ABSTRACT
Intracerebroventricular injections of angiotensin II (ANG) and nicotine activate the subfornical organ (SFO), an essential central nucleus for ANG-induced drinking. Nicotine has been, however, reported to induce little drinking behavior. To clarify this paradox, we investigated effects of nicotine and ANG on activity of SFO neurons and drinking behavior. In extracellular recordings many SFO neurons (57%) were excited by the both drugs. The nicotine-induced excitation was transient, whereas the ANG-induced was long-lasting. After intracerebroventricular injection of nicotine, the latency to drinking was dose-dependently shortened, but the drinking volumes were much smaller than those by ANG. These suggest that central nicotinic activation contributes to induction of drinking behavior while drinking volume is small because effects of nicotine on neurons are short-lasting.
Subject(s)
Drinking Behavior/drug effects , Nicotine/pharmacology , Nicotinic Agonists/pharmacology , Subfornical Organ/drug effects , Angiotensin II/pharmacology , Animals , Drinking/drug effects , Drinking/physiology , Electrophysiology , Injections, Intraventricular , Male , Neurons/drug effects , Neurons/physiology , Organ Culture Techniques , Rats , Rats, Wistar , Subfornical Organ/cytology , Subfornical Organ/physiology , Vasoconstrictor Agents/pharmacologyABSTRACT
Central injection of hypocretins/orexins in rats induces water intake. As the subfornical organ (SFO) plays an important role in drinking behavior, hypocretins may excite SFO neurons. In this study, effects of hypocretins on SFO neurons were investigated electrophysiologically in slice preparations. In extracellular recordings, hypocretin-1 excited SFO neurons, but hypocretin-2 did not or it was little. After the block of synaptic inputs, the excitatory responses to hypocretin-1 remained, but some disappeared. In whole-cell patch-clamp recordings, hypocretin-1 reduced the frequencies of miniature inhibitory presynaptic currents with inward currents occasionally in SFO neurons, but hypocretin-2 did not. These results suggest that hypocretin-1 excites SFO neurons via the activation of hcrtR1 on premembranes and postmembranes.
