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Behaviour of SHR, C57B1/6 male mice and common albino male rats treated intracerebroventricularly or intraperitoneally with kynurenine, quinolinic, kynurenic, picolinic, xanthurenic, anthranilic acids and nicotinamide, was studied in the dark/light chamber. Quinolinic acid and its precursor kynurenine diminished dark preference, increased the number of transitions between dark and light compartments, diminished locomotion in light compartment. Biogenic amine phenylethylamine with its typical anxiogenic activity, exerted a similar action. Diazepam acted in the opposite way. Noncompetitive antagonist of the NMDA receptors, kynurenic acid, prevented the effect of quinolinic acid. The hole reflex appears to be a useful simple object to study neuroactive endogenous compounds on.

It has been shown in the behavioural experiments that combined pretreatment with haloperidol (0.25 mg/kg) and caerulein (40 micrograms/kg), and to a lesser extent pretreatment with caerulein alone caused long-term reversal of amphetamine (2 mg/kg) induced hyperexcitability in rats. Administration of proglumide (50 mg/kg), an antagonist of CCK-8 receptors, did not reverse long-term antiamphetamine effect of caerulein. In mice pretreatment with caerulein (50 and 100 micrograms/kg) alone or in combination with haloperidol (0.25 mg/kg) caused hypersensitivity to the behavioural effect of amphetamine (3 mg/kg). Intraventricular (I ng), but not systemic (100-500 micrograms/kg) administration of caerulein selectively antagonized seizures in mice induced by intraventricular administration of quinolinic acid (5 micrograms) and N-methyl-D-aspartate (0.2 microgram). Pretreatment with proglumide (50 mg/kg) reversed the anticonvulsive effect of caerulein in mice. In rats, caerulein failed to affect the seizures caused by intraventricular administration of quinolinic acid. The results of the present study demonstrate the existence of obvious interspecies differences in the behavioural effects of caerulein, the agonist of CCK-8 receptors, in mice and rats.