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PubMed1988

Screening of clonidine effect on brain acetylcholine content, anticonvulsant and local anaesthetic properties.

Clonidine, a potent centrally acting antihypertensive drug was screened for effect on " free " and " bound " acetylcholine (Ach) in brain of morphine dependent and morphine withdrawal rats, anticonvulsant activity and morphine withdrawal rats, anticonvulsant activity and local anaesthetic activity. " Free " and " total " Ach content in normal (non-dependent) animals as well as in animals dependent to morphine was not changed by clonidine. Naloxone produced abstinence syndrome in dependant rats with highly significant increase in " free " Ach. Clonidine pretreatment decreased the rise of " free " Ach content produced by naloxone. It failed to show any anticonvulsant effect against maximal electroshock convulsions in rats, however, it exhibited significant local anaesthetic activity. Diuresis, piloerection and convulsions were observed with higher doses of clonidine.

Journal Article↗
PubMed2006

[Relation between level of expression of high mobility group protein B1 in hepatic tissue with the severity and prognosis of sepsis in rat].

OBJECTIVE: To investigate whether the levels of expression of high mobility group protein B1 (HMGB1) in hepatic tissue are related with severity and prognosis of sepsis in rat, in order to look for a dependable marker for monitoring and evaluating the efficiency of the treatment of sepsis. METHODS: Ninety SD rats (specific-pathogen free, male, 250-300 g) were randomly divided into sham operation group (group A), cecal ligation and puncture (CLP) group (group B) and CLP followed by ethyl pyruvate (EP) treatment group (group C). Laparo fury was done aseptically, and the cecum was returned to the abdomen (group A) or CLP was carried out (group B and C). The abdominal wall was then closed layer by layer. Normal saline (NS) 2 ml (group A and B) or EP 2 ml (130 mg/kg, group C) was intraperitoneally injected and repeated every 12 hours. Five animals were sacrificed at 0, 6, 12, 24, 48 and 72 hours after the operation, blood samples and 100 grams of hepatic tissue were harvested before the animal died. Before sacrifice, activity, food taking, piloerection, diarrhea, anophthalmia, respiration, distention of intestine, hyperemia, ascites, and omental adhesion to the cecum, and hyperemia of lung were observed. Another group of 20 rats were used to observe the survival rate after CLP. The level of HMGB1 mRNA expression in the hepatic tissue was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR), and the levels of interleukin-1 beta (IL-1 beta), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in plasma were determined by enzyme linked immunoadsorbent assay (ELISA). RESULTS: The mortality of sepsis was higher in group B than other groups (both P<0.01), that of group C was significantly lower than B but higher than A (both P<0.01). The levels of IL-1 beta, IL-6 and TNF-alpha in plasma rose to the peak at 6 hours after CLP in all groups, and group B>group C>group A (P<0.01), and they descended at 12 hours. The HMGB1 mRNA expression level in hepatic tissue was measurable at 6 hours and rose at 12 hours in group B, and maintained a high level up to 48 hours after CLP. The HMGB1 expression was positive correlated with IL-6 (r=0.91). The value in group C was significantly lower than group B at all time points (all P<0.01). The degree of severity and survival rate of sepsis were highly correlated with HMGB1 levels. CONCLUSION: As a late-released inflammatory mediator, HMGB1 plays a key role in lethal effect of sepsis, the surviving time and the severity degree of sepsis are highly correlated with HMGB1 expression level in hepatic tissue.

Animals↗
PubMedDate not supplied

[Pharmacologic study of clofelin].

Clofelin--2-(2,6-dichlorphenylamino)-2-imidasoline, an analoque of foreign-made clonidine (St155, catapresan, hemiton, etc) was subjected to a pharmacological study. In animals the drug produces first a rise and then protracted fall of the arterial pressure, reduces the frequency of cardiac contractions, lessens reflex hypertension that develops on compression of carotid arteries. When used in low doses it depresses the motor activity in unanesthetized animals and produces symptoms that bear evidence to its adrenomimetic action, e.g. exophthalmos, piloerection. Hypertension provoked by clofelin is caused by its peripheral and hypotension--by the central alpha-adrenomimetic action. The results of the present investigation prove clofelin to be identical with corresponding foreign drugs.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Ribavirin-induced behavioral, body temperature and electrocortical spectra effects in the rat.

Behavioral, electrocortical spectra and body temperature effects, following a single intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) injection of ribavirin, were studied in male adult rats. Ribavirin, when administered i.p., induced squatting posture, sedation, electrocortical synchronization, piloerection and a slight decrease of tactile and/or auditory stimuli/responses lasting from 45 min to 16 hr, as well as a longer lasting hypothermic effect. Following i.c.v. administration, ribavirin (50, 100 and 200 micrograms) elicited a soporific effect and produced changes in the electrocortical spectra. Pretreatment, 15 min before, with either prazosin (10 mg/kg, i.p.), an alpha 1-adrenoceptor blocker, or piperoxan (20 mg/kg, i.p.) and yohimbine (1 mg/kg, i.p.), two alpha 2-adrenoceptor blockers, or naloxone (1 mg/kg, i.p.), an opioid antagonist, did not prevent the hypothermic and behavioral effects induced by i.p. or i.c.v. administration of ribavirin. The present findings exclude an involvement of alpha-adrenergic and opioid neurotransmission in mediating the hypothermic, electrocortical and behavioral effects induced by ribavirin.

Animals↗
PubMed1990

General pharmacology of recombinant human tumor necrosis factor. 2nd communication: effects on central nervous system functions.

Effects of recombinant human Tumor Necrosis Factor (rHu-TNF, PT-050) administered s.c. and i.v. on the central nervous system were investigated behaviorally and physiologically in different animal species. With i.v. administration at doses of 10(4) U/kg and less, PT-050 produced no significant changes in most of behavioral and physiological tests, except that a transient increase in rectal temperature in dogs occurred with 0.765 x 10(4) U/kg and acetic acid-induced writhing syndrome in mice was inhibited with 10(4) U/kg. Locomotor activity in mice was inhibited after 3 x 10(4) U/kg. With 10(5) U/kg and more, in addition to the above effects, diverse effects were observed as follows: various symptoms were induced in general behavior in mice such as piloerection, catalepsy, lowering of body position, ptosis and pupil dilatation; rectal temperature was increased in rats and decreased in mice; cortical EEG was synchronized in hippocampal theta waves were disturbed in gallamine-immobilized cats. On the other hand, with s.c. administration, the effect on rectal temperature was seen at 10(4) U/kg in dogs and at 10(5) U/kg in rats. Cortical EEG in conscious rabbits was affected with 10(6) U/kg. At higher dose of 10(7) U/kg. PT-050 (s.c.) further influenced locomotor activity, rectal temperature and acetic acid-induced writhing syndrome in mice. However, even with 10(7) U/kg (s.c.), no effect was found in general behavior, rotarod performance and hexobarbital narcosis in mice. Thus, it is concluded that PT-050 has weaker effects on the central nervous system by s.c. route than by i.v. route. From the present findings and the efficacy of PT-050 as TNF, it is suggested that PT-050, when administered intratumorally, may be useful for cancer therapy without severe side effects.

Analgesics↗
PubMed1990

[The central effects of a steroid alkaloid, Buxaminol-E, in conscious cats].

Buxaminol-E injected i.v. to conscious cats evoked hypothermia, tachypnoe, anorexia, salivation, defecation, decrease of spontaneous activity and sensitivity to painful stimulus and agitation during its administration. The above mentioned effects of B--E, with the exception of the antinociceptive action which was not examined and of the initial excitation, were observed also after intracerebroventricular (i.c.v.) administration of B--E, and they were depressed by atropine administered i.c.v. Our findings suggest a central cholinergic action of B--E in conscious cats. Paroxysmal tonic-clonic convulsions and circling observed only after i.c.v. administration of B--E and piloerection, ataxia and urination were not inhibited by atropine administered i.c.v.

Alkaloids↗
PubMed1989

[Study of behavioral pharmacology on rats. Tranquilizing effects induced by endogenous or exogenous bradykinin].

UNLABELLED: This study was investigated on the mechanism of the sedative state, tranquilization induced by bradykinin (BK) and kallikrein (KAL). The drugs used in this study were as follows: KAL as endogenous BK promoter; prostaglandins (PGs) as a material of analogous action of BK; indomethacin and mepacrine as the inhibitors of PG-synthesis; eugenol as the OH- scavenger and the PGE-synthesis potentiator; angiotensin converting enzyme inhibitor as BK potentiator B. All drugs were dissolved in Hartmann's solution (lactate Ringer's solution) and 10 microliters of solution was injected into the lateral ventricle of rats, according to the Myers' procedure. Then, the rat behavior was estimated, by means of monitoring spontaneous movement. A high performance liquid chromatography (HPLC) was used for detecting alteration of monoamines and prostaglandins in the rat brain on sedative state after BK or KAL injection. RESULTS: 1) A 2-phase alteration of spontaneous movement was occurred within 30 min after BK or KAL icv-injection with behavioral specificity as follows: two exciting states and one sedative state. 2) A great increase of spontaneous movement evoked by BK or KAL was accompanied by exciting state as follows: jumping, wet dog response, struggle and scratching response, rearing and exploration. 3) A great decrease of spontaneous movement evoked by BK or KAL was accompanied with sedative state as follows: crouching with piloerection and closed eyes, catalepsy, preening and moisturizing and grooming. 4) PGE1 icv-injection was also carried out to clarify the involvement in the BK- or KAL-induced behavioral alteration. Consequently caused PGE1 the similar result to BK or KAL. 5) ACEI elongated and enhanced the exciting state or sedative state evoked by BK or KAL. 6) It was clear that BK reduced levels of monoamines in the rat hypothalamus: levels of norepinephrine(NE), epinephrine(E), dopamine(DA) and 5-hydroxytryptamine (5-HT) were decreased to 72.5%, 53.5%, 71.2% and 75.0% of control, respectively. Reduction of catecholamines in the hypothalamus was produced by increase of PGs and subsequently occurred sedative state of rats. 7) BK- or KAL-induced exciting state was enhanced by PG- synthesis inhibitor, especially the cyclo-oxygenase inhibitor indomethacin, but the sedative state was weakened. On the contrary, eugenol, an OH- scavenger, elongated and intensified the sedative state. Detection with HPLC showed remarkable increase of levels of PGs in the rat brain during the sedative state: the level of PGE2 was 27.5% increase of control and the level of PGE2 alpha was also 54.8% increase of control, respectively.

Angiotensin II↗
PubMed1989

Antidiarrheal activity of alpha-2 adrenoceptor agonist SK&F 35886.

Alpha-2 adrenoceptor agonists exhibit antidiarrheal activity in animal models and in humans. However, hypotensive and sedative side effects seriously limit the use of these agents to treat diarrhea. SK&F 35886 (2,6-dimethyl phenylamino imidazoline) is an alpha-2 adrenoceptor agonist with little central nervous system activity. In Ussing chamber preparations of rabbit ileum, SK&F 35886 produces a concentration-dependent decrease in basal short-circuit current (Isc) (EC50 0.2 microM) that is dependent on the presence of mucosal HCO3. This concentration-response curve is shifted to the right of rauwolscine, increasing the EC50 to 30 microM. Prazosin had no effect on this response. Flux studies indicate that SK&F 35886 increases net Cl absorption and enhances HCO3 absorption without altering net Na flux. After PGE2 stimulation of Isc, SK&F 35886, applied either serosally or mucosally, immediately returns the Isc to base line. This effect is due to a reversal of the PGE2-induced inhibition of Na and Cl absorption. In vivo SK&F 35886 dose-dependently inhibits PGE2-induced enteropooling when given orally (ED50 approximately 31 micrograms/kg). This effect is attenuated significantly by rauwolscine (1.0 micrograms/kg s.c.). In cecectomized rats, SK&F 35886 abolishes PGE2-induced diarrhea within 1 hr after oral administration of the drug. SK&F 35886 (500 micrograms/kg p.o.) did not alter hexobarbital sleep time or elicit piloerection or lethargy, whereas clonidine (37.3 micrograms/kg p.o.) significantly enhanced hexobarbital sleep time. These results illustrate the ability of a peripheral acting alpha-2 agonist to promote absorption and inhibit secretion and diarrhea in the mammalian intestine.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Benzodiazepine dependence in mice after ingestion of drug-containing food pellets.

Diazepam was administered to Swiss-Webster mice for 53 days as a mixture of drug in laboratory chow, leading to consumption as high as 1000 mg/kg/day. Low plasma concentrations of diazepam, but very high levels (generally between 5,000 and 10,000 ng/ml) of the active metabolites nordiazepam and oxazepam, were found. Animals appeared healthy throughout drug administration, but some died because of apparent drug-induced aggression. Withdrawal was precipitated by omitting drug from the food. The behavior and physiological state of each animal were observed in detail during treatment and withdrawal phases. Tests that showed stable results in control animals and changes during abstinence were used to measure the withdrawal syndrome. These changes included piloerection, tremor, pelvic elevation and tail elevation, as well as changes in body tone, abdominal tone and pupil size. A composite withdrawal score was plotted against time; this score increased significantly (P less than .01) 1 day after withdrawal and remained significantly elevated for 17 days. This technique provides a quantitative method to study the effect of withdrawal from benzodiazepines in mice.

Aggression↗
PubMed1985

[Effect of muscimol (GABA-agonist) on thalamo-hypothalamic regulation by corticotropic efferents (thalamic model)].

It can be assumed from previous data that the stress-induced polyphasic adrenocortical response involves two phenomenons. First, direct hypothalamic afferents stimulate the adrenocorticotropic axis resulting in a rapid increase in plasma corticosterone levels up to a maximum of about 40 ng . ml-1 at 15 min. Then, a thalamic-hypothalamic loop generates the late rebounding components. Intravenous injection of muscimol (0.5 ml . kg-1) produces only slight and short duration (45 min) disturbances (piloerection; panting; corticosteronemia). Stress application, 1 hr after muscimol administration, elicits only the first peak of corticosterone with magnitude and delay similar to that in control. However, the late rebounding component is no more visible. Thus, GABA-ergic stimulation leads to a situation similar to that seen after section of neural connections between thalamic nuclei and infundibular complex. The hypothalamic-adrenocorticotropic reactivity itself is not affected whereas the function of the regulating thalamo-hypothalamic loop is markedly impaired.

Animals↗
PubMed1978

Percutaneous epidural neurostimulation for paraplegic spasticity.

A case of post-paraplegic, post-traumatic spasticity, alleviated by percutaneous epidural neurostimulation from implanted electrodes at the L1 and L3 intervertebral levels, is presented. Secondary beneficial physiological effects and controls of involuntary activity that were achieved were regulation of a bowel regime, production of sweating below the level of the lesion, increased piloerections, and morning penile erections. Electrical modulation of the involuntary motor and autonomic activities below a complete spinal cord injury is discussed. The main advantages of such treatment in modulating spasticity are the avoidance of all other destructive neurosurgical procedures and the regulation of secondary physiological, autonomic responses. Long-term follow-up and additional therapeutic proofs are necessary to substantiate this preliminary report.

Adult↗
PubMed1986

Pharmacologic characterization of acute chlordiazepoxide dependence in the rat.

A single intoxicating dose of chlordiazepoxide HCl (p.o.) in the rat can induce quantifiable manifestations of physical dependence. Dependence was revealed by antagonist precipitation (Ro 15-1788, CGS-8216) as well as spontaneous emergence of neurobehavioral signs of withdrawal observed by multiple raters blind to treatments. Ro 15-1788 was 45% more effective than CGS-8216 in both reversing chlordiazepoxide intoxication and expressing withdrawal signs. The severity of Ro 15-1788-precipitated withdrawal varied with chlordiazepoxide dose, Ro 15-1788 dose and the agonist-antagonist dose interval. Maximal precipitated dependence was evoked 3 days after chlordiazepoxide HCl (450 mg/kg) by Ro 15-1788 (25 mg/kg i.p.). The precipitated syndrome consisted of tail erection, reduced motor activity, high step, curled claw, arched back, muscle hypertonus and piloerection. Ro 15-1788-precipitated dependence emerged between 28 and 52 hr, peaked at 76 hr and disappeared by 124 hr. Spontaneous withdrawal had emerged from 100 to 124 hr and then faded gradually. The neurobehavioral expression of central nervous system depression and its reversal were necessary but not sufficient conditions for the induction and expression of acute chlordiazepoxide dependence. These results suggest caution in reviving acute benzodiazepine-overdosed patients to avoid iatrogenic withdrawal analogous to naloxone for opiates.

Animals↗
PubMed1987

Evaluation of granulocyte transfusion in healthy neonatal pony foals.

Granulocyte transfusions (GT), 0.98 X 10(9) neutrophils/kg of body weight, were performed on 7 healthy pony foals between 2 and 7 days old. The mean neutrophil count of the foals was significantly (P less than 0.05) greater than base line (4,830 +/- 1,260/microliter) 1 hour after GT (8,870 +/- 3,350/microliter) and was similar to base line by 15 to 18 hours after GT (6,550 +/- 2,310/microliter). Leukocyte concentrates (LC) used for GT were harvested from clinically normal adult horses by continuous-flow centrifugation leukapheresis (CL), 3 to 6 hours after hydrocortisone sodium succinate was administered to increase the blood neutrophil count. The mean neutrophil count of the LC used for GT was 68,050 +/- 13,990/microliter, and the mean LC volume was 377.4 +/- 79.2 ml (14.82 +/- 3.54 ml/kg). The mean time required to collect the LC used for GT was 232.1 +/- 73.4 minutes. Neutrophils from LC had significantly reduced in vitro stimulated migration to zymosan-activated serum, when compared with peripheral blood neutrophils of the donors (P less than 0.05). Neutrophil phagocytosis and bactericidal capacity were not significantly changed in LC. Mean neutrophil migration indices were not significantly different in foals after GT. Mild depression and transient diarrhea was noticed in 1 foal 30 minutes after the start of the GT. The donor of LC for this foal and 1 other donor experienced depression, piloerection, and muscle tremors during CL, indicating that complement had been activated. Problems were eliminated by the use of new disposable plastic materials for blood processing in each CL procedure.

Animals↗
PubMed1987

[Emotional behavior disorders in rats during the formation of a generator of pathologically enhanced excitation in the basomedial nuclei of the amygdaloid complex].

Microinjections of kainic acid and ferrous sulfate into basomedial nuclei of both amygdalae resulted in the formation of the generator of pathologically enhanced excitation (GPEE), as evidenced by the epileptical activity (EpA) registered in both nuclei. EpA of different intensity and pattern could be retained for more than three weeks. Hyperactive basomedial nuclei played the role of a primary pathological determinant which caused the complex of emotional and behavioural disorders. Continuous motor depression at the early stages alternated pathologically enhanced activity at the later stages. A number of signs could be considered as the evidence of the affective disorders (motivation suppression, enhanced irritation, anxious excitation). Stereotype behaviour, immobility, rigidity, different types of vegetative disorders (ptosis, constipation, piloerection, loss of weight, respiratory arrhythmia, dystrophic symptoms) were observed in most animals. The emotional, behavioural and vegetative disorders described are compared to the manifestations of the depressive syndrome.

Affective Symptoms↗
PubMed1986

Toxicological studies on (2"R)-4'-O-tetrahydropyranyladriamycin, a new antitumor antibiotic. Subacute toxicity study in rats.

(2"R)-4'-O-Tetrahydropyranyladriamycin X HCl (THP), a new anthracycline antitumor antibiotic, was administered to Sprague-Dawley rats intraperitoneally for 13 weeks. In rats receiving 0.4 mg/kg/day, piloerection, emaciation, loose feces and thickening of the injection site were evident, and 7 males and 2 females died after week 12. Inferior body weight gain was observed in both sexes starting week 4 approximately 6. The food consumption also decreased. Hematological examination revealed lower counts of total leucocyte and lymphocyte. At termination there were lower spleen, thymus and testes weights, thickening of the walls of the intestine and stomach, gastric ulceration, presence of ascitic fluid, and congestion and thickening at the injection site. Decreases in the lymphocyte populations of the thymus, spleen and lymph nodes were observed microscopically. A decrease in the number of hematopoietic cells in the bone marrow and a degeneration of the germinal epithelium in the testes were also seen, as were gastrointestinal disturbances. These treatment-related effects were mainly confined to rats receiving 0.4 mg/kg/day and to a lesser extent, to rats receiving 0.1 mg/kg/day. The effects on rats receiving 0.025 mg/kg/day were only at the microscopic level. No rats receiving 0.006 mg/kg/day were toxicologically affected.

Animals↗
PubMed1986

Toxicological studies on (2"R)-4'-tetrahydropyranyladriamycin, a new antitumor antibiotic. Chronic toxicity study in rats.

(2"R)-4'-O-Tetrahydropyranyladriamycin X HCl (THP), a new anthracycline antitumor antibiotic, was administered to Sprague-Dawley rats (each group 20 rats) intraperitoneally at dosages of 0.001, 0.008, 0.06 and 0.3 mg/kg/day for 53 weeks. Piloerection, loose feces or perianal staining and thin or emaciated build were observed from week 12 in rats receiving 0.06 or 0.3 mg/kg/day. All rats receiving 0.3 mg/kg/day and 3 males and 1 female receiving 0.06 mg/kg/day died or were prematurely sacrificed in the period from weeks 13 to 44. The overall food consumption and body weight gain of both sexes receiving 0.06 or 0.3 mg/kg/day were lower than those of the controls. Hematological examination showed low leucocyte counts, disturbance in neutrophil and lymphocyte number and low erythrocytic characteristics in animals receiving 0.06 or 0.3 mg/kg/day. At necropsy, macroscopic changes were found at the injection site, throughout the gastrointestinal tract and in the male reproductive system in rats receiving 0.06 or 0.3 mg/kg/day. Microscopic examination revealed decrease in the small lymphocyte population in the hematopoietic and lymphoid system in rats receiving 0.008 to 0.3 mg/kg/day. Degeneration of the germinal epithelium of the subcapsular tubules of the testes, gastric ulceration, epithelial adnexal atrophy of the skin and chronic cellulitis and necrosis at the injection sites were also observed. No rats receiving 0.001 mg/kg/day were affected in these respects.

Animals↗
PubMed1985

Intrathecal clonidine: analgesia and effect on opiate withdrawal in the rat.

Clonidine, an alpha 2 adrenergic agonist, has analgesic properties and recently has been used to suppress opiate withdrawal. These two properties theoretically make it a suitable analgesic substitute in patients tolerant to opioids. The objectives of this study were to see if intrathecal clonidine is analgesic and whether it can modify morphine withdrawal at the spinal level. Rats chronically implanted with catheters in the lumbar subarachnoid space were utilized. In analgesia experiments, intrathecal clonidine produced analgesia with the peak effect in the paw-lick test occurring at 200nM, and in the tail-flick test analgesia was apparent at 100 nM and peaked at 400 nM (in 10 microL Ringer's lactate). In dependency experiments, animals dependent on morphine (300 mg X kg-1) received intrathecal clonidine 25, 50, 200 nM in 10 microliter Ringer's lactate 72 h after morphine. Following this, a naloxone challenge, 3 mg X kg-1 was administered and withdrawal assessed. Clonidine-treated animals showed significant weight loss and decrease in temperature, and those treated with high doses showed marked hypothermia and hind-limb flaccidity. Intrathecal clonidine prevented the hyperalgesia associated with opiate withdrawal but did not affect the occurrence of the majority of behavioral signs (e.g., piloerection, irritability) associated with morphine withdrawal. Intrathecal clonidine prevented the naloxone-induced increase in blood pressure during withdrawal and in animals not treated with morphine-produced hypotension. Thus, intrathecal clonidine is analgesic, and part of the antiwithdrawal action of clonidine may be exerted at the spinal level.

Analgesics↗
PubMed1985

Continuous intravenous infusion of phencyclidine in unrestrained rats results in the rapid induction of tolerance and physical dependence.

The continuous infusion of 45 mg/kg/24 hr of phencyclidine (PCP) into the jugular vein of unrestrained rats induced tolerance to PCP-induced impairment of forced motor activity and physical dependence in 3.5 and 7 days, respectively. In drug-naive rats, an i.v. 2-mg/kg PCP test dose abolished rotarod performance for more than 20 min which returned to pretreatment values at 40 min. Eight hours after the termination of 3.5 days of infusion, rotarod performance of PCP-infused rats was significantly less impaired by the PCP test dose at 20 min than that of saline-infused controls. After infusion of PCP for 7 days, the duration of performance abolition produced by the PCP test dose (given 8 hr after the termination of infusion) was shortened further with performance significantly better than that of saline-infused controls at both 10 and 20 min. The results showed a greater than 2-fold tolerance development to this PCP effect and suggest the observed tolerance to be mainly functional in nature. Abrupt withdrawal of PCP after infusion for 7 days resulted in an abstinence syndrome with the following signs: piloerection, increased susceptibility to audiogenic seizures, transient weight loss and reductions in exploratory activity and rotarod performance. The first withdrawal signs were noted 4 hr after the termination of infusion. At 24 hr of abstinence, most of the withdrawal signs had subsided. The reduced rotarod performance, associated with withdrawal, could be reversed by a single i.v. dose of 2 mg/kg of PCP. The reversibility of this sign supports the interpretation of impaired rotarod performance after withdrawal as being an abstinence sign and adds to the experimental evidence that physical dependence on PCP is inducible within 7 days in rats.

Animals↗