Biomedical subjects

Saïd Kourrich

Publications and source records attributed to Saïd Kourrich.

3 recordsLinked to original sources

PubMed2003

Inwardly rectifying Kir3.1 subunit knockdown impairs learning and memory in an olfactory associative task in rat.

Inward-rectifier potassium channels gated by the direct action of G proteins are activated or inhibited by numerous neurotransmitters and they modulate neuronal excitability. Using an olfactory associative task, the effect of Kir3.1 subunit knockdown was tested on learning and memory. Repeated intracerebroventricular injections of antisense oligodeoxyribonucleotide to the Kir3.1 subunit significantly reduced hippocampal expression of its mRNA target determined by Western blotting. The antisense knockdown had no effect on locomotor and drinking activity or on attention processes. The reduction in Kir3.1 subunit impaired the learning of the odor associations and the procedural side of the task. This reduction correlated with the performance impairment. The results suggest that Kir3.1 channel activity is implicated in the memory processes.

Animals↗

PubMed2002

NMDA receptor-dependent long-term synaptic depression in the entorhinal cortex in vitro.

The entorhinal cortex receives a large projection from the piriform (primary olfactory) cortex and, in turn, provides the hippocampal formation with most of its cortical sensory input. Synaptic plasticity in this pathway may therefore affect the processing of olfactory information and memory encoding. We have recently found that long-term synaptic depression (LTD) can be induced in this pathway in vivo by repetitive paired-pulse stimulation but not by low-frequency (1 Hz) stimulation with single pulses. Here, we have used field potential recordings to investigate the stimulation parameters and transmitter receptors required for the induction of LTD in the rat entorhinal cortex in vitro. The effectiveness of low-frequency stimulation (900 pulses at 1 or 5 Hz) and repeated delivery of pairs of stimulation pulses (30-ms interpulse interval) was assessed. Only repeated paired-pulse stimulation resulted in lasting LTD, and a low-intensity paired-pulse stimulation protocol that induces LTD in vivo was only effective in the presence of the GABA(A) receptor antagonist bicuculline (50 microM). LTD could also be induced in normal ACSF, however, by increasing the number of pulse-pairs delivered and by increasing the stimulation intensity during LTD induction. The induction of LTD was blocked by constant bath application of the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovalerate (50 microM), indicating that LTD is dependent on NMDA receptor activation. However, LTD was not blocked by the group I/II mGluR antagonist (RS)-alpha-ethyl-4-carboxyphenylglycine (500 microM) or by bicuculline (50 microM). The induction of LTD in the entorhinal cortex in vitro is therefore dependent on intense stimulation that recruits activation of NMDA receptors, but does not require concurrent activation of mGluRs or inhibitory synaptic inputs.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Transient hippocampal down-regulation of Kv1.1 subunit mRNA during associative learning in rats.

Voltage-gated potassium channels (Kv) are critically involved in learning and memory processes. It is not known, however, whether the expression of the Kv1.1 subunit, constituting Kv1 channels, can be specifically regulated in brain areas important for learning and memory processing. Radioactive in situ hybridization was used to evaluate the content of Kv1.1 alpha-subunit mRNA in the olfactory bulb, ventral, and dorsal hippocampus at different stages of an odor-discrimination associative task in rats. Naive, conditioned, and pseudoconditioned animals were sacrificed at different times either prior to a two-odor significance learning or after odor discrimination was established. Important decreases of Kv1.1 mRNA levels were transiently observed in the ventral hippocampus before successful learning when compared with the pseudoconditioned group. Moreover, temporal group analysis showed significant labeling alterations in the hippocampus of conditioned and pseudoconditioned groups throughout the training. Finally, Kv1.1 mRNA levels in the hippocampus were positively correlated with odor-reward association learning in rats that were beginning to discriminate between odors. These findings indicate that the Kv1.1 subunit is transiently down-regulated in the early stages of learning and suggest that Kv1 channel expression regulation is critical for the modification of neuronal substrates underlying new information acquisition.

Analysis of Variance↗