title: Post-tetanic hyperpolarization evoked by depolarizing pulses in crayfish stretch receptor neurones in tetrodotoxin.
abstract: A post-tetanic hyperpolarization (p.t.h.) that is quantitatively identical to that evoked by a train of action potentials in stretch receptor neurones of crayfish Procambarus clarki and Pacifastacus leniculus is evoked when the normal Na+ influx is blocked with tetrodotoxin (TTX) and a train of depolarizing pulses is used to simulate a train of action potentials. The p.t.h. evoked by depolarizing pulses in the presence of TTX is attributable to an electrogenic Na-K pump, because it (a) is abolished by strophanthidin, (b) is abolished by removal of external K+, (c) depends in magnitude on internal Na+ concentration, (d) is not associated with a change in membrane conductance and (e) does not exhibit a reversal potential. When each action potential in the stimulus train is followed by a hyperpolarizing pulse, generation of the p.t.h. is prevented even though the action potentials are unchanged. The time constant for build-up of the p.t.h. is longer than the time constant of decay. Increasing the magnitude of depolarizing pulses increases the magnitude of the p.t.h. response in the presence of TTX and also increases the time constant for its build-up. The suppression of the p.t.h. occurring in low external Na+ appears to represent a response to a change in internal Na+ concentration, characterized by a time constant much longer than the decay of the p.t.h. The activity of the pump appears to be regulated by two mechanisms: a Na+-sensitive mechanism with a time constant of the order of a minute and an apparently voltage-sensitive mechanism with a time constant of about 5 s. The hypothesis is proposed that changes in the transmembrane electric field influence the enzymatic systems of the pump and disrupt the steady-state distribution of conformation states. The decay of the p.t.h. represents a relaxation back to the resting distribution.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003400:Astacoidea / Q000502:physiology*; D001693:Biological Transport, Active / Q000187:drug effects; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008465:Mechanoreceptors / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D007473:Ion Channels; D013779:Tetrodotoxin; D012964:Sodium; D011188:Potassium