Abstract
In the cerebellar cortex, previous reports indicated that noradrenaline (NA) enhances inhibitory synaptic transmission via β-adrenoceptor-pathways. However, the effects of α-adrenoceptor activation on cerebellar inhibitory postsynaptic currents (IPSCs) have not yet been fully understood. Therefore, we investigated the effects of the α1- or α2-adrenoceptor agonist on IPSCs recorded from mouse Purkinje cells (PCs). The selective α1-adrenoceptor agonist phenylephrine (PE) increased both the frequency and amplitude of spontaneous IPSCs (sIPSCs). PE also enhanced the amplitude of evoked IPSCs (eIPSCs) and increased the frequency but not the amplitude of miniature IPSCs (mIPSCs). Moreover, PE decreased the paired-pulse ratio of eIPSCs and did not change GABA receptor sensitivity in PCs. Conversely, the selective α2-adrenoceptor agonist clonidine significantly reduced both the frequency and the amplitude of sIPSCs. Neither eIPSCs nor mIPSCs were affected by clonidine. Furthermore, presynaptic cell-attached recordings showed that spontaneous activity of GABAergic interneurons was enhanced by PE, while reduced by clonidine. These results suggest that NA enhances inhibitory neurotransmitter release via α1-adrenoceptors, which are expressed in presynaptic terminals and somatodendritic domains, whereas suppresses the excitability of interneurons via α2-adrenoceptors, which are expressed in presynaptic somatodendritic domains. Thus, cerebellar α-adrenoceptors play roles in a presynaptic dual modulation of GABAergic inputs from interneurons to PCs. [J Physiol Sci. 2006;56 Suppl:S161]
