Presynaptic GABA(B) receptors modulate synaptic facilitation and depression at distinct synapses in fusiform cells of mouse dorsal cochlear nucleus.

The mammalian dorsal cochlear nucleus (DCN) is considered to contribute to the localization of the sound sources. Fusiform cells (FCs), principal projection neurons in the DCN, integrate two excitatory inputs from auditory nerve fibers (ANFs) and parallel fibers (PFs). Although an immunohistochemical study suggested presence of GABA(B) receptors at excitatory presynaptic terminals in the DCN, it has not been elucidated how GABA(B) receptors modulate the synaptic transmission to FCs. Here, we examined effects of baclofen on the transmission in vitro. Baclofen reduced both PF-EPSC and ANF-EPSC by reducing transmitter releases, and it enhanced the facilitation in PF-FC synapses and prevented the depression in ANF-FC synapses. The enhancement and prevention were prominent during high-frequency (50Hz) synaptic input, suggesting the activation of presynaptic GABA(B) receptors may optimize both PF-FC and ANF-FC synapses for high-frequency transmission. Postsynaptic GABA(B) receptors activated GIRK current and would further modulate the activity of FCs.