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The Journal of Neurophysiology Vol. 83 No. 5 May 2000, pp. 2987-2995
Copyright ©2000 by the American Physiological Society
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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