In vivo comparison of the regulation of releasable dopamine in the caudate nucleus and the nucleus accumbens of the rat brain

Abstract

In viva voltammetry has been used to measure the release of dopamine evoked by electrical stimulation of the medial forebrain bundle (MFB). Simultaneous measurements have been made with voltammetric-sensing electrodes ipsilateral to the stimulating electrode in the nucelus accumbens and the caudate nucleus of the anesthetized rat. During the stimulation, the species observed in both regions is voltammetrically identical to dopamine. Further evidence for the identity of dopamine is provided by anatomical, physiological, pharmacological, and postmortem data. Postmortem analysis of these brain regions after a single stimulation demonstrates that dopamine levels are unchanged, while dihydroxyphenylacetic acid (DOPAC) levels are increased in both regions. Systemic application of synthesis inhibitors results in a decrease in evoked release for each brain region. Amfonelic acid results in a restoration of stimulated release after synthesis inhibition. Evoked release is affected differently by pargyline in the two brain regions. The evoked release of dopamine is significantly elevated in the nucleus accumbens as a result of pargyline administration, but similar effects are not seen in the caudate nucleus. Tissue levels of dopamine are increased in both brain regions by pargyline, but the increase is significantly greater in the accumbens. Electrolytic lesions of the striatonigral pathway or systemic administration of picrotoxin eliminates the pargyline-induced difference in evoked release of dopamine. Amphetamine causes a reduction in stimulated release in the caudate nucleus with little effect on that observed in the nucleus accumbens. Administration of pargyline prior to amphetamine results in a diminution of release in both brain regions. Taken together, these data indicate that different factors affect regulation of the releasable pool of dopamine in the nucleus accumbens and caudate nucleus.Several major dopaminergic systems exist in the mammalian brain, including the nigrostriatal and mesolimbic systems. It is known that the mesolimbic system plays an important role in the regulation of normal brain function, and this role is distinct from that played by the nigrostriatal dopamine pathway (Mogenson and Yin, 1981;White and Wang, 1982). It has been shown by unit-recording techniques that these two regions respond in different manners to pharmacological stimuli thought to affect dopaminergic neurons (Rebec and Zimmerman, 1980; Reynolds et al., 1981). The behavioral responses elicited by electrical stimulation of these two pathways differ (van der Heyden, 1984). Lesions of the two regions also produce different behavioral responses (Kelly and Moore, 1976; Pycock and Marsden, 1978). Furthermore, anatomical differences have been shown at an ultrastructural level (Bouyer et al., 1984). A rec- Received June 10, 1985; revised Oct. 7, 1985; accepted Oct. 10, 1985. This work was supported by a grant from the National Science Foundation, Neurobiology Section.Correspondence should be addressed to R. M. Wigbtman, Department...

Differential action of (+)‐amphetamine on electrically evoked dopamine overflow in rat brain slices containing corpus striatum and nucleus accumbens

“…In vivo, electrical stimulation of the median forebrain bundle in the presence of (+ )-amphetamine resulted in an increase in the efflux of [3H]-dopamine from the caudate nucleus (Von Voigtlander & Moore, 1973). By contrast, Kuhr et al (1986) using a voltammetric technique, showed that (+)-amphetamine attenuated electrically evoked endogenous dopamine efflux in the caudate nucleus but had no effect on dopamine efflux in the nucleus accumbens. In vitro, (+ )-amphetamine either enhanced electrically evoked dopamine efflux, when measured by high performance liquid chromatography (h.p.l.c.)…”

“…Actions of (+ )-amphetamine on electrical stimulation during the 35 min period could not be measured. In the in vivo voltammetric study (Kuhr et al, 1986), the effect of (+ )-amphetamine on dopamine release was monitored every 20 min.…”

Presynaptic dopaminergic function is largely unaltered in mesolimbic and mesostriatal terminals of adult rats that were prenatally exposed to cocaine

“…The data presented here and in the literature suggest that the consumption of dopamine is not altered suggesting that dopamine synthesis should also be unaltered. Since the content of dopamine in the terminals mainly reflects storage pools of dopamine [19], this leaves the possibility that the amount of stored dopamine (bound to the cytoskeleton) is decreased. However, this effect should not alter dopaminergic function other than during extreme challenge (e.g.…”

Role of Aberrant Striatal Dopamine D1Receptor/cAMP/Protein Kinase A/DARPP32 Signaling in the Paradoxical Calming Effect of Amphetamine

“…Under these conditions, it is commonly assumed that CPA principally measures striatal extracellular content of DA rather that of NA. Indeed, electrodes are more sensitive to DA than to NA, and the striatal DA innervation and DA tissue content are much greater than NA ones (DA:NA content is 100:1 in the caudate of mammals) (Kuhr et al, 1986;Garris et al, 1993). Striatal slices of WT and DAT-CI mice (n ϭ 6 per genotype and treatment) were superfused with 100 M amphetamine, 30 M nomifensine, or 100 M bupropion (diluted in the artificial CSF).…”