Membrane properties of complex spike firing neurons of the mouse dorsal cochlear nucleus in vitro.
Intracellular recordings were made from complex spike firing neurons of the mouse dorsal cochlear nucleus (DCN) in vitro. The whole cochlear nucleus was dissected out and maintained submerged in rapidly flowing artificial cerebrospinal fluid (CSF). Recordings were made with current clamp techniques in the presence or absence of ion channel blocking drugs tetrodotoxin (TTX, 1 microM), tetraethylammonium (TEA, 20 mM), 4-aminopyridine (4-AP, 5 mM) or verapamil (50, 100, 150, 250 microM). The cells showed both spontaneous firing and responses to injections of depolarising current consisting of a mixture of a tall single action potential and complexes of 2 to 3 smaller wider action potentials superimposed on a plateau depolarisation. The membrane properties were: resting membrane potential -68.8 +/- 8.5 mV, cell resistance 54.1 +/- 26.5 M omega, time constant 9.6 +/- 5.4 ms and capacitance 0.25 +/- 0.5 nF; the first three variables had bimodel distributions. The current/voltage (I/V) relationship at membrane below resting was non-linear. Previously published histological evidence from the mouse DCN has shown that both cartwheel cells and Purkinje-like neurons are present. Both DCN cartwheel cells and cerebellar Purkinje cells are known to fire both tall single action potentials and complexes of smaller wider action potentials. It is therefore possible that the recordings shown here were made from these neuron types. TTX (1 microM) abolished both the tall single and the complexes of smaller action potentials, suggesting that the tall single action potentials are sodium dependent and possibly that a TTX sensitive sodium channel is responsible for the plateau as is suggested for Purkinje cells in the cerebellum. Verapamil (100 microM) abolished only the complex action potentials and the plateau leaving the tall narrow action potentials intact, which is consistent with the smaller complexes being calcium dependent. Higher concentrations abolished all spiking activity. TEA and 4-AP used separately both caused marked depolarisation to around -20 mV, suggesting that there is a large potassium current active at and near resting.
Ağar
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Department of Physiology, Faculty of Medicine, University of Ondokuz Mayis, Samsun, Turkey.
Green
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GG
Sanders
D J
DJ
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001306:Auditory Pathways / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D017626:Cochlear Nucleus / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D051379:Mice; D008807:Mice, Inbred BALB C; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000037:antagonists & inhibitors / Q000494:pharmacology; D014700:Verapamil / Q000037:antagonists & inhibitors / Q000494:pharmacology
D002121:Calcium Channel Blockers; D013757:Tetraethylammonium Compounds; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D014700:Verapamil