Locomotor inhibition induced by procaine injections into the nucleus accumbens core, but not the medial ventral striatum: Implication for cocaine‐induced locomotion

Abstract

We examined whether injections of the local anesthesia procaine into the nucleus accumbens core disrupts locomotion more readily than those into the medial ventral striatum. Spontaneous locomotion decreased during the first 10 min immediately following injections of procaine into the core. When procaine was co-administered with d-amphetamine into the core, the injections also decreased amphetamine-induced locomotion during the initial 10 min. On the other hand, no detectable effect on spontaneous or amphetamine-induced locomotion was found when procaine was injected into the medial ventral striatum, including the medial shell and medial olfactory tubercle. We replicated our recent finding that cocaine injections into the core induced delayed, modest locomotion, while cocaine injections into the medial ventral striatum induced immediate, vigorous locomotion. Injections of amphetamine into the core induced as equally vigorous locomotion as that of the medial ventral striatum. These results show that the neurons of the core involved in locomotion are more vulnerable to local anesthesia than the neurons of the medial ventral striatum. In other words, cocaine at the doses inducing vigorous locomotion in the medial ventral striatum induces local anesthesia when applied to the core.

Evidence for Multiple Sites within Rat Ventral Striatum Mediating Cocaine-Conditioned Place Preference and Locomotor Activation

“…For example, amphet- amine acted with similar potency at either injection site, whereas cocaine stimulated locomotor activity most strongly after injection into medial OT and medial shell (Ikemoto, 2002). Importantly, locomotor responses from accumbens core injections of cocaine may have been weakened by local anesthesia (Ikemoto and Witkin, 2003).…”

“…In addition, only cocaine infusion at amOT sites produced CPP at the doses tested (Ikemoto, 2003). However, the behavioral effects of focal cocaine infusion into the NAcc (shell or core) may be masked by local anesthesia (Ikemoto and Witkin, 2003). Nevertheless, DA antagonist microinjection experiments suggest that it is the medial shell rather than the core that mediates the reinforcing effects of self-administered i.v.…”

“…Intra-NAcc infusion of cocaine produces both locomotor stimulation and rewarding effects (Ikemoto, 2002(Ikemoto, , 2003Rodd-Henricks et al, 2002;Ikemoto and Witkin, 2003). However, the interpretation of such findings is complicated by possible sympathomimetic and anesthetic actions within the target tissue (Ikemoto, 2003;Ikemoto and Witkin, 2003). Even after systemic injection, the precise route of administration can be critical.…”

Quantitative Trait Locus Analysis Identifies Rat Genomic Regions Related to Amphetamine-Induced Locomotion and Gαi3 Levels in Nucleus Accumbens

“…Amphetamine-induced locomotion (AIL) is a well-studied phenomenon in animal models of psychiatric disorders, including stimulant addiction and psychoses (Blackburn and Szumlinski, 1997;Ikemoto and Witkin, 2003;Rajakumar et al, 2005). AIL, regarded as a measure of mesolimbic dopamine function (Dellu-Hagedorn, 2005), is mediated via dopaminergic transmission in the nucleus accumbens (NAc) (Kim and Vezina, 1998;Chausmer and Ettenberg, 1999;Millan et al, 1999;Ikemoto and Witkin, 2003).…”

“…AIL, regarded as a measure of mesolimbic dopamine function (Dellu-Hagedorn, 2005), is mediated via dopaminergic transmission in the nucleus accumbens (NAc) (Kim and Vezina, 1998;Chausmer and Ettenberg, 1999;Millan et al, 1999;Ikemoto and Witkin, 2003). AIL differs from other types of locomotion, such as noveltyinduced locomotion (NIL), which has been associated with stress responses.…”