NORADRENERGIC RESPONSES IN RAT HIPPOCAMPUS - ELECTRO-PHYSIOLOGICAL ACTIONS OF DIRECT-ACTING AND INDIRECT-ACTING SYMPATHOMIMETICS IN THE INVITRO SLICE

  • 1 January 1982
    • journal article
    • research article
    • Vol. 223  (3) , 599-605
Abstract
The effects of perfusion of postulated direct- and indirect-acting sympathomimetics on evoked potentials in the CA1 region of the in vitro rat hippocampus were examined. A selective .alpha.-agonist, 6-fluoronorepinephrine, produced depressions of population spike amplitude which were antagonized by the .alpha.-antagonist phentolamine, but not by the .beta.-antagonist timolol. The selective .beta.-agonist, 2-fluoronorepinephrine, produced increases in population spike amplitude which were antagonized by timolol but not by phentolamine. Weak and variable responses were seen to the indirect-acting sympathomimetic tyramine, wiht lower doses producing increases and higher doses producing decreases in population spike amplitude, respectively. As with 2-fluoronorepinephrine, increases in spike amplitude elicited by tyramine were blocked by timolol but not by phentolamine. Another indirect-acting sympathomimetic, d-amphetamine, produced only increases in population spike amplitude which were blocked by timolol. Phencyclidine, an agent which may produce some of its central effects via noradrenergic synapses, was virtually ineffective in producing catecholamine-like responses in this system. Only nonspecific, local anesthetic effects were observed. Taken together with previous studies, these results support the hypothesis that activation of .alpha.- and .beta.-receptors decreases and increases, respectively, pyramidal cell excitability. Although .alpha.- and .beta.-receptors appear to be capable of interacting with endogenously released norepinephrine, the .beta.-response may predominate.