Transition from random to phasic firing induced in neurons cultured from the hypothalamic supraoptic area.
Intracellular recordings of the spontaneous activity were obtained from neurons in long-term cultures from the area of the supraoptic nucleus of rats. The effects of various substances known from in situ studies to cause vasopressin release were analyzed. Application of nicotine or acetylcholine induced a transition from a random to a phasic discharge pattern. Similar alterations in firing patterns were observed with enkephalin analogues, an effect which was blocked by the opiate antagonist, naloxone. Glutamate excited hypothalamic neurons in a dose-dependent manner, but did not induce phasic firing. Angiotensin II increased the firing rate in randomly firing cells and the duration of bursts in phasic cells. In an attempt to identify the transmitter(s) involved in the generation of phasic activity, several antagonists to excitatory transmitters were applied. Of the agents tested, only saralasin reduced the duration of bursts, but it is questionable whether this effect is due to its angiotensin-antagonistic property.
D000109:Acetylcholine / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D005071:Evoked Potentials / Q000187:drug effects; D005971:Glutamates / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009538:Nicotine / Q000494:pharmacology; D009924:Organ Culture Techniques; D051381:Rats; D013495:Supraoptic Nucleus / Q000187:drug effects / Q000502:physiology*; D014667:Vasopressins / Q000378:metabolism
D005971:Glutamates; D014667:Vasopressins; D000804:Angiotensin II; D009538:Nicotine; D000109:Acetylcholine