Experimental studies on hatching behavior in the chick. IV. Evidence for the role of a noradrenergic mechanism

In the present experiments we have attempted to determine whether one or more of the biogenic amines are involved in the prehatching and hatching behavior of the chick. Injection of reserpine first induces a depression in ongoing spontaneous motility on day 16 of incubation. Prior to this, reserpine has no apparent effect on embryonic behavior. Reserpine injections on days 17-19 induce a similar behavioral depression that lasts for at least six hours; by 24 hours post-injection the behavior of reserpine-treated embryos is comparable to controls. Injection of reserpine on day 20 (post-pip) delays hatching by about nine hours. Injection of reserpine into the yolk-sac of eggs prior to incubation also delays hatching by eight to nine hours. It is unlikely that the well-known cardiovascular effects of reserpine are involved in the above behavioral results since spinal embryos also exhibit a behavioral depression following reserpine treatment. Biochemical estimation of norepinephrine (NE) in the brain of reserpine-treated embryos suggest that it is release, not depletion, of the catecholamines that is responsible for the behavioral effects. Additional suport for this notion comes from experiments in which 16- or 18-day old embryos were injected with NE, L-dopa or amphetamine. In each case, a behavioral depression similar to that produced by reserpine resulted. Clonidine, a NE agonist induces a depression in certain aspects of embryonic behavior (Types 1 and 2), but also selectively enhances a corrdinated motor pattern (type 3 motility) involved in prehatching behavior (tucking). Clonidine first evokes this behavior pattern one or two days prior to its spontaneous appearance on day 16. After pipping on day 19 or 20 clonidine no longer activates Type 3 behavior, even if injected during the actual hatching process (climax). Since the alpha-adrenergic blocking agent phenoxybenzamine blocks the effect of clonidine on Type 3 tucking behavior, whereas the beta-adrenergic blocker propranolol does not, we suggest that tucking and the attainment of the hatching position are mediated by an alpha-adrenergic mechanism in the brain and/or spinal cord. Furthermore, since clonidine affects the Type 3 behavior associated with tucking, but not the somewhat similar coordinated behavior involved in hatching and emergence from the shell (climax), we propose that this later behavior pattern be given a new name, Type 4 motility.