Dopamine prevents muscarinic-induced decrease of glutamate release in the auditory cortex

Atzori, Marco; Kanold, Patrick O.; Pineda, Juan Carlos; Flores‐Hernández, Jorge; Paz, Rodrigo D.

doi:10.1016/j.neuroscience.2005.05.005

Cited by 36 publications

(34 citation statements)

References 88 publications

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“…mitter glutamate through activation of muscarinic receptors (Metherate and Ashe, 1991;Cox et al, 1992;Hasselmo and Cekic, 1996;Atzori et al, 2005;Kremin et al, 2006). Therefore, it is reasonable to speculate that this effect might supersede a cholinergic increase in excitability, and combined with the inhibitory effects of NE (Dinh et al, 2009), synergistically contribute to the various effects of VNS.…”

Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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Abstract-Vagus nerve stimulation (VNS) is an FDA approved treatment for drug-resistant epilepsy and depression.Recently, we demonstrated the capacity for repeatedly pairing sensory input with brief pulses of VNS to induce input specific reorganization in rat auditory cortex. This was subsequently used to reverse the pathological neural and perceptual correlates of hearing loss induced tinnitus. Despite its therapeutic potential, VNS mechanisms of action remain speculative. In this study, we report the acute effects of VNS on intra-cortical synchrony, excitability, and sensory processing in anesthetized rat auditory cortex. VNS significantly increased and decorrelated spontaneous multi-unit activity, and suppressed entrainment to repetitive noise burst stimulation at 6 -8 Hz but not after application of the muscarinic antagonist scopolamine. Collectively, these experiments demonstrate the capacity for VNS to acutely influence cortical synchrony and excitability and strengthen the hypothesis that acetylcholine and muscarinic receptors are involved in VNS mechanisms of action. These results are discussed with respect to their possible implications for sensory processing, neural plasticity, and epilepsy.

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Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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“…Animal studies support both dopamine-dependent and dopamine-independent effects of muscarinic agents. 40,190 The muscarinic and dopaminergic system interact bidirectionally at different levels in the brain and the nature of these interactions is not fully understood. Depending on the brain region and muscarinic receptor subtype involved, stimulation and inhibition of the muscarinic system can result in different effects on the dopaminergic system.…”

Section: Discussionmentioning

confidence: 99%

“…36 In addition, both systems do not function in isolation but closely interact with each other and with other neurotransmitter systems including dopamine, glutamate and GABA. [37][38][39][40][41] The interactions between the muscarinic cholinergic system and the nicotinic cholinergic system as well as other neurotransmitter systems are complex and bi-directional. Given the central role of dopamine in schizophrenia, the interactions between the muscarinic cholinergic system and the dopaminergic system will be reviewed in more detail.…”

Section: Cholinergic Neurotransmissionmentioning

confidence: 99%

Towards a muscarinic hypothesis of schizophrenia

Raedler

Bymaster

Tandon³

et al. 2006

Mol Psychiatry

247

211

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Although the neurotransmitter dopamine plays a prominent role in the pathogenesis and treatment of schizophrenia, the dopamine hypothesis of schizophrenia fails to explain all aspects of this disorder. It is increasingly evident that the pathology of schizophrenia also involves other neurotransmitter systems. Data from many streams of research including preclinical and clinical pharmacology, treatment studies, post-mortem studies and neuroimaging suggest an important role for the muscarinic cholinergic system in the pathophysiology of schizophrenia. This review will focus on evidence that supports the hypothesis that the muscarinic system is involved in the pathogenesis of schizophrenia and that muscarinic receptors may represent promising novel targets for the treatment of this disorder.

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“…Indeed, the available evidence predicts that GABA release, likely from fast-spiking interneurons, silences cortical pyramidal as well as non-pyramidal cells (e.g., [103]) and inhibits ACh release from cholinergic terminals [104–106]. Although these effects would suffice to prevent the prefrontal circuit from up-shifting into the detection mode, activation of other neuromodulators, reflecting a departure from the default-mode state during the intertrial interval, also likely contributes to the suppression of cue-evoked glutamatergic-cholinergic activity [107]. Finally, we need to acknowledge that extremely little is known about the contribution of non-cholinergic afferents from the basal forebrain; these GABAergic and presumably glutamatergic projections may be recruited separately from the cholinergic system and may strongly influence the state of the detection-mediating circuitry in the PFC (e.g., [108,109]).…”

Section: Circuitry Model For Signal Detection: Prefrontal Glutamatmentioning

confidence: 99%

nAChR agonist-induced cognition enhancement: Integration of cognitive and neuronal mechanisms

Sarter

Parikh

Howe

2009

Biochemical Pharmacology

110

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The identification and characterization of drugs for the treatment of cognitive disorders has been hampered by the absence of comprehensive hypotheses. Such hypotheses consist of (a) a precisely defined cognitive operation that fundamentally underlies a range of cognitive abilities and capacities and, if impaired, contributes to the manifestation of diverse cognitive symptoms; (b) defined neuronal mechanisms proposed to mediate the cognitive operation of interest; (c) evidence indicating that the putative cognition enhancer facilitates these neuronal mechanisms; (d) and evidence indicating that the cognition enhancer facilitates cognitive performance by modulating these underlying neuronal mechanisms. The evidence on the neuronal and attentional effects of nAChR agonists, specifically agonists selective for α4β2* nAChRs, has begun to support such a hypothesis. nAChR agonists facilitate the detection of signals by augmenting the transient increases in prefrontal cholinergic activity that are necessary for a signal to gain control over behavior in attentional contexts. The prefrontal microcircuitry mediating these effects include α4β2* nAChRs situated on the terminals of thalamic inputs and the glutamatergic stimulation of cholinergic terminals via ionotropic glutamate receptors. Collectively, this evidence forms the basis for hypothesis-guided development and characterization of cognition enhancers.

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Dopamine prevents muscarinic-induced decrease of glutamate release in the auditory cortex

Cited by 36 publications

References 88 publications

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Towards a muscarinic hypothesis of schizophrenia

nAChR agonist-induced cognition enhancement: Integration of cognitive and neuronal mechanisms

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