A post-synaptic depressant modulatory action of 5-hydroxytryptamine on excitatory amino acid responses in rat entorhinal cortex in vitro

Stimulation of 5‐HT1A receptors in the dorsal hippocampus and inhibition of limbic seizures induced by kainic acid in rats

“…In particular, 5-HTIA receptor activation blocks long-term potentiation induced by primed burst stimulation in the CAI region (Corradetti et al, 1992) and in the entorhinal cortex, 5-HT was able to reduce the depolarization induced by pulses of glutamate during blockade of synaptic transmission (Sizer et al, 1992). These studies provide further evidence of a postsynaptic action of 5-HT mediated by 5-HTIA receptors.…”

“…Autoradiographic analysis of 5-HT receptors in fully kindled rat brain showed a selective increase in 5-HTIA binding in the dentate gyrus (Clark et al, 1993 (Ropert, 1988;Baskys et al, 1989;Beck & Choi, 1991;Ghadimi & Jarolimek, 1994), prompted us to study whether stimulation of 5-HTIA receptors by 8-OH-DPAT reduced EEG seizure activity induced by intrahippocampal infusion of kainic acid. This acute model of seizures was chosen because of (i) its similarities with temporal lobe epilepsy in man (Ben-Ari, 1985), (ii) the pivotal role receptors of excitatory aminoacids in CNS play in various convulsive syndromes (Schwarcz & Meldrum, 1985) and (iii) the functional interactions between 5-hydroxytryptaminergic and glutamatergic neurotransmission in limbic areas (Corradetti et al, 1992;Sizer et al, 1992 1985).…”

Serotonin reduces synaptic excitation in the superficial medial entorhinal cortex of the rat via a presynaptic mechanism

“…Furthermore, it has been shown recently that serotonin inhibits glutamatergic transmission onto rat motoneurons by a presynaptic mechanism (Singer, Bellingham & Berger, 1996). In contrast to our findings, fluorometric enzyme assay experiments in the entorhinal cortex showed no effects of serotonin on the glutamate release (Sizer, Kilpatrick & Roberts, 1992), probably due to a different experimental design. The increase in total cell conductance induced by 5_HT is important for the interpretation of the depressant effects on synaptic responses, since a general membrane conductance increase can reduce the amplitude of synaptic events (Ginsborg, 1973).…”

Effects of serotonin on the intrinsic membrane properties of layer II medial entorhinal cortex neurons

“…Our present results in the medial EC are consistent with these composite intrinsic actions. Although initial studies in the EC (Sizer et al, 1992;Grunschlag et al, 1997) showed prominent 5-HT 1A -mediated hyperpolarizing responses, the bulk of recent studies in the EC have primarily focused on the modulatory action of 5-HT on excitatory synaptic transmission since intrinsic responsiveness was both inconsistent and small (Schmitz et al, 1998c). Our results suggest, in contrast to these latter researchers, that the intrinsic hyperpolarizing action of 5-HT upon medial EC Layer II principal neurons is both consistent and prominent.…”

“…Initial studies of the neurophysiological effects of 5-HT application upon EC principal neurons (Sizer et al, 1992;Grunschlag et al, 1997) were consistent with intrinsic membrane effects found in other central nervous system cells, including a prominent and consistent hyperpolarization concomitant with increased membrane conductance that was mediated by stimulation of 5-HT 1A receptors. These studies also showed that 5-HT depressed electrically mediated excitatory synaptic responses, responsiveness to exogenously applied glutamate, but did not alter glutamate release or paired pulse facilitation, suggesting that any influence on excitatory neurotransmission were mediated by the postsynaptic influence of 5-HT.…”