<i>In vivo</i> release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen

Santiago, Marti; Machado, Alberto; Cano, Josefina

doi:10.1111/j.1476-5381.1993.tb13647.x

Cited by 43 publications

(27 citation statements)

References 44 publications

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“…2). GABA released from these neurons may inhibit dopamine release by activating GABA B receptors in the medial prefrontal area (Santiago et al, 1993). This suggestion is compatible with the coupling of 5-HT 2A receptors to G q proteins and, accordingly, their excitatory rather than inhibitory effect.…”

supporting

confidence: 73%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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supporting

confidence: 73%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

View full text Add to dashboard Cite

“…Thus, the lack of effect of intraCPu baclofen is more likely because CPu GABA B receptors are not involved in acute amphetamine-induced behaviors than to the heterogeneity of the striatum. Similarly, GABA B receptors in the mPFC appear not to be involved in the motor stimulatory effects of acute amphetamine although intra-mPFC baclofen decreases nomifensine-induced extracellular dopamine levels in PFC (Santiago et al, 1993). Similarly, selective quinolinic acid-induced lesions of the prelimbic cortex (Cg3), which only destroy intrinsic neurons, did not affect locomotion and rearing responses induced by amphetamine (Tzschentke and Schmidt, 1998).…”

Section: Effects Of Intracerebral Baclofen On Amphetamine-induced Behmentioning

confidence: 99%

“…In support of the regional differences in baclofen's effectiveness, perfusion of baclofen into the SN decreased basal and nomifensine-induced extracellular dopamine levels in the SN and CPu, but infusion into the CPu did not decrease striatal dopamine levels (Westerink et al, 1992;Santiago et al, 1993;Balon et al, 2002). GABA B receptors are expressed by striatonigral, striatopallidal, and glutamatergic afferents as well as by dopamine and GABA neurons in the SN and VTA (Sugita et al, 1992;Charara et al, 2000;Boyes and Bolam, 2003).…”

Section: Effects Of Intracerebral Baclofen On Amphetamine-induced Behmentioning

confidence: 99%

Intracerebral Baclofen Administration Decreases Amphetamine-Induced Behavior and Neuropeptide Gene Expression in the Striatum

Zhou

Mailloux

McGinty

2004

Neuropsychopharmacol

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In a previous study, systemic administration of the GABA B receptor agonist, R-( þ )-baclofen (2.5 mg/kg, i.p.) blocked acute amphetamine (2.5 mg/kg, i.p.)-induced rearing and neuropeptide (preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII)) mRNA expression in the striatum (Zhou et al, 2004). The purpose of the present study was to investigate the site(s) of action of these baclofen effects in the dorsal and ventral striatal circuitries. Infusion of baclofen (75 ng/side) into the ventral tegmental area (VTA), substantia nigra (SN), nucleus accumbens (NA), caudate-putamen (Cpu), or medial prefrontal cortex (mPFC) had no effect on behavioral activity in saline-treated rats habituated to a photocell apparatus. However, intra-VTA infusion of baclofen (75 ng/ side) completely blocked, whereas intra-NA and intra-SN infusion of baclofen attenuated, amphetamine-induced vertical activity without affecting amphetamine-induced total distance traveled. In contrast, intramedial PFC and intra-CPu infusion of baclofen had no effect on behavioral activity in amphetamine-treated rats. Infusion of baclofen into the VTA, NA, or SN decreased amphetamine-induced neuropeptide gene expression in the striatum. These results indicate that GABA B receptor stimulation within the ventral striatal circuitry is involved in mediating acute amphetamine-induced behaviors and neuropeptide gene expression in the dorsal and ventral striatum. The present study provides information on the potential targets in the brain for baclofen in the initial behavioral and genomic response to amphetamine.

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“…The activation of GABAB receptors both at the somatodendritic (Westerink et al, 1996) and at the terminal level (Santiago et al, 1993) has been suggested to result in decreased mesocorticolimbic DA release. Our present results suggest that the action at the nerve terminal level is not strong enough to inhibit the stressinduced increase in DA release in the PFC.…”

Section: Figmentioning

confidence: 99%

Local Activation of Metabotropic Glutamate Receptors Inhibits the Handling‐Induced Increased Release of Dopamine in the Nucleus Accumbens but Not that of Dopamine or Noradrenaline in the Prefrontal Cortex: Comparison with Inhibition of Ionotropic Receptors

Feenstra

Botterblom

Uum

1998

Journal of Neurochemistry

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On-line in vivo microdialysis was used to determine the effects of a 16-mm handling period on release of dopamine (DA) in the nucleus accumbens and of DA and noradrenaline (NA) in the medial prefrontal cortex of awake, freely moving rats. DA and NA were determined in one HPLC run. Handling resulted in an immediate and strong increase of both catecholamines in the prefrontal cortex. Maximal values for DA were 295%, and for NA 225%, of controls. DA in the nucleus accumbens was also increased (to 135% of controls) but only after a short delay. Local inhibition of ionotropic glutamate receptors by continuous reversed dialysis of the drugs 6-cyano-7-nitroquinoxaline, D-2-amino-5-phosphonopentanoic acid, or dizocilpine did not significantly affect handling-induced increases in cortical DA and NA release. Neither did the agonist of metabotropic glutamate receptors, trans-(1 S,3R)-1 -aminocyclopentane-1 ,3-dicarboxylic acid (ACPD), or the GABA-B agonist baclofen. Reversed dialysis of dizocilpine in the nucleus accumbens was equally ineffective, but ACPD inhibited the increase in DA release in this area. Stimulation of metabotropic glutamate receptors in the nucleus accumbens was previously reported to inhibit activation of DA release in that area after stimulation of glutamatergic or dopaminergic afferents. It is concluded that metabotropic receptors in the nucleus accumbens are important for the control of activation of DA release in the accumbens by physiological stimuli but that a similar mechanism is lacking in the prefrontal cortex.

show abstract

In vivo release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen

Cited by 43 publications

References 44 publications

5-HT Receptor Regulation of Neurotransmitter Release

5-HT Receptor Regulation of Neurotransmitter Release

Intracerebral Baclofen Administration Decreases Amphetamine-Induced Behavior and Neuropeptide Gene Expression in the Striatum

Local Activation of Metabotropic Glutamate Receptors Inhibits the Handling‐Induced Increased Release of Dopamine in the Nucleus Accumbens but Not that of Dopamine or Noradrenaline in the Prefrontal Cortex: Comparison with Inhibition of Ionotropic Receptors

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