Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus.
Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca2+-spikes. The neurons normally discharge such spikes on low-threshold Ca2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca2+-spike firing. A slowly inactivating K+ conductance, sensitive to blockade with 4-aminopyridine (50-100 microM), but not tetraethylammonium (2-10 mM), appeared to suppress excitability and high-threshold Ca2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca2+-spike into a plateau potential. Application of the Ca2+-channel blocker Cd2+ (50 microM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses. Our results suggest that high-threshold Ca2+-spike firing, and a short-term influx of Ca2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K+-conductance may reduce high-threshold Ca2+-spike firing and shorten high-threshold Ca2+-spike duration. A persistent Na+-conductance promotes coupling of the low-threshold Ca2+-spike to a high-threshold Ca2+-spike. Thus, the activation of both voltage-dependent conductances would affect Ca2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states.
Tennigkeit
F
F
Department of Pharmacology and Therapeutics, and The Rotary Hearing Centre, The University of British Columbia, Vancouver, Canada.
Schwarz
D W
DW
Puil
E
E
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001306:Auditory Pathways / Q000502:physiology*; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D005071:Evoked Potentials / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time; D019789:Tetraethylammonium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013788:Thalamus / Q000502:physiology*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D015221:Potassium Channels; D002104:Cadmium; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D002118:Calcium