Single ion channel activity in peptidergic nerve terminals of the isolated rat neurohypophysis related to stimulation of neural stalk axons.
Scanning electron micrographs revealed that the cut face of the sagittally bisected rat neural lobe was characterized by fine fibres bearing multiple rounded swellings (0.5-5 micron in diameter) presumed to be axonal swellings and peptidergic nerve terminals. Patch-clamp electrodes sealed (seal resistance greater than 10(10) omega) on to the cell membrane in such regions revealed (36 out of 43 patches) opening of channels conducting inward current following stimulation of the neural stalk at stimulus frequencies between 5 and 20 Hz. Channel opening did not occur immediately on stimulation (delay 5-15 s) and persisted 1-25 s after stimulation of the axons ceased, implying the possible existence of a depolarization-evoked intracellular messenger. Addition of TTX (5-20 microM) to the bath to block spike propagation abolished stalk stimulation-evoked channel opening but TTX in the patch electrode did not prevent opening. Opening was, however, prevented by addition of 4 mM Co2+ or 4 mM Mn2+. The slope conductance of this channel in medium with 10 mM Ca2+ was approximately 7 pS which was increased to 19 pS in medium containing 95 mM Ba2+. A second inward channel with a slope conductance of 56 pS in medium with 10 mM Ca2+ was also characterized and outward channels were noted in four patches. The electrical properties of nerve terminals are difficult to study because of their small size. The demonstration that ion channel activity can be recorded from mammalian peptidergic nerve terminals thus offers wide scope for future studies on the relation between stimulus and secretion.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007473:Ion Channels / Q000502:physiology*; D008855:Microscopy, Electron, Scanning; D009411:Nerve Endings / Q000502:physiology; D009431:Neural Conduction; D010904:Pituitary Gland, Posterior / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D013779:Tetrodotoxin; D012964:Sodium; D002118:Calcium