PubMed Health⌕ Search

Biomedical subjects

H Vara

Publications and source records attributed to H Vara.

5 recordsLinked to original sources
PubMed2004

Characterization of release-independent short-term depression in the juvenile rat hippocampus.

Short-term depression strongly influences neuronal activity in cerebral circuits and contributes to low-pass temporal filtering of information. In this work, we show that synaptic depression evoked by stimulation of commissural-Schaffer collateral afferents at 10 Hz is associated with a reduction of the fibre volley. This depression of action potentials is also evident in the absence of extracellular Ca(2+), which underlies its release-independent nature. In addition, this reduction of the excitability is independent of failures in action potential propagation since increasing the distance between the stimulus and recording electrodes does not alter this effect. Whole-cell recordings show that tetanic stimulation at supraminimal intensity induces action potential failures preceded by changes in the repolarization rate of the action potentials leading the membrane potential to hyperpolarized values. This activity-dependent hyperpolarization was blocked by ouabain, an indication of the important role of the Na(+)-K(+)-ATPase in this process. Then again, an alteration of the firing threshold was observed when action potentials were elicited either by somatic current injection or by synaptic stimulation, which indicates that this mechanism could alter the EPSP-spike coupling in these cells. The results suggest that these factors act together to reduce gradually the safety factor for action potential generation and to produce failures in action potential initiation; in fact, experiments made at twice the supraminimal intensity show a dramatic decrease in the rate of these failures. Taken together, the results suggest the existence of a release-independent component of short-term depression that is related to failures in action potential initiation.

Action Potentials↗
PubMed2003

Age-dependent alterations of long-term synaptic plasticity in thyroid-deficient rats.

Thyroid hormone deficiency during a critical period of development profoundly affects cognitive functions such as attention, learning, and memory, but the synaptic alterations underlying these deficits remain unexplored. The present study examines the effect of congenital hypothyroidism on long-term synaptic plasticity. This plasticity is believed to be essential for learning and memory and for activity-dependent regulation of synapse formation in the developing brain. We found that the neonatal expression of long-term potentiation (LTP), long-term depression (LTD), depotentiation, and de-depression in hippocampal slices from hypothyroid animals was similar to that of controls. To examine the postnatal development of these plasticities, we used slices from neonatal (2-3 weeks) and adult (7-8 weeks) rats. This work demonstrates that the ability to express all these forms of synaptic plasticity is reduced in an age-dependent manner in control rats. LTP and depotentiation are also downregulated in adult hypothyroid rats, but we have found that de-depression is not affected during maturation. In addition, these animals express LTD at ages at which controls fail to induce it. In contrast, input/output experiments have shown greater levels of basal synaptic efficacy in hypothyroid adults, and this effect is probably related to the higher probability of release observed by paired-pulse experiments. Nevertheless, these effects appear to be unrelated to the differences observed in long-term synaptic plasticity, as no correlation was found between basal synaptic efficacy and the degree of LTD and de-depression. Furthermore, the NMDA-receptor antagonist amino-phosphonopentanoic acid (APV) completely blocked LTD, which suggests a postsynaptic locus of this alteration. Because LTD has been associated with novelty acquisition, we suggest that the greater LTD observed in adult hypothyroid rats might be related to the hyperactivity of these animals. However, other possibilities such as a retarded maturation of synaptic plasticity must be taken into account.

Aging↗
PubMed2002

Thyroid hormone regulates neurotransmitter release in neonatal rat hippocampus.

Thyroid hormone is essential for the normal maturation and function of the mammalian CNS. Thyroid hormone deficiency during a critical period of development profoundly affects cognitive functions such as learning and memory. However, the possible electrophysiological alterations that could underlie these learning deficits in hypothyroid animals remain largely unexplored. In this work, we have studied the possible effect of thyroid hormone on short-term synaptic plasticity, which is hypothesized to be a neural substrate of short-term memory. We compared short-term modification of the excitatory postsynaptic potential in hippocampal slices between control and hypothyroid rats. Electrophysiological studies reveal that paired-pulse facilitation is strongly altered in the hypothyroid rats. In addition, hypothyroid rats exhibit an increase in the Ca(2+)-dependent neurotransmitter release. These alterations are basically reversible when thyroid hormone is administered. In order to examine the possible molecular mechanisms underlying these synaptic changes, we compared the expression of synapsin I, synaptotagmin I, syntaxin, and alpha-Ca(2+)/calmodulin kinase II between control and hypothyroid hippocampus. Our results show that the levels of synapsin I and synaptotagmin I are increased in the hypothyroid rats, which suggests that the genes encoding these proteins are implicated in the action of thyroid hormone on neurotransmitter release. Taken together, the results from this study suggest that thyroid hormone may modulate the probability of neurotransmitter release.

Adenosine↗
PubMedDate not supplied

[Short term synaptic plasticity].

INTRODUCTION: At many chemical synapses, the amount of transmitter released by each action potential can increase or decrease markedly after the onset of specific temporal patterns of activity. OBJECTIVES: This review focuses on mechanisms and functions of short term presynaptic plasticity that last from milliseconds to minutes. The short term enhancement of neurotransmitter release is due to three calcium dependent presynaptic processes differing in their durations: about one second or less (facilitation), about 30 seconds (augmentation) and several minutes (post tetanic potentiation). These forms of short term potentiation are usually attributed to a transient elevation in presynaptic calcium ions (Ca2+) concentration following the arrival of the action potential. Otherwise, presynaptic depression processes, as well as the facilitation ones, depend on neurotransmitter release probability. Thus, synapses with high release probability show few facilitation and are easily depressed because of their ability to deplete faster all synaptic vesicles of the ready releasable pool. CONCLUSIONS: Short term synaptic plasticity appears to serve as a flexible mechanism for temporal information processing in higher cortical integration.

Action Potentials↗