The anterior paraventricular thalamus (aPVT) projects to the SCN, and a lesion of the aPVT leads to phase delays of circadian rhythms, instead of advances, produced by light pulses at CT23. As a first step to understanding the underlying mechanism, the authors characterized the monosynaptic responses of SCN neurons to aPVT in whole-cell recordings from brain slices in rats. Stimulation of aPVT evoked excitatory and inhibitory postsynaptic potentials in SCN neurons. Pharmacological isolation of such components indicated that the excitatory postsynaptic potential (EPSP) involves AMPA and NMDA glutamate receptors while the inhibitory postsynaptic potential (IPSP) involves GABA A receptors. Since the SCN comprises mostly GABA neurons, the persistence of IPSP after the blockade of glutamate receptors ruled out the possibility that GABA was released from SCN interneurons responsive to glutamate released from the paraventricular thalamus. Altogether, the present evidence demonstrates that glutamate and GABA are released in synapses between aPVT and the SCN.
Última actualización: 26/06/2019