Nucleus Accumbens and Dopamine-Mediated Turning Behavior of the Rat: Role of Accumbal Non-dopaminergic Receptors

Abstract

Abstract. Accumbal dopamine plays an important role in physiological responses and diseases such as schizophrenia, Parkinson's disease, and depression. Since the nucleus accumbens contains different neurotransmitters, it is important to know how they interact with dopaminergic function: this is because modifying accumbal dopamine has far-reaching consequences for the treatment of diseases in which accumbal dopamine is involved. This review provides a summary of these interactions, and our current knowledge about them are as follows: A) AMPA receptors are required for dopamine-dependent behavior and vice versa; NMDA receptors modulate the activity at the level of AMPA and/or dopamine D 1 receptors. B) GABA A , but not GABA B , receptors inhibit dopamine-dependent behavior. C) Nicotinic receptors are required for dopamine-dependent behavior, whereas muscarinic receptors inhibit dopamine-dependent behavior. D) α-Adrenoceptors inhibit dopamine-dependent behavior in contrast to β-adrenoceptors, which potentiate this behavior. E) μ-and δ 2 -opioid receptors elicit behavior that requires an intact dopaminergic function and δ 2 -opioid receptors modulate dopamine-dependent behavior. F) Orexin 2 receptors play an important, modifying role in dopamine-dependent behavior. G) Somatostatin receptors potentiate dopamine-dependent behavior. It is suggested that modulation of the above-mentioned nondopaminergic receptors provide new tools to control physiological functions as well as diseases mediated by accumbal dopamine.

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

“…With respect to the interaction of these systems, there is a study showing that the NMDA receptors are localized on the NAc shell neurons which abundantly contain dopamine D 1 receptors [81]. Some evidence has also indicated the modulation of dopamine function through NMDA and AMPA receptors [30]. In an interesting report, Kalivas et al declared that SCH 23390 and sulpiride restore the amphetamine-induced glutamate level decrease in NAc suggesting the involvement of presynaptic dopamine receptors in this phenomenon [36].…”

“…These two dopamine family receptors have a high expression in both parts of NAc while at different distribution patterns. For example, the D 1 -and D 2 -like dopamine receptor families are higher and lower in the NAc shell than in core, respectively [30]. This may partly explain the different physiological functions of the two parts of NAc [40,42].…”

“…Due to the abundant dopaminergic inputs which NAc shell receives from various brain parts and the consequent high contraction level of dopamine in the NAc shell, this part is believed to render a critical role in dopamine-mediated functions [30]. The NAc receives its dopaminergic afferents from the ventral tegmental area (VTA) and the substantia nigra (SN), and the glutamatergic inputs from several brain areas such as prefrontal cortex, amygdala and hippocampus [30].…”

Effects of Hypericum perforatum on turning behavior in an animal model of Parkinson's disease

“…Besides dopamine, H. perforatum also reduces serotonin and noradrenalin uptake, and it has been reported to have a brain-derived neurotrophic-factor-like effect (Leuner et al, 2007). Other authors indicate an interaction of hyperforin with non-dopaminergic receptors (Ikeda et al, 2012). Those effects in other structures, like the subthalamic nucleus, are involved on the modulation of turning behavior (Ikeda et al, 2012;Petri et al, 2013).…”

Dopaminergic Hyperactivity Accompanied by Hyperlocomotion in C57BL/6J-bgJ/bgJ (beige-J) Mice

“…In fact, activation of the mesolimbic dopaminergic system induces several behavioral changes including an increase in locomotor activity in rodents (1,2). Furthermore, psychostimulant-induced hyperlocomotion, which is mediated by activation of the mesolimbic dopaminergic system, has been used as an animal model of schizophrenia (3).…”