Pedunculopontine tegmental stimulation evokes striatal dopamine efflux by activation of acetylcholine and glutamate receptors in the midbrain and pons of the rat

Forster, Gina L.; Blaha, Charles D.

doi:10.1046/j.1460-9568.2003.02511.x

Cited by 152 publications

(141 citation statements)

References 88 publications

(140 reference statements)

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“…These results are consistent with the critical role of M5 receptors in prolonged activation of mesolimbic and striatal dopamine neurons following mesopontine stimulation Forster and Blaha, 2003). Consequently, M5 mutant mice may serve as a model of reduced dopamine function, and M5 blockers may be useful as neuroleptic drugs.…”

Section: Chromosomal Localization Of Mouse and Human M5 Muscarinic Resupporting

confidence: 85%

“…Pharmacological studies suggest that M5 receptors tonically regulate mesolimbic and striatal dopamine functions (Blaha et al, 1996;Miller and Blaha, 2002;Zhang et al, 2002;Basile et al, 2002;Forster and Blaha, 2003). Since decreased dopaminergic activity in the nucleus accumbens enhances latent inhibition in rats (Joseph et al, 2000;Moser et al, 2000;Russig et al, 2002;Gray et al, 1997), the improvement in latent inhibition in M5 mutant mice appears to result from decreased mesolimbic dopamine activation by M5 receptors.…”

Section: Latent Inhibitionmentioning

confidence: 99%

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Decreased Amphetamine-Induced Locomotion and Improved Latent Inhibition in Mice Mutant for the M5 Muscarinic Receptor Gene Found in the Human 15q Schizophrenia Region

Wang

Hayes

et al. 2004

Neuropsychopharmacol

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M5 muscarinic receptors are coexpressed with D2 dopamine receptors in the ventral tegmentum and striatum, and are important for reward in rodents. Previously, we reported that disruption of the M5 receptor gene in mice reduced dopamine release in the nucleus accumbens. In this study, we established a polymerase chain reaction (PCR) genotyping method for M5 mutant mice, and, using RT-PCR, found that M5 mRNA expression was highest in the ventral tegmentum, striatum, and thalamus in wild-type mice. In the M5 mutant mice, D2 mRNA expression was increased in several brain structures, including the striatum. Genome mapping studies showed the M5 gene is localized to chromosome 2E4 in mice, and to 15q13 in humans in the region that has been linked to schizophrenia. Amphetamineinduced locomotion, but not baseline locomotion or motor functions, decreased in M5 mutant mice, consistent with lower accumbal dopamine release. Previous reports found latent inhibition improvement in rats following nucleus accumbens lesions, or blockade of dopamine D2 receptors with neuroleptic drugs. Here, latent inhibition was significantly increased in M5 mutant mice as compared with controls, consistent with reduced dopamine function in the nucleus accumbens. In summary, our results showed that M5 gene disruption in mice decreased amphetamine-induced locomotion and increased latent inhibition, suggesting that increased M5 mesolimbic function may be relevant to schizophrenia.

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Section: Chromosomal Localization Of Mouse and Human M5 Muscarinic Resupporting

confidence: 85%

Section: Latent Inhibitionmentioning

confidence: 99%

Decreased Amphetamine-Induced Locomotion and Improved Latent Inhibition in Mice Mutant for the M5 Muscarinic Receptor Gene Found in the Human 15q Schizophrenia Region

Wang

Hayes

et al. 2004

Neuropsychopharmacol

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“…The convergence of these inputs has raised the possibility that both neurotransmitters may be coreleased from the same terminals, with some evidence that this does occur in the squirrel monkey but not in the rat (Lavoie and Parent, 1994;Wang and Morales, 2009). Stimulation of the PPT elicits burst firing in SN pars compacta dopamine neurons (Lokwan et al, 1999;Floresco et al, 2003) and evokes dopamine release in the striatum, which is inhibited by application of either nicotinic or glutamatergic receptor antagonists into the SN pars compacta (Futami et al, 1995;Forster and Blaha, 2003). Indeed, it has been suggested that cholinergic activation is critical for promoting burst firing (Kitai et al, 1999).…”

Section: Pedunculopontine Nucleusmentioning

confidence: 99%

α6β2* and α4β2* Nicotinic Acetylcholine Receptors As Drug Targets for Parkinson's Disease

Quik

Wonnacott²

2011

Pharmacol Rev

177

185

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“…The PPTg contains cholinergic and glutamatergic cells that project to the ventral tegmental area (VTA) and the substantia nigra (Beninato and Spencer, 1987;Bolam et al, 1991;Futami et al, 1995). Stimulation of these afferents activates midbrain DA cells with short latency (Scarnati et al, 1984;Lokwan et al, 1999) and evokes DA release in the areas of dopaminergic innervation (Forster and Blaha, 2003).…”

Section: Introductionmentioning

confidence: 99%

Pedunculopontine Tegmental Nucleus Controls Conditioned Responses of Midbrain Dopamine Neurons in Behaving Rats

Pan

Hyland²

2005

J. Neurosci.

184

170

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Midbrain dopamine (DA) neurons respond to sensory cues that predict reward. We tested the hypothesis that projections from the pedunculopontine tegmental nucleus (PPTg) are involved in driving this DA cell activity. First, the activity of PPTg and DA neurons was compared in a cued-reward associative learning paradigm. The majority of PPTg neurons showed phasic responses to the onset of sensory cues, at significantly shorter latency than DA cells, consistent with a PPTg-to-DA transmission of information. However, unlike DA cells, PPTg responses were almost entirely independent of whether signals were associated with rewards. Second, DA neuron responses to the cues were recorded in free-moving rats during reversible inactivation of the PPTg by microinfusion of local anesthetic. The results showed clear suppression of conditioned sensory responses of DA neurons after PPTg inactivation that was not seen after saline infusion or in non-DA cells. We propose that the PPTg relays information about the precise timing of attended sensory events, which is integrated with information about reward context by DA neurons.

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Pedunculopontine tegmental stimulation evokes striatal dopamine efflux by activation of acetylcholine and glutamate receptors in the midbrain and pons of the rat

Cited by 152 publications

References 88 publications

Decreased Amphetamine-Induced Locomotion and Improved Latent Inhibition in Mice Mutant for the M5 Muscarinic Receptor Gene Found in the Human 15q Schizophrenia Region

Decreased Amphetamine-Induced Locomotion and Improved Latent Inhibition in Mice Mutant for the M5 Muscarinic Receptor Gene Found in the Human 15q Schizophrenia Region

α6β2* and α4β2* Nicotinic Acetylcholine Receptors As Drug Targets for Parkinson's Disease

Pedunculopontine Tegmental Nucleus Controls Conditioned Responses of Midbrain Dopamine Neurons in Behaving Rats

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