Serotonin 5-HT1A Receptor-Mediated Reduction of Excitatory Synaptic Transmission in Layers II/III of the Parasubiculum. (15th May 2019)

• Record Type: Journal Article
• Authors: Carter, Francis; Chapman, C. Andrew
• Is Part Of: Neuroscience. Volume 406(2019)
• Page Start: 325
• Page End: 332
• Publication Date: 2019-05-15
• Subjects: 5-HT 5-hydroxytryptamine, or serotonin -- ACSF artificial cerebrospinal fluid -- fEPSPs field excitatory postsynaptic potentials -- GABA gamma aminobutyric acid -- N-K Newman–Keuls test -- NMDA N-methyl-D-aspartate; parasubiculum -- EPSP -- rat -- serotonin -- 5-HT1A receptor; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2019.03.024
• Languages: English
• ISSNs: 0306-4522

Abstract

Abstract: Serotonin (5-HT) has important effects on cognitive function within the hippocampal region where it modulates membrane potential and excitatory and inhibitory synaptic transmission. Here, we investigated how 5-HT modulates excitatory synaptic strength in layers II/III of the parasubiculum in rat brain slices. Bath-application of 1 or 10 μM 5-HT resulted in a strong, dose-dependent, and reversible reduction in the amplitude of field excitatory postsynaptic potentials (fEPSPs) recorded in the parasubiculum. The 5-HT reuptake blocker citalopram (10 μM) also reduced fEPSP amplitudes, indicating that 5-HT released within the slice inhibits synaptic transmission. The reduction of fEPSPs induced by 5-HT was blocked by the 5-HT1A receptor blocker NAN-190 (10 μM), but not by the 5-HT7 receptor blocker SB-269970 (10 μM). Moreover, the 5-HT1A agonist 8-OH-DPAT induced a reduction of fEPSP amplitude similar to that induced by 5-HT. The reduction was prevented by the 5-HT1A receptor blocker NAN-190. The reduction in fEPSPs induced by either 5-HT or by 8-OH-DPAT was accompanied by an increase in paired-pulse ratio, suggesting that it is due mainly to reduced glutamate release. Our data suggest that the effects of serotonin on cognitive function may depend in part upon a 5-HT1A -mediated reduction of excitatory synaptic transmission in the parasubiculum. This may also affect synaptic processing in the entorhinal cortex, which receives the major output projection of the parasubiculum. Highlights: Serotonin reduces the amplitude of evoked field excitatory postsynaptic potentials in the parasubiculum in vitro. The reduction of excitatory synaptic transmission induced by serotonin is concentration-dependent and reversible. The reduction is mimicked by the 5-HT1A receptor agonist 8-OH-DPAT, and is blocked by the 5-HT1A receptor blocker NAN-190. The serotonin reuptake blocker citalopram also reduces the amplitude of excitatory synaptic responses. Serotonin and 8-OH-DPAT increase paired-pulse ratio, consistent with a reduction in glutamate release.