The role of norepinephrine and acetylcholine in mediating escape deficits produced by inescapable shocks.
This study examined the role of neurochemical changes produced by inescapable shock, specifically the depletion of norepinephrine (NE) and enhancement of acetylcholine (ACh), in mediating subsequent inescapable shock-induced deficits in escape acquisition in rats. Enhancement of these neurochemical changes by injections of the NE synthesis inhibitor, FLA-63 (10 mg/kg), or the anticholinesterase, eserine sulphate (3 X 0.5 mg/kg), during the inescapable shock enhanced the subsequent escape deficits observed 3 days later. In contrast, these drugs had no effect on the subsequent escape behavior of rats that were not exposed to inescapable shock. Since these effects could not be attributed to carry-over or state-dependent effects of the drugs, these data suggest that the magnitude of the escape deficit produced by prior inescapable shock is dependent on the magnitude of the initial inescapable shock-induced changes in NE and ACh.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D005406:Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide; D001921:Brain / Q000503:physiopathology*; D004924:Escape Reaction / Q000502:physiology*; D006801:Humans; D008297:Male; D009638:Norepinephrine / Q000502:physiology*; D010830:Physostigmine; D051381:Rats; D011919:Rats, Inbred Strains; D013315:Stress, Psychological / Q000503:physiopathology*
D005406:Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide; D010830:Physostigmine; D000109:Acetylcholine; D009638:Norepinephrine