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J Neurophysiol 83: 2987-2995, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 83 No. 5 May 2000, pp. 2987-2995
Copyright ©2000 by the American Physiological Society

Current and Voltage Clamp Studies of the Spike Medium Afterhyperpolarization of Hypoglossal Motoneurons in a Rat Brain Stem Slice Preparation

Remigijus Lape and Andrea Nistri

Biophysics Sector and INFM Unit, International School for Advanced Studies (SISSA), 34014 Trieste, Italy

Lape, Remigijus and Andrea Nistri. Current and Voltage Clamp Studies of the Spike Medium Afterhyperpolarization of Hypoglossal Motoneurons in a Rat Brain Stem Slice Preparation. J. Neurophysiol. 83: 2987-2995, 2000. Whole-cell patch clamp recordings were performed on hypoglossal motoneurons (HMs) in a brain stem slice preparation from the neonatal rat. The medium afterhyperpolarization (mAHP) was the only afterpotential always present after single or multiple spikes, making it suitable for studying its role in firing behavior. At resting membrane potential (-68.8 ± 0.7 mV), mAHP (23 ± 2 ms rise-time and 150 ± 10 ms decay) had 9.5 ± 0.7 mV amplitude, was suppressed in Ca2+-free medium or by 100 nM apamin, and reversed at -94 mV membrane potential. These observations suggest that mAHP was due to activation of Ca2+-dependent, SK-type K+ channels. Carbachol (10-100 µM) reversibly and dose dependently blocked the mAHP and depolarized HMs (both effects prevented by 10 µM atropine). Similar mAHP block was produced by muscarine (50 µM). In control solution a constant current pulse (1 s) induced HM repetitive firing with small spike frequency adaptation. When the mAHP was blocked by apamin, the same current pulse evoked much higher frequency firing with strong spike frequency adaptation. Carbachol also elicited faster firing and adapting behavior. Voltage clamp experiments demonstrated a slowly deactivating, apamin-sensitive K+ current (IAHP) which could account for the mAHP. IAHP reversed at -94 mV membrane potential, was activated by depolarization as short as 1 ms, decayed with a time constant of 154 ± 9 ms at -50 mV, and was also blocked by 50 µM carbachol. These data suggest that mAHP had an important role in controlling firing behavior as clearly demonstrated after its pharmacological block and was potently modulated by muscarinic receptor activity.




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