The physiological role of pre- and postsynaptic GABAB receptors in membrane excitability and synaptic transmission of neurons in the rat's dorsal cortex of the inferior colliculus

In the inferior colliculus (IC), GABAergic inhibition mediated by GABAA receptors has been shown to play a significant role in regulating physiological responses, but little is known about the physiological role of GABAB receptors in IC neurons. In the present study, we used whole-cell patch clamp recording in vitro to investigate the effects of activation of GABAB receptors on membrane excitability and synaptic transmission of neurons in the rat's dorsal cortex of the inferior colliculus (ICD). Repetitive stimulation of GABAergic inputs to ICD neurons at high frequencies could elicit a slow and long-lasting postsynaptic response, which was reversibly abolished by the GABAB receptor antagonist, CGP 35348. The results suggest that postsynaptic GABAB receptors can directly mediate inhibitory synaptic transmission in ICD. The role of postsynaptic GABAB receptors in regulation of membrane excitability was further investigated by application of the GABAB receptor agonist, baclofen. Baclofen hyperpolarized the cell, reduced the membrane input resistance and firing rate, increased the threshold for generating action potentials (APs), and decreased the amplitude of the AP and its associated after-hyperpolarization. The Ca2+-mediated rebound depolarization following hyperpolarization and the depolarization hump at the beginning of membrane depolarization were also suppressed by baclofen. In voltage clamp experiments, baclofen induced inward rectifying K+ current and reduced low- and high-threshold Ca2+ currents, which may account for the suppression of membrane excitability by postsynaptic GABAB receptors. Application of baclofen also reduced excitatory synaptic responses mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and inhibitory synaptic responses mediated by GABAA receptors. Baclofen increased the ratios of 2nd/1st excitatory and inhibitory postsynaptic currents to paired-pulse stimulation of the synaptic inputs. These results suggest that fast glutamatergic and GABAergic synaptic transmission in ICD can be modulated by presynaptic GABAB receptors.