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L C Wang

Publications and source records attributed to L C Wang.

9 recordsLinked to original sources

[The synaptic architecture of propriospinal neurons in cultured mouse spinal cord].

An electron microscopic analysis of the synaptic architecture in propriospinal neurons of cultured fetal mouse spinal cord has been undertaken. The size of the perikarya in the cultured spinal cord represents a range from small- to medium sized neurons, which form many synapses each other. There are many axo-dendritic and axo-somatic synapses in the culture but direct dendro-dendritic apposition is rarely seen. Four morphological types of synaptic boutons, S, F, M and G are classified according to criteria used by previous investigators. The ultrastructural details available suggest that the propriospinal neurons receive synaptic input from propriospinal fibers through simple synapses. It may indicate that their impulses can be controlled only postsynaptically.

Animals

Effects of central injection of biogenic amines during arousal from hibernation.

Simultaneous measurements of heat production (HP) and heat loss (HL) and brain and rectal temperatures were made in Richardon's ground squirrels (Spermophilus richardsonii) rewarming from hibernation at an ambient temperature of 6.0 +/- 0.5 degrees C. Calculations from HP and HL measurements from control animals showed that due to differential rewarming, there was a reduction of apparent specific heat of the animal to 0.59 cal/g. degrees C. This resulted in an energy saving of 30%. Three intracerebroventricular injections of 5-hydroxytryptamine (5-HT) of 56 microgram each at brain temperatures of 10, 20, and 30 degrees C caused initial suppression of HP and a greater overall HL, which resulted in a slower rate of arousal as compared to the controls. Injections of norepinephrine (NE) of 12.5 microgram each at similar brain temperatures caused a greater rate of HP, which resulted in a faster rate of arousal as compared to the controls. The respective actions of 5-HT and NE on thermoregulation during rewarming are similar to those in some euthermic hibernators and nonhibernating species. Our data indicated that these substances evoke thermoregulatory responses during arousal in much the same manner as during normothermia.

Animals

A microampere radiotelemetry transmitter for measurement of temperature from unrestrained subjects.

A miniature radiotelemetry transmitter is described suitable for chronic or acute monitoring of temperatures from animal or human subjects. The transmitters can be easily constructed with little or no electronics background from discrete components readily available from any electronics supplier. Transmitters weighed from 2.5-20 g, had volumes of 0.8-3.5 ml, had normal currents of 50-120 muA with potential transmitter lives of 35 h to greater than 1 yr, and transmission ranges of 10-30 m. Transmitters could be implanted, swallowed, or connected to chronically or acutely attached temperature probes. The design of the telemetry system allows for reception on any commercial FM receiver. Depending on mode of decoding the temperature data transmitter signal can be accurate to measure changes of from 0.15 to 0.015 degrees C. Thus with a minimum of expense and little electronics background a temperature-dependent transmitter system can be constructed for monitoring temperatures from unrestrained subjects.

Animals

Changes in plasma glucose, FFA, corticosterone, and thyroxine in He-O2-induced hypothermia.

Unanesthetized, male rats were exposed to normal air (NA), or NA and a 4 h-exposure of He-O2 (79% helium, 21% oxygen) at ambient temperature (Ta) of 22 or - 10 degrees C. Blood samples from each individual were taken from a chronically implanted carotid cannula at 1) preexposure, 2) during exposure, 3) 2.5 h after exposure, and 4) 19-20 h after exposure. Exposure to He-O2 at 22 degrees C caused an increase in plasma free fatty acids (FFA) and corticosterone of 45% and 49%, respectively, with little change in plasma glucose and thyroxine. Exposure to He-O2 at 10 degrees C for 3 h invariably induced hypothermia with body temperature (Tb) decreased to 23.7 +- 0.5 degrees C (N = 10). During hypothermia, plasma glucose, FFA, and corticosterone were significantly higher (P LESS THAN 0.05) than those at preexposure and those after exposure to NA at -10 degrees C. During spontaneous recovery from hypothermia, at Ta = 19 degrees C and NA, glucose, corticosterone, and thyroxine returned to normal, but FFA remained significantly higher than at preexposure. The ability of animals to rewarm spontaneously from hypothermia and the quick return of metabolic substrates and hormones to normal after rewarming indicates the preservation of regulatory mechanisms for metabolism at depressed Tb when hypothermia is induced by He-O2 and cold.

Animals

Metabolic and respiratory responses during Helox-induced hypothermia in the white rat.

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.

Animals