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Query: UNIPROT:P08908 (
5-HT1A
)
5,574
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Motoneuron membrane potentials were recorded from the ventral roots of isolated, hemisected frog spinal cords using sucrose gap techniques. The effects of the selective 5-HT3 agonist 2-methyl-serotonin (2-Me-5HT) on the changes in motoneuron membrane potential produced by dorsal root stimulation and by superfusion of excitatory amino acid agonists were evaluated. Application of 2-Me-5HT (100 microM) did not alter motoneuron membrane potential, but did substantially reduce (approximately 20%) the polysynaptic ventral root potentials evoked by dorsal root stimulation. 2-Me-5HT did not change motoneuron depolarizations generated by addition to the Ringer's solution of the excitatory amino acid agonists AMPA (10-30 microM), kainate (30 microM), or t-ACPD (100 microM), but NMDA-induced motoneuron depolarizations (100 microM) were significantly and reversibly reduced (approximately 20%) by exposure to 2-Me-5HT (100 microM). 2-Me-5HT-evoked decreases of NMDA depolarizations were blocked by the 5-HT3 antagonists ICS 205 930 (50-100 microM) and D-tubocurarine (3-10 microM), but not by MDL 72222 (20-100 microM), the 5-HT2 receptor antagonist ketanserin (10 microM), or the
5-HT1A
/5-HT2A antagonist spiperone (10 microM). Two lines of evidence support the hypothesis that the effects of 2-Me-5HT are generated by an indirect mechanism involving interneurons: (1) TTX (0.781 microM) eliminated the effect of 2-Me-5HT on NMDA-induced motoneuron depolarizations, and (2) 2-Me-5HT reduced spontaneous ventral root potentials that result from interneuronal discharges. We attempted to establish the identity of a putative transmitter released by interneurons responsible for the effects on NMDA-depolarizations produced by 2-Me-5HT, but the AMPA receptor antagonist, CNQX (10 microM), the GABAA receptor antagonist, bicuculline (50 microM), the GABAB receptor antagonist, saclofen (100 microM), the opioid antagonist, naloxone (100 microM), and the adenosine antagonists,
CPT
(20-100 microM) and CSC (10-100 microM) did not alter 2-Me-5HT-induced reductions of NMDA-depolarizations. In sum, the site of interaction between 2-Me-5HT and NMDA appears to be at interneuronal locus, but the mechanism remains unclear.
...
PMID:Modulation of frog spinal cord interneuronal activity by activation of 5-HT3 receptors. 878 13
Cognitive control processes may depend on contextual information, sometimes improving performance, but impairing performance if expectancies about forthcoming events induce pre-potent responses. The neurobiological bases of these effects are not understood. Here, we examine context-dependent variations of response control processes using the AX-
CPT
task with respect to the relevance of the functional serotonin 1A receptor polymorphism (
5-HT1A
C(-1019)G) in a sample of healthy subjects (N=90) by means of event-related potentials (ERPs). The results show that, when context information is helpful to drive behavioural performance, carriers of the -1019G allele reveal compromised cognitive control. Yet, they show enhanced task performance when strong context representations would lead to declines in behavioural control. These findings are paralleled by modulations of the (Nogo)-P3 ERP-component. These results show for the first time that, even though the -1019G allele enhances the risk to develop anxiety disorders, it also confers an advantage to its carriers in terms of better cognitive control processes in conditions where contextual information compromises cognitive control. Effects of the
5-HT1A
C(-1019)G polymorphism were further modulated by anxiety sensitivity. As the functional effect of the
5-HT1A
C(-1019)G polymorphism has previously been shown to be rather specific for serotonergic 1A autoreceptors in the dorsal raphe nucleus (DRN), the results suggest that contextual modulations in cognitive control may be exerted by the DRN.
...
PMID:The functional 5-HT1A receptor polymorphism affects response inhibition processes in a context-dependent manner. 2164 34