Lesions in the septal region of the forebrain oftein produce a state of hyperirrilability in rats characterized chiefly by an exaggerated startle response lo tactile stimuli applied to the animal's back and intense and aggressive resistance to handling (Brad}' & Nauta, 1953). These behavioral manifestations (septal syndrome) tend to abate over a period of weeks (Brady & Nauta, 1955). The specific ncuroanatomic structures which must be destroyed to produce the septal syndrome have not been clearly specified (Harrison & Lyon). Nor do we understand the behavioral mechanisms which are altered by the lesions. Brady and Nauta (1953) reported that the lesions weakened a conditioned emotional response but had no effect on the acquisition of the CER. Results obtained by Tracy and Harrison suggest that septal lesions abolish lever pressing to escape an avcrsive noise stimulus but do not interfere with acquisition or retention of lever pressing for food reward with the same noise used as a discrimination stimulus (Tracy & Harrison, 1956). On the other hand, King (1958) found that rats with septal lesions learn conditioned avoidance responses in a double-grill box with even greater facility than normal controls. Subsequent lesions in the amygdala abolish the septal syndrome. Hunt (1957) has reported that rats with the septal syndrome are much more sensitive to the behavioral effects of meprobamate, alcohol, and mephenesin than are normal rats or rats with lesions in other parts of the brain.

No abstract

The right or left coronary arteries were constricted by cholinergic agents and dilated by adrenergic agents. The receptors mediating cholinergic responses are muscarinic. Comparison with the ear artery indicates that the adrenergic receptors mediating dilatation in the coronary artery resemble β₁ rather than β₂. However, the ratios of the dilator potencies of noradrenaline, adrenaline and isoprenaline on the coronary artery were 1:0.23:2.6 compared with ratios of their positive inotropic potencies of 1:1.1:33 on the rabbit papillary muscle. The markedly smaller relative potency of noradrenaline on the papillary muscle may be due to uptake₁, since the potentiating effect of cocaine on noradrenaline on this tissue was approximately 12-fold, but was negligible on the coronary artery. The contribution of uptake₂ is unclear, since histochemical observations indicated selective accumulation of noradrenaline in the wall of the artery, whereas the dilator responses were not appreciably altered by uptake₂ inhibitors.

No abstract

The isolated central artery of the rabbit ear is highly sensitive to catecholamines when perfused with Krebs solution containing 5‐hydroxytryptamine. The preparation responds to 1 ng of noradrenaline and is extremely long lasting. It does not discriminate between noradrenaline and adrenaline.