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1 Neuroscience Program, Ottawa Health Research Institute & University of Ottawa, Ottawa, Ontario, Canada
* To whom correspondence should be addressed. E-mail: lprenaud{at}ohri.ca.
Cardiovascular and behavioural responses to circulating angiotensin require intact connectivity along the upper lamina terminalis joining the subfornical organ (SFO) with the median preoptic nucleus (MnPO). Whole cell patch-clamp recordings in saggital rat brain slice preparations revealed that 70% of MnPO neurons responded to electrical stimulation of SFO efferents with bicuculline-sensitive GABAA receptor-mediated inhibition, and glutamate-mediated postsynaptic excitation involving AMPA and NMDA receptor subtypes, blockable with NBQX and D-APV, respectively. Bath applications of baclofen induced a concentration-dependent (0.3-10µM) reduction in these SFO-evoked postsynaptic currents, attenuation of SFO-evoked paired-pulse depression and reduction in frequency (but not amplitude) of miniature postsynaptic currents, consistent with an action at presynaptic GABAB receptors. Baclofen effects on miniature currents lacked sensitivity to barium, 
-conotoxin GVIA and cadmium. Acting at postsynaptic GABAB receptors, baclofen hyperpolarized a majority of MnPO neurons by increasing a G protein-coupled inwardly rectifying potassium conductance, and also suppressing a N-type high voltage-activated calcium conductance. The latter contributed to reduction in action potential afterhyperpolarization, enhanced cell firing and spike frequency adaptation when tested with a depolarizing stimulus. All baclofen-induced effects were blockable with CGP52432. CGP52432 alone had no significant effect on SFO-evoked postsynaptic current amplitudes or paired-pulse ratios, but did induce an increase in mIPSC frequency in 2/4 cells tested, indicating that ambient levels of GABA could activate presynaptic GABAB receptors on undefined inputs. These observations indicate that MnPO neurons receive both a GABAergic and glutamatergic innervation from SFO. Both forms of rapid neurotransmission are subject to modulation via pre-and postsynaptic GABAB receptors.
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