The electrophysiological effects of neurotensin on neurones of guinea-pig prevertebral sympathetic ganglia.
1. The membrane effects of neurotensin on neurons of guinea-pig prevertebral ganglia were investigated by means of intracellular recording techniques in vitro. 2. Neurotensin (2-5 microM) applied by superfusion caused depolarizing responses in fifty-seven of seventy-four neurones tested in the inferior mesenteric ganglion and thirty-seven of forty-seven neurones tested in the coeliac plexus. The remaining neurones tested showed no membrane response. 3. Responses to neurotensin could be discriminated into two different types of membrane depolarizations on the basis of their different time courses and pharmacological characteristics: a steady-state type of depolarization and a transient type of depolarization. Seven of fifty-seven responsive neurones tested in the inferior mesenteric ganglion and ten of thirty-seven responsive neurones tested in the coeliac plexus responded to neurotensin with a depolarization which was maintained constant as long as neurotensin was superfused over the preparation (steady-state type). Forty-eight of fifty-seven responsive neurones tested in the inferior mesenteric ganglion and twenty of thirty-seven responsive neurones tested in the coeliac plexus responded with a transient depolarization which was followed by a repolarization in the maintained presence of neurotensin (transient type). A combination of both types of responses was observed in two neurones tested in the inferior mesenteric ganglion and in seven neurones tested in the coeliac plexus. 4. Steady-state type responses were characterized by a slowly developing membrane depolarization which reached a plateau and lasted throughout the presence of neurotensin. Amplitude and time course of this response were not altered in a solution containing hexamethonium (10 microM) and atropine (10 microM) or by a solution low in calcium (1 mM) and high in magnesium (15 mM). 5. Transient type depolarizations evoked by neurotensin were faster in reaching their maximum and were followed by a repolarization during the maintained presence of neurotensin. Responses similar in time course and amplitude were obtained in solutions containing hexamethonium (10-100 microM) and atropine (10 microM). However, transient responses were abolished in a solution low in calcium (1 mM) and high in magnesium (15 mM) and were markedly attenuated in ganglia treated with capsaicin (3 microM). 6. Both types of depolarizations were associated with increases in membrane input resistance. Both responses converted subthreshold depolarizing electrotonic potentials and subthreshold fast EPSPs to action potentials. 7. Both types of depolarizations were observed when the C-terminal hexapeptide fragment neurotensin 8-13 was used.(ABSTRACT TRUNCATED AT 400 WORDS)
Stapelfeldt
W H
WH
Department of Physiology and Biophysics, Mayo Foundation, Rochester, MN 55905.
Szurszewski
J H
JH
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects; D005728:Ganglia, Sympathetic / Q000187:drug effects*; D006168:Guinea Pigs; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D066298:In Vitro Techniques; D007552:Isotonic Solutions / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects*; D009496:Neurotensin / Q000494:pharmacology*; D013997:Time Factors
D006584:Hexamethonium Compounds; D007552:Isotonic Solutions; C051865:Krebs-Ringer solution; D009496:Neurotensin; D018738:Hexamethonium; D001285:Atropine; D008274:Magnesium; D002211:Capsaicin; D002118:Calcium