). Electrical stimuli applied to the N. VIII tract evoked an orthodromic excitatory postsynaptic potential (EPSP) that lasted about 50 ms following a 0.5 to 1.5 ms delay between the stimulus artifact and synaptic potential. These orthodromic EPSPs were insensitive to the following antagonists: atropine, hexamethonium, dephenhydramine, and caffeine. Based on these results we conclude that the primary afferent excitatory transmitter is not acetylcholine, histamine, or adenosine, respectively. However, kynurenic acid, a general excitatory amino acid receptor antagonist, blocked the orthodromic EPSP while having no effect on the resting membrane potential, input resistance, or action potential configuration of MVN neurons. Our data suggest that an excitatory amino acid, or amino acid‐like substance, is responsible for primary afferent excitatory transmission in the rat medial vestibular nucleu

ISSN:0887-4476    

DOI:10.1002/syn.890030206

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractHigh‐dose treatment with pilocarpine hydrochloride, a cholinergic muscarinic agonist, induces seizures in rodents following systemic or intracerebral administration. Pilocarpine seizures are characterized by a sequential development of behavioral patterns and electrographic activity. Hypoactivity, tremor, scratching, head bobbing, and myoclonic movements of the limbs progress to recurrent myoclonic convulsions with rearing, salivation, and falling, and status epilepticus. The sustained convulsions induced by pilocarpine are followed by widespread damage to the forebrain. The amygdala, thalamus, olfactory cortex, hippocampus, neocortex, and substantia nigra are the most sensitive regions to epilepsy‐related damage following convulsions produced by pilocarpine. Spontaneous seizures are observed in the long‐term period following the administration of convulsant doses of pilocarpine.Developmental studies show age‐dependent differences in the response of rats to pilocarpine. Seizures are first noted in 7–12 day‐old rats, and the adult pattern of behavioral and electroencephalographic sequelae of pilocarpine is seen in 15–21‐day‐old rats. During the third week of life the rats show an increased susceptibility to the convulsant action of pilocarpine relative to older and younger animals. The developmental progress of the convulsive response to pilocarpine does not correlate with evolution of the brain damage. The adult pattern of the damage is seen after a delay of 1–2 weeks in comparison with the evolution of seizures and status epilepticus. The susceptibility to seizures induced by pilocarpine increases in rats aged over 4 months.The basal ganglia curtail the generation and spread of seizures induced by pilocarpine. The caudate putamen, the substantia nigra, and the entopeduncular nucleus govern the propagation of pilocarpine‐induced seizures.The antiepileptic drugs diazepam, clonazepam, phenobarbital, valproate, and trimethadione protect against pilocarpine‐induced convulsions, while diphenylhydantoin and carbamazepine are ineffective. Ethosuximide and acetazolamide increase the suspectibility to convulsant action of pilocarpine. Lithium, morphine, and aminophylline also increase the susceptibility of rats to pilocarpine seizures.The pilocarpine seizure model may be of value in designing new therapeutic

ISSN:0887-4476    

DOI:10.1002/syn.890030207

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

ISSN:0887-4476    

DOI:10.1002/syn.890030201

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY