Abstract
To clarify modulatory synaptic transmission in autonomic neurons in the brain, neurons in slices(200 μm in thickness) of the area postrema (AP) from rats (aged 12-24 days) were studied using whole-cell patch clamp techniques. When glycine (100 μM) or GABA (10 μM) was applied to the AP neurons from a ‘Y-tube’, large outward currents were induced (average peak amplitudes of about 230 pA and 170 pA at -10 mV, respectively). Both of the currents showed reversal potential of -67 mV, which was approximately the estimated Cl− equilibrium potential. At a holding potential of -10 mV, application of high K+ (20 mM) to the AP neurons evoked massive inhibitory synaptic currents (IPSCs) in the neurons. Most of the evoked currents were sensitive to bicuculline but resistant to strychnine, indicating that GABAergic but not glycinergic transmissions were prevalent in AP neurons. When nicotine (5-100 μM) was applied to AP neurons, robust IPSCs were evoked, indicating GABAergic identity. Interestingly, a fraction of nicotine-induced IPSCs still appeared in the presence of tetorodotoxin (1 μM) but were blocked in the presence of 5 mM Mg2+, indicating that functional nicotinic ACh receptors were present at GABAergic presynaptic terminals and induced Ca2+ influx after activation of the receptors. By application of cytisine, DMPP and ACh around an AP neuron, similar presynaptic facilitation of GABA release was observed. The observations revealed that presynaptic facilitation of GABA release by nicotine occurs in AP neurons of the rat. [Jpn J Physiol 55 Suppl:S147 (2005)]
