Histamine H3 receptor activation selectively inhibits dopamine D1 receptor-dependent [3H]GABA release from depolarization-stimulated slices of rat substantia nigra pars reticulata

Garcia, M.C.; Florán, Benjamí­n; Arias‐Montaño, José‐Antonio; Young, J. M.; Aceves, Jorge

doi:10.1016/s0306-4522(97)00100-0

Cited by 124 publications

(87 citation statements)

References 35 publications

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“…It has been demonstrated, for example, that increased activity of H3 receptors may result in the inhibition of release of other neurotransmitters, like serotonin (Fink et al, 1990), norepinephrine (Di Carlo et al, 2000), glutamate (Doreulee et al, 2001), and GABA (Garcia et al, 1997). All of these systems are affected by methamphetamine administration, and they have extended connections with the dopaminergic system.…”

Section: Discussionmentioning

confidence: 99%

“…This potentiation of methamphetamine's subjective effects by thioperamide was reversed by coadministering the histamine H3 agonist R-a-methylhistamine, demonstrating that the effects were mediated by histamine H3 receptors. In in vitro studies selective histamine H3 receptor antagonists can potentiate dopamine efflux in mouse striatum (Schlicker et al, 1993) and dopamine D1 receptor-dependent release of GABA in rat substantia nigra (Garcia et al, 1997) and striatum (Arias-Montano et al, 2001). Moreover, histamine H3 agonists inhibit the synthesis of dopamine in striatal areas and this is blocked by selective H3 antagonists, suggesting that endogenous histamine levels modulate dopamine synthesis (Schlicker et al, 1993;Molina-Hernandez et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Munzar

Justinová²,

Goldberg³

2004

Neuropsychopharmacol

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Methamphetamine administration increases brain levels of histamine and neuronal histamine attenuates several of methamphetamine's behavioral effects. The role of different subtypes of histamine receptors in this negative feedback, however, remains unclear. There is some evidence on possible involvement of histamine H3 receptors in these actions of methamphetamine. The aim of the present study was to evaluate the effects of two histamine H3 receptor antagonists, clobenpropit and thioperamide, on rewarding and neurochemical effects of methamphetamine utilizing three in vivo methodologies, drug self-administration, drug discrimination, and microdialysis in Sprague-Dawley rats. In rats self-administering methamphetamine intravenously under a fixed-ratio schedule, presession treatment with thioperamide (1.0-3.0 mg/kg, subcutaneous, s.c.) or clobenpropit (1.0-3.0 mg/kg, s.c.) potentiated the reinforcing effects of methamphetamine, as indicated by a dose-dependent increase in responding for a low 0.03 mg/kg dose of methamphetamine, that by itself failed to maintain responding above saline substitution levels, and a decrease in responding for a higher 0.06 mg/kg training dose of methamphetamine. In contrast, neither thioperamide nor clobenpropit treatment increased responding during saline substitution. In other rats trained to discriminate intraperitoneal (i.p.) injection of 1.0 mg/kg methamphetamine from i.p. injection of saline, both thioperamide and clobenpropit (0.3-3.0 mg/kg, s.c.) dose dependently increased methamphetamine-appropriate responding when administered with a low 0.3 mg/kg i.p. dose of methamphetamine, which by itself produced predominantly saline-appropriate responding. However, thioperamide and clobenpropit produced only saline-appropriate responding when administered with saline vehicle. Finally, thioperamide and clobenpropit potentiated methamphetamine-induced elevations in extracellular dopamine levels in the shell of the nucleus accumbens, but did not increase brain dopamine levels when given alone. These findings point to histamine H3 receptors as a new and important receptor system modulating the reinforcing, subjective, and neurochemical actions of methamphetamine.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Munzar

Justinová²,

Goldberg³

2004

Neuropsychopharmacol

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“…Previous evidence has indicated that H 3 Rs in the SNr inhibit GABA release (Garcia et al, 1997;Garcia-Ramirez et al, 2004). The possibility that H 3 Rs present on GABAergic or glutamatergic terminals in the SNr contribute to H 3 R-mediated regulation of 5-HT release was investigated using receptor antagonists for GABA or glutamate.…”

Section: H 3 R Control Of 5-ht Release In the Snrmentioning

confidence: 99%

“…Among the inputs to the SNr is a projection from histamine (HA)-containing neurons of the tuberomammillary nucleus (Panula et al, 1989). Although there is limited information on the actions of HA in the SNr, HA has been implicated in the modulation of GABA release at striatonigral synapses (Garcia et al, 1997) and in the local regulation of motor functions (GarciaRamirez et al, 2004). In Parkinson's disease (PD), there is an increase in HA levels and in the varicosity size and density of HA fibers in the SN (Anichtchik et al, 2000a).…”

Section: Introductionmentioning

confidence: 99%

“…Regions that express H 3 R mRNA and project to the SNr include the striatum, subthalamic nucleus, and raphe nuclei but not the dopaminergic neurons in the substantia nigra pars compacta (SNc)-ventral tegmental area (Pillot et al, 2002). The H 3 R is predominantly a presynaptic receptor that has been shown to inhibit release of HA (Arrang et al, 1983), glutamate (Brown and Reymann, 1996;Brown and Haas, 1999;Molina-Hernandez et al, 2001), GABA (Garcia et al, 1997;Yamamoto et al, 1997;Arias-Montano et al, 2001), norepinephrine (Schlicker et al, 1989(Schlicker et al, , 1992(Schlicker et al, , 1999, dopamine (DA) (Schlicker et al, 1993), acetylcholine (Arrang et al, 1995;Giorgetti et al, 1997;Prast et al, 1999), and 5-hydroxytryptamine (5-HT) in cortex (Schlicker et al, 1988;Fink et al, 1990). The present study was designed to elucidate the role of H 3 receptors (H 3 Rs) in the SNr.…”

Section: Introductionmentioning

confidence: 99%

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Histamine H₃Receptors Inhibit Serotonin Release in Substantia Nigra Pars Reticulata

et al. 2004

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Modulation of endogenous GABA release by an antagonistic adenosine A1 / dopamine D1 receptor interaction in rat brain limbic regions but not basal ganglia

Mayfield

Jones

Miller

et al. 1999

Synapse

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Behavioral and biochemical studies suggest that a negative interaction exists between adenosine A(1) and dopamine D(1) receptors in the brain and that this may contribute to the psychomotor effects of adenosine receptor agonists and antagonists. We examined the functional significance of A(1) and D(1) receptor subtypes in modulating electrically evoked endogenous GABA release from slices/punches of rat basal ganglia (striatum, globus pallidus, striatum containing globus pallidus, and substantia nigra reticulata) and limbic regions (ventral pallidum and nucleus accumbens). In basal ganglia, stimulation of A(1) receptors with the selective agonist R-PIA (1-100 nM) resulted in a concentration-dependent decrease in GABA release. The selective A(1) antagonist DPCPX (10-100 nM) increased GABA release, suggesting that endogenous adenosine tonically inhibits GABA release. However, in basal ganglia, consistent dopamine D(1) receptor modulation of GABA, release was not observed in response to either D(1) agonists or antagonists. Furthermore, the A(1) receptor-mediated inhibition of GABA release was not changed by concurrent activation of D(1) receptors, thus confirming the lack of D(1) receptor modulation under these conditions. In contrast, in ventral pallidum and nucleus accumbens, stimulation of D(1) receptors with SKF-82958 (1 microM) increased GABA release significantly. The D(1) receptor-mediated increase in GABA release was attenuated by concurrent activation of adenosine A(1) receptors. These results are consistent with the hypothesis that an antagonistic A(1)/D(1) receptor interaction may be important in modulating GABA release in limbic regions.

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Histamine H3 receptor activation selectively inhibits dopamine D1 receptor-dependent [3H]GABA release from depolarization-stimulated slices of rat substantia nigra pars reticulata

Cited by 124 publications

References 35 publications

Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Histamine H₃Receptors Inhibit Serotonin Release in Substantia Nigra Pars Reticulata

Modulation of endogenous GABA release by an antagonistic adenosine A1 / dopamine D1 receptor interaction in rat brain limbic regions but not basal ganglia

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Histamine H3 receptor activation selectively inhibits dopamine D1 receptor-dependent [3H]GABA release from depolarization-stimulated slices of rat substantia nigra pars reticulata

Cited by 124 publications

References 35 publications

Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Histamine H3 Receptor Antagonists Potentiate Methamphetamine Self-Administration and Methamphetamine-Induced Accumbal Dopamine Release

Histamine H3Receptors Inhibit Serotonin Release in Substantia Nigra Pars Reticulata

Modulation of endogenous GABA release by an antagonistic adenosine A1 / dopamine D1 receptor interaction in rat brain limbic regions but not basal ganglia

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Histamine H₃Receptors Inhibit Serotonin Release in Substantia Nigra Pars Reticulata