Elsevier

Neuropharmacology

Volume 33, Issues 3–4, March–April 1994, Pages 449-456
Neuropharmacology

Effects of chlorisondamine and restraint on cortical [3H]ketanserin binding, 5-HT2A receptor-mediated head shakes, and behaviours in models of anxiety

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Abstract

A recent study has indicated that ganglionic transmission mediates acute restraint-elicited increases in brain tryptophan (5-HT precursor) levels, 5-HT synthesis and (possibly) release. Because restraint-induced release of 5-HT has been shown to be associated with a paradoxical increase in cortical 5-HT2A receptor binding, we have examined the influence of 5-HT synthesis/release upon cortical 5-HT2A receptor binding and 5-HT2A receptor-mediated head shakes in 3-hr restrained rats pretreated with the ganglionic blocker chlorisondamine. In keeping with past reports regarding the effects of restraint and ganglionic blockade upon anxiety, we have also measured the behavioural effects of restraint and/or chlorisondamine in two animal models of anxiety, the elevated plus-maze and the social interaction test. Chlorisondamine pretreatment (2.5 mg/kg, 20 min beforehand) prevented restraint-elicited defaecation and body weight decreases. Although stress amplified the head shake response to the injection of the 5-HT2A/5-HT2C receptor agonist 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane (DOI, 1 or 2 mg/kg 2 hr after the end of restraint), cortical [3H]ketanserin binding remained unaltered. Chlorisondamine treatment was inactive, except for the amplification of the head shake response to DOI (2 mg/kg) in restrained rats. When exposed to the social interaction test, neither restraint nor chlorisondamine affected social interaction, locomotion, or rearings. In the elevated plus-maze, the percent number of open arms entered and the total number of arms enterd were decreased by acute restraint, whilst chlorisondamine pretreatment was inactive.

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    Moreover, changes in receptor expression within a specific subset of neurons in a particular brain area (e.g., within the PVN but not the rest of the hypothalamus) could have escaped detection with the methods used in the present study. Nevertheless, it is worth noting that other investigators have reported instances in which DOI-induced head twitches were altered with no concomitant changes in frontal cortical 5-HT2A receptor binding (Chaouloff et al., 1994; Izumi et al., 2002). In a recent study of cocaine withdrawal, enhanced sensitivity of neuroendocrine responses to DOI was found to be associated with increased Gαq and Gα11, alpha subunits of G proteins that are coupled to the 5-HT2A receptor (Carrasco et al., 2004).

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