Abstract

The goal of this study was to determine whether the dopamine D 3 receptor in limbic structures plays a role in the shell-specific and dopamine-dependent display of jaw movements in rats. When combined with the dopamine D 1 receptor agonist (±)-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine (SKF 82958, 5 μg), the putative dopamine D 3 receptor agonist (±)-7-hydroxy- N,N-di- n-propyl-2-aminotetralin (7-OH-DPAT, 10 μg) produced repetitive jaw movements following injection into the shell, but not the core, of the nucleus accumbens. This behaviour was only partially inhibited by local blockade of dopamine D 1 receptors ( R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine, SCH 23390, 500 ng), dopamine D 2 receptors (domperidone, 50 and 100 ng) or dopamine D 2 3 receptors (l-sulpiride, 25 ng). Combined blockade of both dopamine D 1 and D 2 receptors in the shell completely antagonized the jaw movements elicited by the cocktail of SKF 82958 and 7-OH-DPAT. Replacing 7-OH-DPAT by another putative dopamine D 3 receptor agonist, S(+)-(4 aR, 10 bR)-3,4,4 a,10 b-tetrahydro-4-propyl-2 H,5 H-[1]benzopyrano[4,3- b]-1,4-oxazin-9-ol (PD 128,907, 10 μg), in the cocktail did not produce jaw movements, when administered into the shell. Injection of the cocktail of SKF 82958 and 7-OH-DPAT into the ventrolateral striatum, which contains nearly no dopamine D 3 receptors, also elicited jaw movements. It is concluded that mesolimbic dopamine D 3 receptors play no role in the dopamine-dependent and shell-specific jaw movements: the contribution of 7-OH-DPAT in the cocktail of SKF 82958 and 7-OH-DPAT to the display of jaw movements is solely due to its ability to activate dopamine D 2 receptors.

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