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H Rijk

Publications and source records attributed to H Rijk.

6 recordsLinked to original sources
PubMed1987

Facilitation of amphetamine-induced rotation by muscarinic antagonists is correlated with M2 receptor affinity.

This study examined the relationship between the affinity of cholinergic drugs for muscarinic receptor subtypes and their potency in potentiating or inhibiting amphetamine-induced rotation. The ascending nigrostriatal dopaminergic pathway was unilaterally lesioned in male Wistar rats using 6-hydroxydopamine. In these rats, ipsiversive rotation induced by amphetamine sulphate (1 mg/kg, s.c.) was dose-dependently inhibited by the cholinergic agonists oxotremorine, RS86 and pilocarpine and by the acetylcholinesterase inhibitor physostigmine. In contrast the cholinergic antagonists scopolamine, secoverine and dicyclomine facilitated amphetamine-induced rotation. Agonist and antagonist potencies were then compared with M1 and M2 binding site affinities estimated by displacing [3H]pirenzepine from forebrain and [3H]QNB from brainstem homogenates. The data suggest a relationship between antagonist potency and M2 binding site affinity.

Animals↗
PubMed1983

Facilitation of hot-plate response learning by pre- and posttraining naltrexone administration.

Retention performance for shock-motivated learning is generally enhanced by opiate antagonists. To test the hypothesis that opioid systems mediate learning and memory in nonshock-motivated tasks, the effects of naltrexone on hot-plate response learning were investigated. Naltrexone (0.1 or 1.0 mg/kg IP) 10 min before hot-plate exposure produced hyperalgesia, as measured by decreased latencies of naltrexone-injected mice to escape. Jump latencies, however, were not significantly decreased by naltrexone given 10 min before initial testing. Nevertheless, jump latencies of naltrexone-injected mice, but not saline-injected mice, decreased further on subsequent test trials 1 and 4 days later although treatment was discontinued, suggesting that the opiate antagonist also influenced learning or memory. Mice given naltrexone (0.3-10.0 mg/kg IP) immediately after their first hot-plate exposure also exhibited learning of the jump response, on a test trial 48 h later. The decreases in jump latencies on test trials were smaller after posttraining, than pretraining naltrexone administration. The results indicate that the effect of naltrexone on learning and memory can be at least partially separated from its hyperalgesic activity.

Animals↗
PubMed1982

A mouse model of alcoholism.

A model of alcoholism should demonstrate self-administration of alcohol by the animal and a withdrawal syndrome when the animal no longer has access to the drug. A mouse model is described that meets these criteria and enables the induction of "alcoholism" in a large number of animals within a short period of time. Mice were injected daily with pyrazole, an inhibitor of alcohol dehydrogenase. The animals self-administered ethanol by inhaling vapour containing a relatively constant concentration of ethanol. Self-administration was voluntary: the mice could move to a chamber without ethanol vapour. During the first six days of each experiment, the animals were prompted to select the ethanol chamber by darkening that chamber. Most mice continued to self-administer ethanol without any prompting for at least 3 days; thereafter, preference for ethanol waned. Self-administration led to measurable levels of ethanol in blood and to the development of withdrawal when infusion of vapour was stopped.

Alcohol Withdrawal Delirium↗
PubMed1980

Tolerance to ethanol and severity of withdrawal in mice are enhanced by a vasopressin fragment.

Mice were rendered physically dependent on ethanol by inhalation of ethanol vapour and treatment with pyrazole for 3 days. On Day 4, withdrawal convulsions were measured and on Day 5 or later, residual tolerance to the hypothermic effect of an i.p. challenge dose of 3 g/kg ethanol was assessed. Mice continuously infused with the vasopressin fragment des-Gly9-[Arg8]-vasopressin dicitrate (DGAVP) throughout the periods of dependence induction and withdrawal testing exhibited exacerbated withdrawal convulsions. DGAVP also tended to exacerbate withdrawal when injected s.c. repeatedly (10 micrograms/injection/mouse) during testing for withdrawal. The data indicate that these effects were not likely to have been due to subconvulsive activity of DGAVP by itself or to changes in blood levels of ethanol. Continuous infusion of DGAVP enhanced residual tolerance on Day 5 but did not maintain tolerance when the time interval between withdrawal and testing for tolerance was increased. Restricting treatment with DGAVP to the period of induction of dependence (Days 1-3) also enhanced tolerance on Day 5. The data indicate that the vasopressin fragment modulates the development and/or the decay of tolerance to ethanol. In addition it exacerbates withdrawal convulsions, an effect that may be due to modulation of physical dependence.

Animals↗