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Abstract
We studied the effects of GABA(B) receptor activation on either glycine or GABA(A)
receptor-mediated synaptic transmission to hypoglossal motoneurons (HMs, P8-13) using
a rat brainstem slice preparation. Activation of GABA(B) receptors with baclofen,
a GABA(B) receptor agonist, inhibited the amplitude of evoked glycine and GABA(A)
receptor-mediated inhibitory postsynaptic currents. Additionally, with blockade of
postsynaptic GABA(B) receptors baclofen decreased the frequency of both glycine and
GABA(A) receptor-mediated spontaneous miniature inhibitory postsynaptic currents (mIPSCs),
indicating a presynaptic site of action. Conversely, the GABA(B) receptor antagonist
CGP 35348 increased the frequency of glycine receptor-mediated mIPSCs. Application
of the GABA transport blocker SKF 89976A decreased the frequency of glycinergic mIPSCs.
Lastly, we compared the effects of baclofen on the frequency of glycine and GABA(A)
receptor-mediated mIPSC during HM development. At increased postnatal ages (P8-13
versus P1-3) mIPSC frequency was more strongly reduced by baclofen. These results
show that presynaptic GABA(B) receptors inhibits glycinergic and GABAergic synaptic
transmission to HMs, and the presynaptic sensitivity to baclofen is increased in P8-13
versus P1-3 HMs. Further, endogenous GABA is capable of modulating inhibitory synaptic
transmission to HMs.