In vivo voltammetric monitoring of catecholamine release in subterritories of the nucleus accumbens shell

Abstract

Fast-scan cyclic voltammetry (FSCV) at carbon-fiber microelectrodes has been used to demonstrate that sub-second changes in catecholamine concentration occur within the nucleus accumbens (NAc) shell during motivated behaviors, and these fluctuations have been attributed to rapid dopamine signaling. However, FSCV cannot distinguish between dopamine and norepinephrine, and caudal regions of the NAc shell receive noradrenergic projections. Therefore, in the present study, we examined the degree to which norepinephrine contributes to catecholamine release within rostral and caudal portion of NAc shell. Analysis of tissue content revealed that dopamine was the major catecholamine detectable in the rostral NAc shell, whereas both dopamine and norepinephrine were found in the caudal subregion. To examine releasable catecholamines, electrical stimulation was used to evoke release in anesthetized rats with either stimulation of the medial forebrain bundle, a pathway containing both dopaminergic and noradrenergic projections to the NAc, or the ventral tegmental area/substantia nigra, the origin of dopaminergic projections. The catecholamines were distinguished by their responses to different pharmacological agents. The dopamine autoreceptor blocker, raclopride, as well as the monoamine and dopamine transporter blockers, cocaine and GBR 12909, increased evoked catecholamine overflow in both the rostral and caudal NAc shell. The norepinephrine autoreceptor blocker, yohimbine, and the norepinephrine transporter blocker, desipramine, increased catecholamine overflow in the caudal NAc shell without significant alteration of evoked responses in the rostral NAc shell. Thus, the neurochemical and pharmacological results show that norepinephrine signaling is restricted to caudal portions of the NAc shell. Following raclopride and cocaine or raclopride and GBR 12909, robust catecholamine transients were observed within the rostral shell but these were far less apparent in the caudal NAc shell, and they did not occur following yohimbine and desipramine. Taken together, the data demonstrate that catecholamine signals in the rostral NAc shell detected by FSCV are due to change in dopamine transmission.

Frequency-Dependent Effects of Ethanol on Dopamine Release in the Nucleus Accumbens

“…Ethanol studies examining non-stimulated phasic activity using electrophysiological and voltammetric techniques have shown that ethanol increases phasic firing activity in the VTA (Mereu et al, 1983), as well as increased frequency of phasic release events in the NAc core (Cheer et al, 2007; Robinson et al, 2009). Although phasic release in the NAc may occur spontaneously in in vivo anesthetized preparations (Park et al, 2010), it is typically mimicked using high-frequency multiple-pulse stimulations of the midbrain, or the medial forebrain bundle (Yavich and Tiihonen, 2000; Jones et al, 2006). In in vivo voltammetry studies, ethanol has a biphasic effect on electrically evoked DA release, slightly increasing evoked DA release at low doses (0.1 g/kg, I.P.)…”

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

“…On the other hand, the rostral part of the NAc as well as the dorsal striatum have scattered NE innervations [46-48]. These data were recently confirmed by direct catecholamine assay, in situ voltammetry, stimulations of the median forebrain bundle and various pharmacological manipulations [49]. The origin of these fibers is only partly attributed to LC, although this issue remains under debate [25].…”

Norepinephrine and dopamine transmission in 2 limbic regions differentially respond to acute noxious stimulation

“…Animals were maintained at a body temperature of 37°C with a heating pad (Harvard Apparatus, Holliston, MA) during surgical procedures, which have been described previously [38; 41]. Briefly, animals were anesthetized with urethane (1.5 g/kg, i.p.…”