Experimental studies on genetically determined predisposition to catatonia in rats as a model of schizophrenia.

To check experimentally the hypothesis of schizophrenia being a manifestation of extremely low threshold of hypnotic (catatonic) type of reaction, changes of some neurophysiologic and neurochemical systems in rats with a genetic predisposition to catalepsy were compared to analogous changes found so far in schizophrenia or chronic amphetamine intoxication considered nowadays as the most adequate pharmacological model of schizophrenia. It is found that in rats predisposed to catalepsy the threshold of audiogenic seizures is elevated; the activity of tryptophan hydroxylase in striatum is higher in rats predisposed to catalepsy genetically and due to a chronic methylphenidate intoxication as compared to control animals; noradrenaline content and noradrenaline/dopamine ratio is lower in the diencephalon of rats predisposed to catalepsy than in controls; cataleptic rats have a higher content of homovanillic acid in N.accumbens , and a higher frequency of inversion of hemispheric asymmetry as estimated by levels of dopamine and dioxyphenylacetic acid in N.accumbens and caudate nucleus, than normal rats; MAO-B/MAO-A ratio is higher in the brain stem of cataleptic than normal rats. The effects of haloperidol and apomorphine on motor activity of cataleptic and normal animals point to a higher sensitivity of postsynaptic dopamine receptors in the former. Conditioned avoidance reaction is formed slower, but preserved longer in rats predisposed to catalepsy. Blood serum of wild rats predisposed to akinetic catatonic reactions, unlike the serum of normal wild rats, inhibits the electric activity of snail neurons. The above indicated changes are analogous to those known to be present in schizophrenia and/or chronic intoxication with amphetamine or its pharmacological analogues, which witnesses in favour of the proposed hypothesis.