Add time:07/15/2019         Source:sciencedirect.com

The role of 5-HT1A and 5-HT2 receptors in mediating foot-shock-induced ultrasonic vocalisation has been studied in rats. Furthermore, behavioural effects were correlated to receptor reserves in the brain by means of receptor inactivation with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ). The dose-dependent inhibition of ultrasonic vocalisation by the 5-HT precursor, l-5-hydroxy-l-tryptophan (110–450 μmol/kg), was abolished by pretreatment with the 5-HT1A/1B antagonist, (−)-penbutolol (27 μmol/kg), and the 5-HT2A/2C antagonist, ritanserin (10 μmol/kg). The inhibitory actions of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and the 5-HT2A/5-HT2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) were reversed by the 5-HT1A antagonist, (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclohexanecarboxamide (WAY-100 635), and the 5-HT2A antagonist, (±)α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorphenyl)ethyl]-4-piperidine-methanol (MDL 100 151), respectively. Pretreatment with EEDQ (24 h, subcutaneous [s.c.]) inhibited foot-shock-induced ultrasonic vocalisation (effective dose50=0.95 μmol/kg) and decreased [3H]-8-OH-DPAT and [3H]-ketanserin binding in the brain. Pretreatment with WAY-100 635 (0.3–20 μmol/kg) 20 min prior to EEDQ administration (1.3 μmol/kg, s.c.) did not reverse the EEDQ-induced inhibition of ultrasonic vocalisation but protected the 5-HT1A receptors against EEDQ inactivation. Pretreatment with MDL 100 151 (0.83–54 μmol/kg) 20 min prior to EEDQ administration both reversed the EEDQ-induced inhibition of ultrasonic vocalisation and protected the 5-HT2A receptors against EEDQ inactivation. These findings demonstrate that 5-HT1A and 5-HT2 receptors are involved in the regulation of ultrasonic vocalisation in rats. However, the function of 5-HT1A and 5-HT2 receptors in this model seems to differ as vocalisation was preserved after protection of 5-HT2 but not 5-HT1A receptors.

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