Amphetamine Microinfusion in the Dorso-Ventral Axis of the Prefrontal Cortex Differentially Modulates Dopamine Neurotransmission in the Shell-Core Subterritories of the Nucleus Accumbens (original) (raw)
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Journal of Neuroscience Methods, 1991
The present study was designed to test the hypothesis that the active neurotransmitter processes of release and uptake affect the in vivo microdialysis recovery of dopamine (DA) in the nucleus accumbens (N ACC) of the rat. The in vivo recovery for DA was established for rats which had received either unilateral infusions of the neurotoxin 6-hydroxydopamine (6-OHDA, 8 #g) or vehicle (0.2 p,g ascorbate). In the quantitative dialysis method used (point of no net flux method), DA is added to the perfusate at concentrations above and below the expected extracellular concentration (0, 5, 10 and 20 nM) and DA is measured in the dialysate from the brain to generate a series of points. A linear fit is performed, the slope of which is the in vivo recovery of the dialysis probe. The in vivo recovery of the 6-OHDA group was 30 + 3% which was significantly lower (P < 0.002) than the in vivo recovery of the control group which was 60 + 3% (mean + SEM; n = 6/group). The zero intercept of this regression is the point of no net flux, which is the extracellular concentration of DA independent of the probe sampling characteristics. The extracellular DA concentration for the 6-OHDA group was 7.8 + 1.1 nM, which was not significantly different than the control group which was 6.9 + 0.7 nM. The tissue DOPAC/DA ratios of the 6-OHDA lesioned hemispheres were significantly higher than the contralateral hemispheres of the same animals (0.62 + 0.1 vs. 0.27 + 0.1; P < 0.02) while the DOPAC/DA ratios in the control group were not significantly different (0.24 + 0.1 vs. 0.27+ 0.1). The fractional DA efflux from the terminals in the 6-OHDA group was significantly higher than the fractional DA efflux of the control group (0.52 + 0.08 vs. 0.03 __. 0.003; P < 0.0001), indicating that the remaining terminals have increased turnover of DA. Despite the increased turnover, however, the number of remaining release and uptake sites are not sufficient to maintain the high in vivo recovery observed in the control group.
Journal of Neuroscience Methods, 1990
This study describes the results of a systematic characterization of extracellular dopamine (DA) and y-aminobutyric acid (GABA) recovered from dorsolateral striatum using in vivo microdialysis in rats following acute (2.5 h) and chronic (1 day, 2 day and 4 day) implantation of the probe. The voltage and calcium dependence of DA and GABA overflow was characterised by perfusion with the sodium channel blocker tetrodotoxin (TFX 10-6M) and with Ca2+-frec Ringers perfusion medium. In addition, the effect of halothane anaesthesia on the responsiveness of these neurotransmitter substances to TI'X and Ca2+-free perfusion medium was investigated. Perfusion with TFX decreased basal DA levels by at least 60% in all groups. The TTX-induced decrease was most profound in halothane-anaesthetised rats, 24 h after implantation of the probe. Responsiveness of GABA to TTX infusion was different between the groups. In acutely implanted halothane-anaesthetised rats basal GABA levels were unaltered by perfusion with TI'X while in the remaining groups at least a 35% reduction was observed. In awake rats 2 days following implantation of the probe removal and replacement of the Ca 2+ from the perfusion medium resulted in a reversible reduction of basal DA by 87%. In addition, basal GABA levels were decreased by 52%. This decrease was delayed and was not reversed 1.5 h after the Ca2+-free perfusion medium was replaced with normal perfusion medium although basal GABA levels returned to pre~experimental levels by the following day. The present study demonstrates that the responsiveness of striatal DA and GABA to manipulations of both voltage-dependent (TTX) and vesicular release (Ca2+-free perfusion) is influenced by the length of time elapsed after the implantation of the dialysis fiber and the conscious state of the animal.
Psychopharmacology, 1993
Concentric dialysis probes were vertically implanted in rats in the nucleus accumbens (Acc) of one side and in the dorsal caudate-putamen (CPu) of the other side. On the day after the implant the output of dopamine was monitored and the changes elicited by d-amphetamine sulphate were compared in the two areas. Amphetamine preferentially stimulated dopamine release in the Acc in a wide range of doses (0.25, 0.5, 1.0, 2.0 mg/kg SC) when Acc probes were located in the medial aspect of the Acc. In contrast, no significant differences between the Acc and the dorsal CPu were obtained in response to amphetamine (0.5 mg/kg SC) when Acc probes were located about 0.7 mm lateral to the previous site. It is concluded that the preferential effect of amphetamine in the Acc is related to precise topographical boundaries. This in turn might be related to the existence of a sharp anatomical and functional heterogeneity within the Acc.
Naunyn-Schmiedeberg's Archives of Pharmacology, 1990
Brain microdialysis experiments were performed to assess the effects of calcium (1.2 retool/1 and 3.4 retool/l) in the perfusio solution on a variety of pharmacological treatments known to affect the release of dopamine (DA) and/or acetylcholine (ACh). Intrastriatal infusion of the muscarinic receptor agonist oxotremorine (100 ~tM), the selective dopamine D-2 receptor agonist (-)-N-0437 (1 gM), and the indirect DA agonists (+)amphetamine (10 ~tM) and nomifensine (1 ~tM) via the dialysis probe did not affect the overflow of ACh when the perfusion fluid contained 3.4 mmol/1 calcium. In contrast, these compounds produced pronounced decreases in the overflow of ACh at 1.2 retool/1 calcium. Intrastriatal infusion of the muscarinic receptor antagonist atropine (1 laM) increased the output of ACh both at 1.2 retool/1 and 3.4 mmol/1 calcium. The selective DA D-2 receptor antagonist (-)-sulpiride (1 gM) did not affect the overflow of ACh at either calcium concentration. Infusion of oxotremorine and atropine had no effect on the overflow of DA at either 1.2 retool/1 or 3.4 retool/1 calcium. (-)-N-0437 decreased and (-)-sulpirde increased DA overflow, both effects being independent of the calcium concentration in the perfusion fluid. Nomifensine and (+)amphetamine caused relatively (but not absolutely) larger increases in the overflow of DA at 1.2 retool/1 calcium. These findings emphasize the critical importance of the calcium concentration of the perfusion fluid in determining the nature of pharmacological responses in microdialysis experiments, and demonstrate that locally applied dopaminergic drugs can modulate striatal cholinergic function.
Journal of Neuroscience Methods, 2002
Dual probe microdialysis was employed to characterize the origins of dialysate glutamate, aspartate and gamma-aminobutyric acid (GABA) in the medial prefrontal cortex (mPfc) and to investigate functional interactions between the mPfc and ventral tegmental area (VTA) in awake, freely moving rats. Perfusion with elevated potassium (K ' ; KCl, 100 mM, 20 min), low Ca 2' (0.1 mM, 60 min) or tetrodotoxin (TTX, 10 mM, 100 min) was performed in the mPfc and dialysate levels of glutamate, aspartate and GABA were measured locally and in the VTA. Elevated K ' in the mPfc rapidly increased dialysate glutamate and aspartate locally ('/909/10 and '/419/9% from basal, respectively) and in the VTA ('/719/14 and '/429/14%, respectively). MPfc GABA was also rapidly increased ('/2419/62%) while VTA GABA was not affected. Perfusion with low Ca 2' in the mPfc decreased local glutamate, aspartate and GABA ((/269/8; (/359/7 and (/459/8%, respectively) and decreased only GABA ((/409/5%) in the VTA. Intra-mPfc TTX increased glutamate and aspartate locally ('/829/23 and '/549/27%, respectively) and in the VTA ('/849/18 and '/389/17%, respectively). In contrast, intra-mPfc TTX decreased local GABA ((/33'/6%) while VTA GABA levels were not affected. Taken together, these data confirm the influence of the mPfc upon the ipsilateral VTA and provide evidence for two neuronal pools which contribute to basal extracellular mPfc and VTA glutamate, aspartate and GABA levels, the first pool derived from Na ' -and Ca 2' -dependent release and the second derived from voltage-dependent reuptake. #
Brain Research Bulletin, 1987
~rt/rn,7c,r,rr.s tr7ic,rcrclicr/~sis and crmphctcminr, injbsion in the nw/~~~s crc~c~rcmhor.s and striatrrm c!ffrz~!\: mo~+ng rats: Inc~rcwsc~ i/l r.utrrrc~c~//rt/nr doprrrxitle rrnd serofotzin. BRAIN RES BULL 19(6f 623-628, 1987.-To test the effects of systemic and local amphetamine on dopamine and serotonin release in freely moving rats, guide cannulas were implanted in the nucleus accumbens and ventral striatum for removable 200 i* microdialysis probes. Comparing 4.5 min samples before and after IP amphetamine (2 mgikg), dopamine (DA) in dialysate from the accumbens increased from a baseline of 3 pg/20 ~1 to I I pg/20 yl; whereas dopamine metabolites. DOPAC and HVA decreased. This was probably due to block of DA reuptake and inhibition of monoamine oxidase, MAO. Accumbens serotonin increased from a baseline of 8 to 11 pg/ZO ~1. Changes in the ventral striatum were similar. In the second experiment, microdialysis was performed before and after local injection of amphetamine (4 pg) to reveal effects of
Brain Research, 2001
The present study was undertaken to investigate and compare the properties of noradrenaline release in the locus coeruleus (LC) and prefrontal cortex (PFC). For that aim the dual-probe microdialysis technique was applied for simultaneous detection of noradrenaline levels in the LC and PFC in conscious rats. Calcium omission in the LC decreased noradrenaline levels in the LC, but increased its levels in the PFC. Novelty increased noradrenaline levels in both structures. Infusion of the a-adrenoceptor agonist clonidine decreased 2 extracellular noradrenaline in the LC as well as in the PFC. Infusion of the a-adrenoceptor antagonist BRL44408, or the 2A a-adrenoceptor agonist cirazoline into the LC or PFC caused a similar dose-dependent increase in both structures. When BRL44408 or 1 cirazoline were infused into the LC, few effects were seen in the PFC. Infusion of the 5-HT-receptor agonist flesinoxan into the LC or 1A the PFC decreased the release of noradrenaline in both structures. When flesinoxan was infused into the LC, no effects were seen in the PFC. When the GABA antagonist bicuculline was applied to the LC, noradrenaline increased in the LC as well as in the PFC. It is A concluded that the release of noradrenaline from somatodendritic sites and nerve terminals responded in a similar manner to presynaptic receptor modulation. The possible existence of dendritic noradrenaline release is discussed.
Neuroscience, 1996
In the present study we employed the dual probe approach to investigate functional interactions between the nigrostriatal dopaminergic and striatonigral GABAergic pathways in the awake, freely moving rat and their role in motor function. One microdialysis probe of concentric design was implanted in the substantia nigra pars reticulata and another in the ipsilateral dorsolateral striatum. Perfusion with a low-Ca 2+ (0.1 mM) medium and with the voltage-dependent Na+-channel blocker tetrodotoxin (10 # M) was alternatively performed in both brain regions and the dialysate dopamine, glutamate and GABA levels were simultaneously measured in the dorsolateral striatum, whereas GABA levels alone were monitored in the substantia nigra. Perfusion with a low-Ca 2+ medium in the substantia nigra pars reticulata did not affect local GABA levels, but transiently increased striatal dopamine release (+40%) without modifying striatal glutamate and GABA levels. Conversely, intranigral perfusion with tetrodotoxin transiently increased local GABA levels (+40%), while it decreased striatal dopamine (-60%) and increased glutamate (+70%) and GABA (+ 50%) levels. Perfusion with a low-Ca 2+ medium in the dorsolateral striatum reversibly decreased local dopamine (-70%), glutamate (-20%) and GABA (-20%) levels, while local perfusion with tetrodotoxin decreased dopamine (-70%), increased glutamate (+ 30%) but did not affect dialysate GABA levels in this brain area. Neither of these intrastriatal treatments significantly affected GABA levels in the substantia nigra. Intranigral but not intrastriatal perfusion with tetrodotoxin was also associated with an increase in spontaneous locomotor activity as expressed by contralateral turning. Intranigral and intrastriatal perfusion with low-Ca 2+ medium did not influence locomotor activity. On the basis of these neurochemical and behavioural findings, we propose a new dynamic model for the study of motor behaviour as mediated by basal ganglia circuitry.