Plateau-generating neurones in the dorsal horn in an in vitro preparation of the turtle spinal cord.
1. In transverse slices of the spinal cord of the turtle, intracellular recordings were used to characterize and analyse the responses to injected current and activation of primary afferents in dorsal horn neurones. 2. A subpopulation of neurones, with cell bodies located laterally in the deep dorsal horn and dendrites radiating towards the pial surface, was distinguished by the ability to generate plateau potentials. Activation of the plateau potential by a suprathreshold depolarizing current pulse produced an increasing firing frequency during the first few seconds and a sustained after-discharge. 3. The plateau potential was assumed to be mediated by L-type Ca2+ channels since it was blocked by Co2+ (3 mM) and nifedipine (10 microM) and enhanced by Bay K 8644 (0.5-2 microM). 4. The threshold for activating the plateau potential declined during the first few seconds of depolarization. The decline in threshold gradually subsided over 3-10 s after repolarization. 5. Frequency potentiation of the plateau potential contributed to wind-up of the response to depolarizing current pulses and primary afferent stimuli repeated at frequencies higher than 0.1-0.3 Hz. 6. The sustained after-discharge mediated by the plateau potential was curtailed by a slow after-hyperpolarization (sAHP) evoked by strong depolarizations. The relative strength of the plateau potential and sAHP varied among cells. In some cells the plateau potential and sAHP interacted to produce damped oscillations upon depolarization. The sAHP was mediated by both apamin and tetraethylammonium (TEA)-sensitive K+ channels. 7. Our findings suggest that basic properties of sensory integration may reside with the specialized intrinsic response properties of particular subtypes of neurones in the dorsal horn.
Russo
R E
RE
Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
Hounsgaard
J
J
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D003035:Cobalt / Q000494:pharmacology; D004594:Electrophysiology; D066298:In Vitro Techniques; D009474:Neurons / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D013116:Spinal Cord / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014426:Turtles / Q000378:metabolism
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D001030:Apamin; D003035:Cobalt; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine