ATP-sensitive K+ channels control the spontaneous firing of a glycinergic interneuron in the auditory brainstem

Autor(es)

Strazza, Jr., Paulo S. ^[1] ; de Siqueira, Daniela V. F. ^[1] ; Leao, Ricardo M. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF PHYSIOLOGY-LONDON; v. 599, n. 5 JAN 2021.
• Citações Web of Science: 0

Resumo

Cartwheel neurons from the dorsal cochlear nucleus (DCN) are glycinergic interneurons and the primary source of inhibition on the fusiform neurons, the DCN's principal excitatory neuron. Most cartwheel neurons present spontaneous firing (active neurons), producing a steady inhibitory tone on fusiform neurons. In contrast, a small fraction of these neurons do not fire spontaneously (quiet neurons). Hyperactivity of fusiform neurons is seen in animals with behavioural evidence of tinnitus. Because of its relevance in controlling the excitability of fusiform neurons, we investigated the ion channels responsible for the spontaneous firing of cartwheel neurons in DCN slices from rats. We found that quiet neurons presented an outward conductance not seen in active neurons, which generates a stable resting potential. This current was sensitive to tolbutamide, an ATP-sensitive potassium channel (K-ATP) antagonist. After inhibition with tolbutamide, quiet neurons start to fire spontaneously, while the active neurons were not affected. On the other hand, in active neurons, K-ATP agonist diazoxide activated a conductance similar to quiet neurons' K-ATP conductance and stopped spontaneous firing. According to the effect of K-ATP channels on cartwheel neuron firing, glycinergic neurotransmission in DCN was increased by tolbutamide and decreased by diazoxide. Our results reveal a role of K-ATP channels in controlling the spontaneous firing of neurons not involved in fuel homeostasis. (AU)

• Processo FAPESP: 19/13458-1 - Alterações durante o desenvolvimento das correntes iônicas e neurotransmissão de neurônios ligados a processamento auditivo: efeitos do ambiente acústico
• Beneficiário: Ricardo Mauricio Xavier Leão
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 16/01607-4 - Estimulação auditiva de alta intensidade e plasticidade sináptica
• Beneficiário: Ricardo Mauricio Xavier Leão
• Modalidade de apoio: Auxílio à Pesquisa - Regular