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Rats with bilateral lesions in the medial forebrain bundle demonstrate both an increased sensitivity to electric shock, as reflected by a lowered jump threshold, and a decrease in the concentration of serotonin in the brain. Both effects of the lesion are characterized by a delayed time of onset and gradual development, which approximates the time required for progressive nerve degeneration in the central nervous system. It is suggested that this behavioral effect of bilateral lesions in the medial forebrain bundle may be due to a central denervation supersensitivity.

The rate of glucose-supported respiration in cortical slices taken from control rats and rats with bilateral lesions in the caudate nucleus was increased by 92 to 95 percent after the addition of potassium chloride. In cortical slices taken from rats with bilateral lesions in the septal area the respiratory rate increased by only 40 percent.

Infusions of adrenaline failed to produce a significant increase in the adrenaline and noradrenaline content of cat uterus and kidney and of rat uterus and spleen, using normal and reserpine-treated animals. The adrenaline content of extracts of the organs was assayed on the isolated rat uterus, which was stimulated electrically; the noradrenaline content was assayed on the blood pressure of the pithed rat. The tissues studied contained relatively small quantities of adrenaline and this was not decreased by reserpine. Our results show a difference between the stores of adrenaline and noradrenaline in these tissues; the noradrenaline stores are larger, they are depleted by reserpine, and they are increased by an infusion of noradrenaline.

1. Sample from the neocortex and piriform cortex of guinea pigs and rats were incubated in inulin-containing glucose-saline. Their intracellular (non-inulin) space contained 19-27muequiv. of Na(+)/g. of original tissue. These values were stable between 30 and 100min. after incubation commenced, but addition of (22)NaCl to the neocortical samples showed them to be associated with a flux of 400muequiv. of Na(+)/g. of tissue/hr. 2. Addition of 0.5-10mm-l-glutamic acid or 0.1mm-N-methyl-dl-aspartic acid rapidly increased the tissue's Na(+) content; N-acetyl-dl-aspartic acid was without action. 3. During the first 1-1.5min. after the addition of l-glutamic acid to neocortical samples their Na(+) content increased at 600muequiv./g. of tissue/hr., and the rate of (22)Na(+) influx corresponded to 1230muequiv. of Na(+)/g./hr. These rates were calculated to be sufficiently rapid to account for loss of the tissue's normal membrane potential within 1-2sec. of the addition of the acid. 4. In addition, a rapid but more limited loss of K(+) took place after the addition of l-glutamic acid or the methylaspartic acid; on continued incubation tissue K(+) content increased, as also did the intracellular volume of the tissue, from its original 670mul./g. to 1100mul./g. 5. Interpretation of these and of associated changes is offered in terms that involve a cation pump and the permeability changes associated with the nerve impulse.

In the cat, phenoxybenzamine prevented the uptake of noradrenaline by the kidney but not by the uterus; dichloroisoprenaline prevented the uptake of noradrenaline by the uterus but not by the kidney. In the rat, a single dose of phenoxybenzamine prevented the uptake of noradrenaline by the heart, spleen and uterus and reduced the uptake by the duodenum. Prolonged treatment with phenoxybenzamine prevented the uptake by the heart and uterus but not by the spleen or duodenum. Both phenoxybenzamine and dichloroisoprenaline lowered the noradrenaline content of some tissues of the rat. Phenoxybenzamine did not antagonize the responses to noradrenaline of the nonpregnant cat uterus in situ, not the responses of rat isolated ventricles, uterus or duodenum. It is concluded that the way in which these noradrenaline antagonists affect the storage sites for noradrenaline varies between organs. The effects of the drugs on the receptors for noradrenaline are not related to their effects on storage sites.

Rats with electrolytic lesions in the septal forebrain show increased sleeping times after injection with thiopental sodium or barbital, as compared with normal and other control rats and rats with lesions in the cerebral cortex or caudate nucleus.