Antidromic firing occurs spontaneously on thalamic relay neurons: triggering of somatic intrinsic burst discharges by ectopic action potentials.
Eighty-two identified thalamocortical relay neurons were recorded extracellularly in the ventral posterior thalamic nucleus in 29 urethane-anaesthetized rats. Electrical stimulations were applied to the contralateral vibrissae or to the ipsilateral neocortex for ortho- or antidromic activation. The critical period following a known somatic action potential and during which no antidromic response could reach the soma was systematically determined for each cell using a collision test. Thus, the possible ectopic axonal origin of a given impulse could be determined. Thalamic neurons displayed either tonic or phasic firing modes, the latter characterized by episodes of rhythmic high-frequency burst discharges. The present results suggest that such bursts were generated at the soma and probably involved an intrinsic mechanism, since: (1) a modulation of the somatic excitability with an excitatory or inhibitory amino acid affected the intra-burst structure; (2) an antidromic test action potential collided with the second or any of the later impulses of such bursts; (3) an orthodromic activation could evoke a burst structurally similar to a natural one; and (4) the duration of the first interval of such an evoked burst was always inferior to the sum of the critical period plus the antidromic conduction time, ruling out the possibility that it might have been entirely ectopically generated on thalamic terminals. The results further show that a spontaneous ectopic axonal impulse could trigger a somatic burst, since: (1) an electrically-evoked antidromic action potential could trigger a burst structurally similar to a spontaneous one; (2) on 42% of the tested thalamic cells, a known antidromic action potential delivered during the critical period following a spontaneous single impulse could not collide with it: in many cases such non-collisions were seen with the first action potential of a burst; and (3) with increasing ionophoretic doses, GABA could: (i) convert bursts to single action potentials, while the ortho- but not the antidromic responses were abolished, (ii) block these single impulses at similar doses than those which abolished known antidromic ones, and (iii) multiply by a factor of 3 the probability of testing an ectopic action potential. On 70% of the cells tested, such GABA-isolated impulses could be proved to have been ectopically generated. Finally, ectopic impulses have never been observed during periods of tonic firing, indicating that such a feature was not an experimental artifact.(ABSTRACT TRUNCATED AT 400 WORDS)
Pinault
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Unité de Recherches sur l'Epilepsie, INSERM U97, Centre Paul Broca, Paris, France.
Pumain
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D000200:Action Potentials; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D004558:Electric Stimulation; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013787:Thalamic Nuclei / Q000502:physiology*