Electrophysiological responses of trigeminal root ganglion neurons in vitro.
The membrane electrical properties of neurons and their responses to endogenous compounds or other neuroactive substances were investigated in vitro with intracellular recording techniques in slices of trigeminal root ganglia of guinea-pigs. The mean resting membrane potential of these neurons was -60 mV. Intracellular injections of hyperpolarizing current pulses evoked time-dependent rectification with varying degrees of dependence on membrane voltage in 107 of 110 neurons. Membrane potential oscillations were observed following the termination of the hyperpolarizing pulses and after similar injections of depolarizing current. This phenomenon appeared to be voltage-dependent at levels that were subthreshold for spike genesis; the more pronounced oscillations were evident at the more depolarized levels and were insensitive to tetrodotoxin applications. Two groups of neurons could be distinguished on the basis of certain characteristics in their action potentials. The majority exhibited short duration (0.6 ms) spikes with mean amplitude of 72 mV in response to intracellular depolarizing current. The brief (3 ms) afterhyperpolarizations that followed such spikes were blocked by intracellular injections of Cs+ or by bath applications of tetraethylammonium. Action potentials in the minority group exhibited a hump in their repolarization phase. The humped spikes had a mean peak amplitude of 78 mV and a longer duration (2 ms). Both the duration (6 ms) and the amplitude (16 mV) of the afterhyperpolarization were significantly greater in this latter group of neurons. Some fast spikes were easily blocked whereas others, including humped spikes, were resistant to tetrodotoxin (10(-6) M). Spikes which were resistant, were also not affected by perfusion with Co2+ (10(-3) M) and were reduced in amplitude during perfusion with Na+-deficient solution. Bath applications of S-glutamate (10(-4)-10(-2) M) depolarized only two of ten neurons by less than 3 mV. Similarly, 5-hydroxytryptamine produced a small depolarization in only two of thirteen neurons. Perfusion of gamma-aminobutyrate (10(-5)-10(-2) M) resulted in an increase in input conductance that waned despite continued application and was associated with a depolarization (2-14 mV) in 44/50 neurons. In some neurons, gamma-aminobutyrate application enhanced their repetitive firing ability, possibly as a result of the increased oscillatory behavior of the membrane at certain depolarized potentials. The effects of gamma-aminobutyrate were blocked by the GABAA-receptor antagonist, bicuculline (10(-4) M) but were unaffected by the GABAB-receptor agonist, baclofen (10(-4) M).(ABSTRACT TRUNCATED AT 400 WORDS)
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002412:Cations / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D018377:Neurotransmitter Agents / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000187:drug effects; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D012668:Trigeminal Ganglion / Q000187:drug effects / Q000502:physiology*; D014276:Trigeminal Nerve / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002412:Cations; D007473:Ion Channels; D018377:Neurotransmitter Agents; D011963:Receptors, GABA-A; D013757:Tetraethylammonium Compounds; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid