Search

Since lesions placed more caudally failed to produce degeneration of terminals in the telencephalon, this suggests that histaminergic cell bodies are present in the upper mesencephalon or posterior hypothalamus.

SummaryAcute pulmonary edema is induced by bilateral injections of dilute solutions of aconitine into the preoptic area of the hypothalamus of rats. The severity of the edema is greatly reduced but not abolished by lesions of the posterior hypothalamus. Deep barbiturate anesthesia greatly reduces aconitine edema. Systemic injections of aconitine up to fatal dose levels do not induce pulmonary edema.

Electrical stimulation of the posterior hypothalamus elicited wheel running in rats. The speed of running was directly related to the intensity of the electrical stimulus. Results suggest that hypothalamic mechanisms mediate locomotor behavior.

Posterior hypothalamic selfstimulation of male rats, in which monopolar,platinum electrodes had been belaterally implanted, increased after systdmic injection of testosterone. constant stimulation to the same site elicited immediate copulation with estrous female rats. During constant stimulation males would press a bar to open a door for access to females. Even after ejaculation, males continued to open the door and to display sexual activity until stimulation terminated. Posterior hypothalamic stimulation is like normal sexual stimulation; it is rewarding, the reward varies with the amount of the sex hormone, and it elicits motivated copulation.

Independent groups of rats received posterior hypothalamic stimulation of 0.5, 1.0, 3.0, or 5.0 sec duration as a reward for performance in a brightness discrimination task. Acquisition of this discrimination was found to be inversely and linearly related to the duration of rewarding stimulation. It is suggested that long durations of hypothalamic stimulation, while generating strong approach tendencies, may retard learning by interfering with critical association and/or consolidation processes.

Norepinephrine has been assayed in the hypothalamus of rats during different phases of the estrous cycle. The content of catecholamine in the anterior and middle hypothalamus was minimal at estrus, rose significantly during diestrus, and reached maximal levels during proestrus. In the posterior hypothalamus no significant changes were detected. (Endocrinology 81: 1405, 1967)

Six rats were trained to operantly control the duration of electrical stimulation to the posterior hypothalamus. The duration of the stimulus was equal to the duration of the lever deflection response. Under normoxic conditions (21% 02), increasing stimulus current levels yielded increasing response rates, decreasing response durations and decreasing inter-response times. Hypoxia (8% 02) did not affect response duration at any current level, but lengthened inter-response time. The magnitude of this effect was inversely related to current level. Results are interpreted as suggesting that hypoxia does not affect the neural response concurrent with electrical stimulation but affects the after-effects of stimulation.

In Figure 13 we have tried to summarize the interactions of thermal and nonthermal control of effector responses, the effects these responses have on the body during exercise, and the ways the changing state of the body feeds back on the central control systems. These systems were depicted in Figure 3 and are included in condensed form in Figure 13. Exercise affects thermoregulatory responses not only by increasing heat production, but also through a number of other mechanisms. For example, the thermoregulatory responses tend to reduce central venous pressure, and sweating without fluid replacement will increase plasma osmolality. The secondary effects of these changes on the control of the thermoregulatory responses may themselves have an important effect on the rise in Tc during prolonged exercise or exercise in the heat. In concluding, it is appropriate to briefly answer the questions raised in the introduction. In our view, the concept of shifting the set point is not different from the concept of resetting the "thermostat," and the temperature regulatory system is governed by only one set point, which does not change during exercise. Tsk does not change the set point as we have defined it. Rather it combines with thermal information from the core and other deep body thermo-detectors to produce a thermoregulatory command signal Tws distributed to all effector responses. To demonstrate a set point shift, one must show that the Tws thresholds for initiating all heat-dissipating responses shift in the same direction. Although this does not occur with exercise, it does occur with time of day, heat acclimation, endurance training, and fever. A hyperosmolar state also can raise the threshold for sweating and vasodilation uniformly, and therefore may also raise the set point. However, a change in posture, for example, which alters the threshold for vasodilation but not for sweating, does not alter the set point. We believe that a shift in threshold for a given effector may be produced by either a central or a peripheral mechanism. For example, an ion-osmotic influence on the sweating: Tc threshold may be at the level of the central nervous system or the sweat gland itself. However, a set point shift must be a central event, since it influences all effector responses uniformly. Is the set point governed by the ratio of sodium to calcium ions in the posterior hypothalamus? This is unlikely. Shifts in ion concentration can influence effector responses, but they do not appear to shift all effectors uniformly.

IT is supposed by several authors1–9 that adrenaline-induced EEG-arousal, which originates in the mesencephalic reticular formation and the posterior hypothalamus, is caused by a direct action of adrenaline on these structures. Discharges were recorded from single cells within the posterior hypothalamus10,11. The firing-rate of these cells was affected by intravenous injection of adrenaline or by mechanically induced changes of blood pressure. There is no effect of adrenaline if the blood pressure is kept constant artificially. We therefore tested the hypothesis that the adrenaline-induced arousal is a secondary effect of the rising blood pressure.