Palmar and non-palmar sweating were continuously measured by Hydrograph (Mitsuwa Denshi) in 3 human subjects during sleep and in 30 subjects during wakefulness. The measurements were processed on line by a personal computer, simultaneously with parotid gland salivary secretion and heart rate measurements. Nonpalmar sweating was recorded from the 3 subjects during sleep, and there was little difference between the sweating rate in REM and non-REM sleep. Slight palmar sweating was only seen in one subject during sleep. Palmar sweating was recorded from every subject during wakefulness but with little non-palmar sweating. The palmar sweating rate was higher in a passionate state and a stressful state than in a relaxed state similar to heart rate, but there was not so clear a difference between an indifferent state and a relaxed state in the sweating rate as heart rate. The sweating manner was different from the salivary secretion, whose rate decreased from a passionate state to a relaxed state, to a stressful state and was lowest in an indifferent state. A certain connection was seen between the palmar sweating, salivary secretion and heart rate in a subject. with a
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PERSISTENT SODIUM CHANNELS BORN RAT MEDULLA IN VITRO Dept. Physiol., Showa Univ. School of Med. Hiroshi Onimaru,
OF RESPIRATORY
A subject
NEURONS IN THE NEW-
Ikuo Homma
In the brainstem-spinal cord preparation from 0- to 4-day-old rats, Na+ channels of respiratory neurons in the ventrolateral medulla were analyzed by whole-cell recordings. Burst generation of respiratory neurons was completely blocked by superfusion of TTX-containing solution, whereas it was retained in low Ca2+/high Mg2+ solution in some pre-inspiratory (Pre-I) neurons. After complete inhibition of the burst activity due to Ca2+ membrane potential oscilchannel blockade by 0.1 mM Cd 2+ , Pre-I neurons showed depolarization-dependent lation and slow depolarizing responses to current pulse injection. The activation threshold was -45 to -40 mV. Subsequent K+ channel blockade induced spontaneous bursting activity and depolarizing plateau potentials. These responses were blocked by addition of 0.5 PM TTX. We suggest that intrinsic slow depolarization in Pre-I neurons due to activation of TTX-sensitive persistent Na+ channels is important in rising phase of spontaneous burst activity.
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IS THE PONTINE PNEUMOTAXIC CENTER NECESSARY FOR EUPNEIC RESPIRATION? Dept. Pharmacol. Fat. Med. Toyama Med. Pharmaceut. Univ., 2630 Sugitani, Toyama, 930-01, Japan Akira Haji, Mari Okazaki, Ryuji Takeda The pontine pneumotaxic center (PC) has been thought to play an essential role in the inspiratory off-switching (10s) mediated by NMDA receptors. We studied the involvement of PC in an apneusis (prolonged inspiration) induced by blockade of NMDA receptors. In decerebrate and vagotomized cats, a eupneic respiration continued after the pontine transection caudal to PC in a half of animals tested. For these cases, a NMDA receptor antagonist dizocilpine produced an apneusis similar to that induced in animals with an intact brainstem. In the remaining animals, the transection caused an apneustic pattern dissimilar to the dizocilpine-induced apneusis but identical to that caused by pentobarbital. The results suggest that the NMDA receptor-mediated 10s mechanism responsible for a eupnea locates in the lower brainstem respiratory network.