Conversely striato-pallidal GABAergic output neurons express selleck inhibitor D2-like receptors [28, 29]. Localization of D2 and D5 receptors has also been demonstrated on GABAergic interneurons [1]. Dopamine enhances GABA release [30] and D1-like receptors selleck bio have been implicated in this effect [31-33]. Evidence about the effect of GABA on dopamine transmission is conflicting. In vitro studies using fast cyclic voltammetry suggest that Inhibitors,Modulators,Libraries GABA enhances dopamine release, as blockade of striatal Inhibitors,Modulators,Libraries GABAA receptors with picrotoxin caused a decrease in evoked dopamine release [34]. Other studies have also shown that GABA potentiates potassium stimulated 3H-dopamine release from striatal slices but did not alter spontaneous release [35].

However other in vitro studies suggest that GABA inhibits dopamine release [36-38].

In vivo studies have shown Inhibitors,Modulators,Libraries that perfusion of picrotoxin directly into the caudate nucleus, resulted in an increase in dopamine release [39]. Adenosine A1 receptors have been reported to be present on GABAergic terminals, Inhibitors,Modulators,Libraries where A1 receptor activation has been shown to be inhibitory [40]. With this in mind, the effect of GABA and adenosine receptor activity on dopamine release was also investigated.2.?Experimental Section2.1. Brain slicesMale Wistar Inhibitors,Modulators,Libraries rats (50-75g) were killed by decapitation. The brain was quickly removed into ice-cold artifical cerebrospinal fluid (aCSF). Blocks of tissue containing the caudate putamen and nucleus accumbens were prepared. 350 ��m thick slices were sectioned using a Campden vibrotome.

Brain slices were then transferred to a Inhibitors,Modulators,Libraries holding chamber containing aCSF (see below) at room temperature (20-21��C) to equilibrate for 1 h. A single slice was then transferred to a recording chamber and perfused with Inhibitors,Modulators,Libraries oxygenated aCSF at 5 ml.min-1 at 30��C Inhibitors,Modulators,Libraries for 1 h before electrical stimulation.2.2. Measurement of endogenous dopamine releaseFollowing 1 h equilibration, a bipolar tungsten-stimulating electrode with a tip separation of GSK-3 200 ��m (A-M Systems, Inc.) was placed in the dorsolateral CPu (see figure 1). A carbon fibre electrode (CFE; 7 ��m diameter carbon fibre; 50-100 ��m exposed length) was placed 100-200 ��m from the stimulating electrode.

In these Carfilzomib set of experiments we manufactured the CFEs by hand and mechanically broke back the fibre to 50 – 100 ��m from the glass seal (by a fine forceps) rather than spark etch the eletrodes (see reference [41] for more details on carbon fibre manufacture).

Fast cyclic voltammetry (FCV; Millar Voltammeter; Dr. Julian Millar, Queen Mary & Westfield College, www.selleckchem.com/products/Oligomycin-A.html University of London, UK) at the CFE was used to detect changes in extracellular concentrations of dopamine following electrical stimulation of the brain slice www.selleckchem.com/products/Belinostat.html [17, 42]. A triphasic voltage waveform (ranging from -1 to +1.4V; 20 ms duration), generated using a Millar voltammeter [43] was applied to the CFE at 2 Hz (every 500 ms; figure 2A).