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1.
J Neurosci ; 31(4): 1213-8, 2011 Jan 26.
Artigo em Inglês | MEDLINE | ID: mdl-21273406

RESUMO

Ryanodine receptors (RyRs) are highly conductive intracellular Ca(2+) release channels which are widely expressed in the CNS. They rapidly increase the intracellular Ca(2+) concentrations in neuronal cells in response to Ca(2+) influx through voltage-gated Ca(2+) channels. A previous study reported that RyRs were expressed in thalamocortical (TC) neurons, but their physiological function has remained elusive. Here, we show that the activation of RyRs in TC neurons in mice decreases their tonic firing rate while blocking them induces the opposite response. Furthermore, activation of RyRs in ventroposteriomedial/ventroposteriolateral nuclei reduces the behavioral responses to inflammatory pain and blocking them increases the responses. This study highlights the importance of the intracellular Ca(2+) release via RyRs in controlling the excitability of TC neurons and in inflammatory pain signal processing in the thalamus.


Assuntos
Neurônios/fisiologia , Dor/fisiopatologia , Canal de Liberação de Cálcio do Receptor de Rianodina/fisiologia , Tálamo/fisiopatologia , Potenciais de Ação , Animais , Agonistas dos Canais de Cálcio/farmacologia , Bloqueadores dos Canais de Cálcio/farmacologia , Inflamação/fisiopatologia , Masculino , Camundongos , Medição da Dor , Núcleos Talâmicos/fisiopatologia
2.
J Neurosci ; 28(49): 13331-40, 2008 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-19052225

RESUMO

Two firing modes of thalamocortical (TC) neurons, tonic and burst firings, are thought to reflect the divergent states of sensory signal transmission from the thalamus to the cortex. However, the behavioral consequences of changes in the thalamic firing between the two modes have not been well demonstrated. Moreover, although the firing modes of TC neurons are known to be affected by corticothalamic inputs via thalamic metabotropic glutamate receptor type 1 (mGluR1)-phospholipase C beta4 (PLCbeta4) pathway, its molecular mechanisms have not been well elucidated. We addressed these questions using PLCbeta4-deficient mice, which show decreased visceral pain responses. We demonstrate that burst and tonic firings of TC neurons are concomitantly regulated by PLCbeta4 pathway. Blocking of this pathway by the mutation simultaneously increases bursting and decreases tonic firing of TC neurons through concurrent upregulation of T- and L-type Ca(2+) currents. The mice with increased bursting and decreased tonic firing of TC neurons showed reduced visceral pain responses. Furthermore, we show that modulation of the Ca(2+) channels or protein kinase C (PKC), a downstream molecule of PLCbeta4, altered the firing modes of TC neurons and pain responses in the predicted ways. Our data demonstrate the molecular mechanism and behavioral consequences of altered firing modes of TC neurons in relaying the visceral pain signals. Our study also highlights the thalamic PLCbeta4-PKC pathway as a "molecular switch" for the firing modes of TC neurons and thus for pain sensory gating.


Assuntos
Potenciais de Ação/genética , Canais de Cálcio/metabolismo , Neurônios/metabolismo , Dor/metabolismo , Fosfolipase C beta/genética , Tálamo/metabolismo , Animais , Canais de Cálcio Tipo L/metabolismo , Canais de Cálcio Tipo T/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Inibição Neural/genética , Dor/genética , Dor/fisiopatologia , Limiar da Dor/fisiologia , Proteína Quinase C/metabolismo , Receptores de Glutamato Metabotrópico/metabolismo , Transdução de Sinais/genética , Transmissão Sináptica/genética
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