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Results for “synaptic plasticity”

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At least 1,153 records · Page 64Linked to original sources
PubMed1988

Effects of pentobarbital on behavioral and synaptic plasticities in crayfish.

Intra-abdominal injections of 90 mg/kg (3.5 x 10(-4) M estimated body concentration) sodium pentobarbital (PB) eliminated the cheliped closing response and eyestalk withdrawal response in crayfish (Procambarus clarkii). Repeated injections produced tolerance to both of these behavioral measures within several days. At glutamatergic synapses of the opener muscle, PB at dosages from 10(-7) to 10(-4) M had no significant effect on non-facilitated transmitter release evoked by 1 Hz stimuli. Facilitated transmitter release at 10 Hz stimuli was significantly decreased by 10(-3) M PB but was not significantly affected at lower concentrations. At 10(-4) M and 10(-3) M, PB significantly reduced the ratio of excitatory postsynaptic potential (EPSP) amplitudes at 10 Hz to those at 1 Hz. The frequency of spontaneous miniature EPSPs (MEPSPs) was reduced by 10(-4) M PB to about half of the control level, while MEPSP amplitudes and time constants were not significantly affected. These results suggest that the ability of PB to depress various crayfish behaviors is due, at least in part, to a presynaptic ability of the drug to depress facilitation of transmitter release at glutamatergic synapses.

Action Potentials↗
PubMed1991

Modulation of synaptic plasticity in the dentate gyrus of the rat by electrical stimulation of the median raphe nucleus.

The effects of median raphe nucleus (MRN) stimulation on the induction of long-term potentiation (LTP) was investigated in the dentate gyrus (DG) of urethane-anaesthetized rats. LTP of both DG population spike amplitude and population EPSP slope was induced when tetanic electrical stimulation (100 Hz, 1 s) of the perforant path (PP), at an intensity which did not produce significant LTP alone, was presented concurrently with tetanic stimulation of the MRN. Tetanic stimulation of either the PP alone or of the PP and MRN together did not affect the short-term enhancement of population spike amplitude produced by single stimuli to the MRN. These findings suggest that serotonergic afferents from brainstem raphe nuclei may modulate the induction of LTP in the dentate gyrus.

Animals↗
PubMed1993

Chronic effects of trimipramine, an antidepressant, on hippocampal synaptic plasticity.

The effects of trimipramine (TRIM), an antidepressant agent, on both the induction and the maintenance of long-term potentiation (LTP) was investigated in area CA1 of hippocampal slice preparations. Chronic administration (7-9 days) of TRIM in rat caused a large reduction in the magnitude of LTP induced by a theta burst stimulation (TBS) paradigm. Results indicate that the reduction of LTP produced by trimipramine does not seem to result from major changes in the physiological properties of the slice preparations. First, paired-pulse facilitation was not impaired following the drug administration suggesting that transmitter release was not modified in TRIM-treated slices. Second, the burst responses evoked by high-frequency stimulation exhibited the typical buildup of depolarization, which is due to both a reduction of IPSPs and the activation of NMDA receptors. Finally, the treatment did not change the amount of short-term potentiation induced by TBS nor did it modify the component of excitatory postsynaptic potentials (EPSPs) mediated by the activation of NMDA receptors, suggesting that the NMDA receptor functions remained intact in TRIM-treated slices. Taken together the present data suggest that the loss of LTP maintenance in TRIM-treated animals is more likely the result of the disruption by trimipramine of cellular processes that follow LTP induction. In addition, the results provide evidence for a possible correlation between the reduction in LTP expression and learning deficits produced by chronic administration of trimipramine.

Animals↗
PubMedDate not supplied

Synaptic plasticity in the red nucleus and learning.

Pairing of the stimulus to the cerebral peduncle (CP) with that to the forearm skin leads cats to flex their forearms within a 10-day training period in response to stimulus to CP, which was initially ineffective. Behavioral study and extracellular unit analysis suggested that the cellular mechanism for this conditioning lies at the corticorubral (CR) synapses. Since formation of new CR synapses occurs in parallel with the recovery from behavioral deficits after brain damage and peripheral nerve cross-innervation, we explored the possibility that the formation of new CR synapses underlies conditioning. We investigated the time course of the CR excitatory postsynaptic potentials (EPSPs) as well as the distribution of the CR synapses on the somadendritic membrane of the red nucleus neurons and compared them with those observed in control animals. In conditioned animals, the times-to-peak of the CR EPSPs were significantly shorter than those in control animals. Electron microscopic studies demonstrated that more CR synapses make contact with large, i.e. proximal, dendrites and somata of red nucleus neurons in conditioned cats than in control ones. These results support the view that the formation of new synapses on the proximal dendrites and soma underlies classical conditioning in the cat.

Animals↗
PubMed1996

Sleep states, memory processes and synaptic plasticity.

There is now a substantial body of data to suggest a relationship between sleep states, particularly paradoxical sleep (PS) or rapid eye movement (REM) sleep, and learning. In animal studies, PS increases have been observed following acquisition in formal tasks and following exposure to enriched environments (EE). Further, PS deprivation at certain post-training times is known to impair memory for recently acquired tasks. PS deprivation following EE exposure has been reported to impair the neural changes normally observed. It is argued that the prolonged PS increases observed following either formal training or EE exposure reflect the same kinds of neural change. It is proposed that accelerated neural plasticity takes place during elevated post-training PS and is especially vulnerable to disruption at specific post-training time periods called PS windows. Further, it is proposed that similar processes take place in the post-training sleep of humans.

Animals↗
PubMed1988

Glutamate and dopamine modulate synaptic plasticity in horizontal cell dendrites of fish retina.

Horizontal cell dendrites protruding into the cone pedicles in fish retina exhibit a light-dependent plasticity. In a light-adapted retina they form numerous spinules having membrane densities at their tips. These spinules disappear during dark adaptation. Experiments with light- or dark-adapted retinas which were incubated in glutamate or its agonists and antagonists, respectively, revealed that this putative cone transmitter is able to reduce the expression of spinules in a light-adapted retina. Dopamine, on the other hand, induces the formation of spinules in a dark-adapted retina and haloperidol reduces the expression in a light-adapted retina. These data suggest a control of spinules plasticity through two retinal neurotransmitter systems.

Animals↗
PubMed1992

Cytochalasin inhibits light-dependent synaptic plasticity of horizontal cells in teleost retina.

Previous studies have shown that the horizontal cell-->cone photoreceptor negative feedback synapse in teleost fish retinae is 'plastic', being suppressed in the dark and potentiated by light adaptation. The possible involvement of filamentous actin in ultrastructural and electrophysiological aspects of this plasticity has been investigated using cytochalasins, which inhibit actin turnover, in the cyprinid fish (roach) retinae. Cytochalasin B or D (40 microM) inhibited both the light-dependent formation and maintenance of spinules, and enhancement of the feedback interaction involved in generation of biphasic spectral responses in horizontal cells. The results suggest that actin turnover is essential for both ultrastructural and electrophysiological plasticity of horizontal cell feedback and that spinules could mediate this dynamic interaction.

Animals↗
PubMed1991

Differences in hippocampal synaptic plasticity in rats with inborn high or low learning ability may be related to different sensitivity of aspartate receptors.

Rats with an inborn high (HP) or low (LP) learning capacity were used to study the sensitivity to the blocking effect of 2-amino-phosphonopentanoic acid (AP5; 10 and 20 microM) on long-term potentiation (LTP) produced in hippocampal slices by a 1-s tetanus at 200 Hz. The potential evoked by stimulation of the perforant path was recorded from the granule cell layer of the dentate gyrus in 400 microns slices perfused with standard Krebs' solution or the AP5. Under perfusion with 10 microM of AP5, in 100% of slices from HP rats, LTP generation was not blocked; when AP5 20 microM was used, in 85% of the cases LTP was not blocked. In 60% of slices from LP rats, AP5 10 microM and in 100% of the cases at 20 microM AP5 blocked LTP generation. These results are coherent with the hypothesis that the different inborn learning ability of HP and LP rats is related to the different population or sensitivity of N-methyl-D-aspartate (NMDA) receptors.

2-Amino-5-phosphonovalerate↗