Systemic administration of baclofen and the GABAB antagonist, CGP 35348, does not affect GABA, glutamate or aspartate in microdialysates of the striatum of conscious rats

Pc, Waldmeier; Stöcklin, K.; Jj, Feldtrauer

doi:10.1007/bf00168947

Cited by 16 publications

(7 citation statements)

References 14 publications

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“…U-tastical on dopaminergic terminals in the ST, as baclofen infusion nn-Whitney U-test): had no effect on dopamine release. These results are in agreement with those obtained by Bonano & Raiteri (1987) who reported that baclofen was without effect on dopamine release from synaptosomes, while Waldmeier et al (1992) have also indicated by microdialysis that baclofen does not affect striatal GABA release. Arias-Montano et al (1991) suggested that GABAB receptors on dopaminergic terminals could control the synthesis of dopamine and the increase in DOPAC found in the present study after baclofen perfusion ** * ** * into the ST would support this view, since it has been suggested that DOPAC is formed from newly synthesized ** ** ** dopamine (Zetterstrom et al, 1988 Bunney, 1984;Pinnock, 1984;Lacey et al, 1988;Kalivas et al, 1990).…”

Section: Discussionsupporting

confidence: 93%

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

Santiago

Machado

Cano

1993

British J Pharmacology

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1 The effect of baclofen, a GABAB receptor agonist, on the release of dopamine from the striatum (ST), substantia nigra (SN) and prefrontal cortex (PFC) of the rat was examined by intracerebral microdialysis. 2 Perfusion of baclofen 50 LM did not affect the striatal release of dopamine. However, dopamine release was markedly reduced in the SN and PFC. 3 3,4-Dihydroxyphenylacetic acid and homovanillic acid output increased in the ST and decreased in the SN and PFC when baclofen was perfused through the microdialysis probe. 5-Hydroxyindoleacetic acid levels were not affected in any experimental condition by baclofen perfusion. 4 The results suggest that GABAB receptors modulate the release of dopamine in the SN and PFC, but do not affect the striatal release of dopamine, which indicates that the role of GABA receptor activation is different in the dopaminergic terminals of the ST and PFC.

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Section: Discussionsupporting

confidence: 93%

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

Santiago

Machado

Cano

1993

British J Pharmacology

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“…Administration of CGP-35348, a GABAB antagonist, at a dose that has been shown to suppress almost completely SWD in GAERS (Marescaux et al, 1992b), also did not affect dialysate GABA levels, again in agreement with previous findings (Waldmeier et al, 1992b) . This lends further support to the hypothesis that enhanced extracellular GABA levels are not merely a consequence of SWD activity .…”

Section: Discussionsupporting

confidence: 90%

“…However, this decrease was not statistically significant, possibly because of the poor time resolution of the microdialysis technique when limited by the sensitivity of the detection method, as is the case with dialysate basal GABA content measurements . A similar lack of response to ( -) -baclofen administration, measured in rat striatum, has been re-ported previously (Waldmeier et al, 1992b) . As argued by these authors, these findings do not preclude the possibility of presynaptic GABAB receptors operating in vivo but highlight the current limitations of microdialysis to address such questions .…”

Section: Discussionsupporting

confidence: 82%

Extracellular GABA in the Ventrolateral Thalamus of Rats Exhibiting Spontaneous Absence Epilepsy: A Microdialysis Study

Richards

Lemos

Whitton

et al. 1995

Journal of Neurochemistry

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There is compelling evidence that excessive GABA‐mediated inhibition may underlie the abnormal electrical activity, initiated in the thalamus, associated with epileptic absence seizures. In particular, the GABAB receptor subtype seems to play a critical role, because its antagonists are potent inhibitors of absence seizures, whereas its agonists exacerbate seizure activity. Using a validated rat model of absence epilepsy, we have previously found no evidence of abnormal GABAB receptor density or affinity in thalamic tissue. In the present study, we have used in vivo microdialysis to monitor changes in levels of extracellular GABA and other amino acids in this brain region. We have shown that basal extracellular levels of GABA and, to a lesser extent, taurine are increased when compared with values in nonepileptic controls. However, modifying GABAergic transmission with the GABAB agonist (−)‐baclofen (2 mg/kg i.p.), the GABAB antagonist CGP‐35348 (200 mg/kg i.p.), or the GABA uptake inhibitor tiagabine (100 µM) did not produce any further alteration in extracellular GABA levels, despite the ability of these compounds to increase (baclofen and tiagabine) or decrease (CGP‐35348) seizure activity. These findings suggest that the increased basal GABA levels observed in this animal model are not simply a consequence of seizure activity but may contribute to the initiation of absence seizures.

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“…Furthermore, it is difficult to observe the obvious effects of GABAB antagonists even on GABA release because of their weak affinities for their receptors. Waldmeier et a!. (1992) reported that systemic administration of baclofen and CGP 35348, a GABAB antagonist, did not affect GABA in microdialysates of the striatum of conscious rats.…”

Section: Discussionmentioning

confidence: 99%

Endogenous GABA Modulates Histamine Release from the Anterior Hypothalamus of the Rat

Okakura-Mochizuki

Mochizuki

Yamamoto³

et al. 1996

Journal of Neurochemistry

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Using a microdialysis method, we investigated the effects of the nipecotic acid-induced increase in content of endogenous GABA on in vivo release of histamine from the anterior hypothalamus (AHy) of urethane-anesthetized rats. Nipecotic acid (0.5 mM), an inhibitor of GABA uptake, decreased histamine release to -~60%of the basal level. This effect was partially antagonized by picrotoxin (0.1 mM), an antagonist of GABAA receptors, or phaclofen (0.1 mM), an antagonist of GABAB receptors. These results suggest that histamine release is modulated by endogenous GABA through both GABAA and GABAB receptors. When the tuberomammillary nucleus, where the cell bodies of the histaminergic neurons are localized, was stimulated electrically, the evoked release of histamine from the nerve terminals in the AHy was significantly enhanced by phaclofen, suggesting that GABAB receptors may be located on the histaminergic nerve terminals and modulate histamine release presynaptically. On the other hand, picrotoxin caused an increase in histamine release to~-~1 70% of the basal level, and this increase was diminished by coinfusion with -) -2-amino-5-phosphonopentanoic acid (0.1 mM), an antagonist of NMDA receptors. Previously, we demonstrated tonic control of histamine release by glutamate mediated through NMDA receptors located on the histaminergic terminals in the AHy. These results suggest the possible localization of GABAA receptors on glutamatergic nerve terminals and that the receptors may regulate the basal release of histamine indirectly.

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Systemic administration of baclofen and the GABAB antagonist, CGP 35348, does not affect GABA, glutamate or aspartate in microdialysates of the striatum of conscious rats

Cited by 16 publications

References 14 publications

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

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

Extracellular GABA in the Ventrolateral Thalamus of Rats Exhibiting Spontaneous Absence Epilepsy: A Microdialysis Study

Endogenous GABA Modulates Histamine Release from the Anterior Hypothalamus of the Rat

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