Wet Shake Behavior Research Articles

THE ROLE OF THE SEROTONERGIC SYSTEM IN THE "WET DOG" SHAKE BEHAVIOUR INDUCED BY SODIUM N-DIPROPYL ACETATE

It is known that experimental animals used in pharmacological research behave in certain ways with the influence of various neurotransmitters in the central nervous system. In this research, we have studied the effect of buspiron on the wet shake behaviour, with respect to its relationship with the serotonergic system, after the administration of n-dipropyl acetate which is used in the treatment of epilepsy and 5-hydroxytryptophan which is a serotonin precursor. Key words: Wet dog shake, n-dipropyl acetate, serotonin, buspiron.

Butorphanol precipitates abstinence in morphine dependent rats

Butorphanol precipitated a withdrawal syndrome in rats receiving continuous intracerebroventricular infusions of morphine for three days. However, the potency of butorphanol to induce defecation, urination, teeth chattering and escape behavior was one to two orders of magnitude less on a molar basis than that of naloxone. Wet shake behavior, a prominent feature of naloxone precipitated withdrawal, was absent in morphine dependent animals challenged with butorphanol. These data indicate qualitative as well as quantitative differences in the withdrawal syndromes induced by butorphanol and naloxone.

Neuropharmacological profile of R 18 503-induced wet-shake behavior in the rat: noradrenergic and opiate components.

R 18 503 (alpha-(p-chlorophenyl)-beta,beta-dimethylimidazole-1-ethanol) 40 mg/kg IP produced a mean of 168 (SEM +/- 4) wet shakes in the 35 min following its administration to 100 g male Wistar rats. No other behavioural abnormalities were seen at this dose. The wet-shakes were not caused by reduced body temperature. However, 20-30 min after R 18 503, body temperature was significantly elevated in comparison with saline treated controls. This supports a role for wet-shakes in thermogenesis in the rat, but suggests that R 18 503-induced wet-shakes are not adapted towards the maintenance temperature homeostasis. R 18 503-induced wet-shakes were potently antagonized by 5 narcotic analgesics, but not by aspirin-like drugs. A further 18 non-narcotic compounds including putative serotonin antagonists, neuroleptics and compounds thought to act on the alpha-adrenergic system, also antagonized R 18 503-induced wet-shakes. Spectral map analysis showed a close link between ED50-values of the non-narcotic R 18 503 wet-shake antagonists and their ED50's to antagonize noradrenaline-induced lethality; this was further confirmed by a highly significant Spearman Rank correlation between the two tests (rs = 0.77, p less than 0.001). However, the spectral mapping and Spearman correlation analysis showed no relationship between antagonism of R 18 503-induced wet-shakes and antagonism of apomorphine-induced stereotypy, tryptamine-induced bilateral forepaw clonus, mescaline-induced head twitches, and 5 HT-induced contractions of rat caudal artery. It is postulated that R 18 503-induced wet-shakes result from an interaction between the opiate system and the alpha-adrenergic system.