Biomedical subjects

I Cavus

Publications and source records attributed to I Cavus.

4 recordsLinked to original sources

PubMed2002

[Augmentation of selective serotonin reuptake inhibitors (SSRI) with atypical antipsychotics in the treatment of depression].

The treatment of severe depression represents a difficult task in the daily psychiatric practice. In certain cases, augmentation therapies in order to improve the efficacy of SSRIs can be useful. Recently, it has become possible to use atypical antipsychotics for SSRI augmentation. This option adds to the existing strategies in the treatment of depression and primary systematic studies show encouraging results. In this review, the possibility of a SSRI augmentation by additionally administering risperidone or olanzapine is critically discussed.

Antipsychotic Agents↗

PubMed1998

NMDA receptor-independent LTP in basal versus apical dendrites of CA1 pyramidal cells in rat hippocampal slice.

The ability of hippocampal CA1 basal synapses to express N-methyl-D-aspartate (NMDA) receptor-independent long-term potentiation (non-NMDA LTP) was studied and compared to the simultaneously induced apical dendritic non-NMDA LTP. Non-NMDA LTP in basal and apical dendrites was induced using stimulation pattern similar to the sharp wave-associated CA3 bursts. Basal dendritic non-NMDA LTP was input-specific and displayed similar development and magnitude to the apical dendritic non-NMDA LTP. Both apical and basal dendritic non-NMDA potentiations were inhibited by the voltage-dependent calcium channel (VDCC) inhibitor verapamil and the tyrosine kinase inhibitors genistein and levandustin A. However, the difference in the degree and time course of these inhibitions suggests involvement of distinct mechanisms in the two dendritic subfields.

Animals↗

PubMed1995

Synaptic plasticity in the hippocampal slice: functional consequences.

There are 3 known forms of synaptic plasticity at CNS synapses: long-term potentiation (LTP) mediated by NMDA receptor activation, LTP mediated by voltage-dependent calcium channel (VDCC) activation, and long-term depression (LTD) mediated by the NMDA receptor. All 3 forms of synaptic plasticity can be observed in hippocampal CAl cells, all are induced by afferent activation, all involve Ca2+ influx, and all activate Ca(2+)-dependent mechanisms. We consider the functional consequences of the presence of 3, sometime opposing, forms of synaptic plasticity at the same synapse. We suggest that the 2 forms of LTP have different consequences for the synapse. We postulate that the co-existence of potentiating and depressing capabilities influences the network processing capabilities of neural networks.

Animals↗

PubMed1994

Multideterminant role of calcium in hippocampal synaptic plasticity.

Hippocampal CA1 cells possess several varieties of long-lasting synaptic plasticity: two different forms of long-term potentiation (LTP) and at least one form of long-term depression (LTD). All forms of synaptic plasticity are induced by afferent activation, all involve Ca2+ influx, all can be blocked by Ca2+ chelators, and all activate Ca(2+)-dependent mechanisms. The question arises as how different physiological responses can be initiated by activation of the same second messenger. We consider two hypotheses which could account for these phenomena: voltage-dependent differences in cytosolic Ca2+ concentration acting upon Ca2+ substrates of differing Ca2+ affinities and compartmentalization of the Ca2+ and its substrates.

Animals↗