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Hakan Kayir

Publications and source records attributed to Hakan Kayir.

18 recordsLinked to original sources

Effects of tianeptine on onset time of pentylenetetrazole-induced seizures in mice: possible role of adenosine A1 receptors.

Depression is a common psychiatric problem in epileptic patients. Thus, it is important that an antidepressant agent has anticonvulsant activity. This study was organized to investigate the effects of tianeptine, an atypical antidepressant, on pentylenetetrazole (PTZ)-induced seizure in mice. A possible contribution of adenosine receptors was also evaluated. Adult male Swiss-Webster mice (25-35 g) were subjects. PTZ (80 mg/kg, i.p.) was injected to mice 30 min after tianeptine (2.5-80 mg/kg, i.p.) or saline administration. The onset times of 'first myoclonic jerk' (FMJ) and 'generalized clonic seizures' (GCS) were recorded. Duration of 600 s was taken as a cutoff time in calculation of the onset time of the seizures. To evaluate the contribution of adenosine receptors in the effect of tianeptine, a nonspecific adenosine receptor antagonist caffeine, a specific A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a specific A2A receptor antagonist 8-(3-chlorostyryl) caffeine (CSC) or their vehicles were administered to the mice 15 min before tianeptine (80 mg/kg) or saline treatments. Tianeptine (40 and 80 mg/kg) pretreatment significantly delayed the onset time of FMJ and GCS. Caffeine (10-60 mg/kg, i.p.) dose-dependently blocked the retarding effect of tianeptine (80 mg/kg) on the onset times of FMJ and GCS. DPCPX (20 mg/kg) but not CSC (1-8 mg/kg) blocked the effect of tianeptine (80 mg/kg) on FMJ. Our results suggest that tianeptine delayed the onset time of PTZ-induced seizures via adenosine A1 receptors in mice. Thus, this drug may be a useful choice for epileptic patients with depression.

Adenosine A1 Receptor Agonists↗

Effects of escitalopram on ethanol withdrawal syndrome in rats.

The present study was designed to investigate the effects of escitalopram, a selective serotonin reuptake inhibitor, on ethanol withdrawal syndrome in rats. Adult male Wistar rats (266-278 g) were subjects. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair fed with an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Escitalopram (2.5, 5 and 10 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After the second and sixth hours of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes, tremors and audiogenic seizures were recorded or rated. A second series of injections was given 30 min before sixth hour of withdrawal test. Effects of escitalopram on the locomotor activities of the naïve (no ethanol-dependent) rats were also evaluated. Escitalopram (5 mg/kg) reduced the increased stereotyped behaviors at the sixth hour of ethanol withdrawal. It inhibited tremors at the second hour of ethanol withdrawal at doses of 5 and 10 mg/kg. Escitalopram (2.5 and 5 mg/kg) also produced some significant attenuations in the incidence of wet dog shakes at the second and sixth hours of the observation period. It was found ineffective on locomotor hyperactivity, agitation and audiogenic seizures. Escitalopram (2.5 and 5 mg/kg) did not cause any significant effect on locomotor activities of the naïve rats. Our results suggest that acute escitalopram treatment has some limited beneficial effects on ethanol withdrawal syndrome in rats.

Alcohol Drinking↗

Acute and chronic tianeptine treatments attenuate ethanol withdrawal syndrome in rats.

Effects of acute and chronic tianeptine treatments on ethanol withdrawal syndrome were investigated in rats. Ethanol (7.2% v/v) was given to adult male Wistar rats by a liquid diet for 30 days. Acute or chronic (twice daily) tianeptine (5, 10 and 20 mg/kg) and saline were administered to rats intraperitoneally. Acute and last chronic tianeptine injections and saline were done 30 min before ethanol withdrawal testing. After 2nd, 4th and 6th hours of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs which included locomotor hyperactivity, agitation, tremor, wet dog shakes, stereotyped behavior and audiogenic seizures were recorded or rated. Locomotor activity in naive (no ethanol-dependent rats) was also tested after acute tianeptine treatments. Acute but not chronic tianeptine treatment attenuated locomotor hyperactivity and agitation in ethanol-dependent rats. Both acute and chronic tianeptine treatment produced some significant inhibitory effects on tremor, wet dog shakes, stereotyped behaviors and audiogenic seizures during the ethanol withdrawal. Our results suggest that acute or chronic tianeptine treatment attenuates ethanol withdrawal syndrome in ethanol-dependent rats and this drug may be useful for treatment of ethanol-type dependence.

Animals↗

The prevention of myocardial ultrastructural changes by perindopril, atenolol and amlodipine in chronic alcohol administered rats.

The effects of perindopril, an angiotensin converting enzyme inhibitor, atenolol, a beta adrenergic receptor blocker and amlodipine, a calcium channel blocker were investigated in chronic alcohol administered rats. Adult male Wistar rats (240-320 g) were used in the present study. Alcohol was given to rats by a modified liquid diet for 21 days. Perindopril (2.5 and 5 mgkg(-1)), atenolol (5 and 10 mg kg(-1)) and amlodipine (5 and 10 mg kg(-1)) were injected to rats in different groups intraperitoneally for 21 days. Control rats were pair fed by an isocaloric liquid diet containing sucrose as a caloric substitute for alcohol. Saline was injected to control rats for 21 days. Rats were anesthetized with ether. Their hearts were removed and 1 mm3 samples from left ventricles were fixed. Five fields per heart were examined and photographed with transmission electron microscope. Blood alcohol levels were also measured spectrophotometrically. Daily alcohol consumption of the rats was in a range of 12.09-15.5 g kg(-1). Blood alcohol concentrations were found as 145.63 mg dl(-1) at 21st day of alcohol consumption. Chronic alcohol consumption caused some marked myocardial injuries. Perindopril and atenolol but not amlodipine produced some significant beneficial effects on alcohol-induced myocardial damages. Our results imply that perindopril and atenolol but not amlodipine have protective effects on heavy chronic alcohol consumption-induced myocardial injury in rats.

Adrenergic beta-Antagonists↗

Discriminative stimulus properties of tianeptine.

RATIONALE: In view of the difficulties in using antidepressant agents as training drugs in drug discrimination research, it was reasoned that tianeptine, because of its short duration of action and its lack of toxicity associated with long-term administration, would be well-suited to establish a discriminative stimulus cue in rats and, hence, a valuable tool in the investigation of the neural basis of depression. OBJECTIVES: A drug discrimination procedure was used to determine whether tianeptine was associated with a specific discriminative stimulus effect, and substitution tests were conducted to determine whether this effect was mediated by serotonergic mechanisms. METHOD: Rats were trained to discriminate 10 mg/kg tianeptine from saline and were tested with fluoxetine, a selective serotonin (5-HT) reuptake inhibitor; venlafaxine, a 5-HT/noradrenaline reuptake inhibitor; 8-hydroxy-(2-di-n-propylamino)tetralin (8-OH-DPAT), a selective 5-HT1A agonist; and caffeine, a nonselective antagonist of adenosine receptors. RESULTS: Tianeptine induced a specific, robust, and sustained discriminative stimulus in rats. Fluoxetine and 8-OH-DPAT partially substituted for tianeptine by producing >50% of tianeptine-appropriate lever responding. In contrast, venlafaxine and caffeine induced responding on a saline-associated lever. CONCLUSION: The discriminative stimulus effect of tianeptine is mediated by serotonergic mechanisms, but what is surprising is that this mechanism seems to be, at least partially, enhanced by serotonergic transmission.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Nicotine antagonizes caffeine- but not pentylenetetrazole-induced anxiogenic effect in mice.

RATIONALE: Nicotine and caffeine are widely consumed licit psychoactive drugs worldwide. Epidemiological studies showed that they were generally used concurrently. Although some studies in experimental animals indicate clear pharmacological interactions between them, no studies have shown a specific interaction on anxiety responses. OBJECTIVES: The present study investigates the effects of nicotine on anxiety induced by caffeine and another anxiogenic drug, pentylenetetrazole, in mice. The elevated plus-maze (EPM) test was used to evaluate the effects of drugs on anxiety. METHODS: Adult male Swiss Webster mice (25-32 g) were given nicotine (0.05-0.25 mg/kg s.c.) or saline 10 min before caffeine (70 mg/kg i.p.) or pentylenetetrazole (15 and 30 mg/kg i.p.) injections. After 15 min, mice were evaluated for their open- and closed-arm time and entries on the EPM for a 10-min session. Locomotor activity was recorded for individual groups by using the same treatment protocol with the EPM test. RESULTS: Nicotine (0.05-0.25 mg/kg) itself did not produce any significant effect in the EPM test, whereas caffeine (70 mg/kg) and pentylenetetrazole (30 mg/kg) produced an anxiogenic effect, apparent with decreases in open-arm time and entry. Nicotine (0.25 mg/kg) pretreatment blocked the caffeine- but not pentylenetetrazole-induced anxiety. Administration of each drug and their combinations did not produce any effect on locomotor activity. CONCLUSIONS: Our results suggest that the antagonistic effect of nicotine on caffeine-induced anxiety is specific to caffeine, instead of a non-specific anxiolytic effect. Thus, it may extend the current findings on the interaction between nicotine and caffeine.

Animals↗

Investigation of the effects of tianeptine and fluoxetine on pentylenetetrazole-induced seizures in rats.

The effects of tianeptine and fluoxetine on pentylenetetrazole (PTZ)-induced seizures in rats were investigated. Female Wistar rats (172-278 g) were used in the study. Tianeptine (1.25, 2.5, 5, 10 and 20 mg/kg) and fluoxetine (2.5, 5, 10 and 20 mg/kg) or saline were injected to rats intraperitoneally 30 min before PTZ (50 mg/kg) injections. Immediately after PTZ administrations, latency and intensity of the PTZ-induced seizures was recorded and scored, respectively. Fluoxetine (2.5-20 mg/kg) did not produce any significant difference in latency and intensity of the PTZ-induced seizures. Although tianeptine (1.25-20 mg/kg) also did not affect the latency time, it produced significant attenuations in the intensity of the seizures. Tianeptine did not cause any significant change in the locomotor activity of the rats. The results of this preliminary study suggest that tianeptine but not fluoxetine has some inhibitory effects on PTZ-induced seizures in rats.

Animals↗

Chronic heavy ethanol consumption is associated with decreased platelet aggregation in rats.

Although moderate alcohol consumption seems to be protective against atherosclerosis, coronary artery disease rate increases with its higher doses. Platelet aggregation is an important process which contributes to the atherosclerosis. The aim of this study was to determine whether heavy ethanol consumption stimulates or inhibits platelet aggregation. Fourteen adult male Wistar rats were used. Ethanol (7.2%, v/v) in a modified liquid diet was given to eight rats for 21 days, which mimicked characteristics similar to human chronic alcoholism. Six rats constituted the control group. Adenosine diphophate (ADP) and collagen-induced platelet aggregation was measured in whole blood. We found reduced ADP-induced mean maximal aggregation in the alcoholic rat group compared to the control group at dose of 5 microM (p < 0.005). We also found decreased platelet aggregation responses to collagen in the alcoholic group (p < 0.006 for 2 microg/ml collagen, and p < 0.05 for 5 microg/ml collagen). In conclusion, chronic heavy ethanol consumption results in the decreased platelet aggregation in a rat model of alcoholism. Therefore, increased mortality from coronary artery disease in chronic alcoholism may be explained by other factors such as dietary imbalances and coexisting conditions, which include hypertension and depression.

Adenosine Diphosphate↗

The effects of chronic ethanol consumption and withdrawal on passive avoidance task and serum cholinesterase level in rats.

The effects of chronic ethanol consumption and ethanol withdrawal on serum cholinesterase (ChE) activity and passive avoidance task in rats were investigated. Ethanol was administered to rats by a modified liquid diet with 4.8% (v/v) ethanol for 3 days followed by 25 days on a liquid diet in which the ethanol concentration was increased to 7.2%. Control rats were pair fed with an isocaloric liquid diet not containing ethanol. ChE activity and blood ethanol concentration were measured at the end of the 4.8% ethanol consumption and after 25 days of ethanol (7.2%) feeding and, just before and 24th and 72nd h of ethanol withdrawal period. Passive avoidance acquisition was evaluated for 150 s (cut-off time) in three individual groups of ethanol-administered, ethanol withdrawn (24th and 72nd h of withdrawal) and control rats. Locomotor activity of the rats was also measured and evaluated. The daily ethanol consumption of the rats ranged from 11.5 to 14.9 g/kg. ChE activities of the ethanol feeding rats were significantly increased as compared to control rats at the 3rd (4.8% ethanol) and 25th days of chronic ethanol (7.2%) consumption and 24th h of ethanol withdrawal. It returned to control values at the 72nd h of the withdrawal. Blood ethanol levels were measured as 200 and 2.2 mg/dl at just before ethanol withdrawal and 24th h of ethanol withdrawal, respectively. Both chronic ethanol consumption and late period of ethanol withdrawal produced some significant decreases in passive avoidance latency of the rats. Our results suggest that chronic ethanol consumption and late period of ethanol withdrawal may be related to impairment of passive avoidance task in rats. In addition, serum ChE levels do not seem to be involved in impairment of cognitive functions in ethanol dependent-rats.

Alcohol Drinking↗

Evidence for the role of nitric oxide in nicotine-induced locomotor sensitization in mice.

RATIONALE: Nitric oxide (NO) is implicated in both acute effects of addictive drugs and development of dependence to them. We investigated the role of NO in nicotine-induced locomotor sensitization. OBJECTIVES: The effects of Nomega-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, and a combination of a NO precursor L-arginine and L-NAME on nicotine-induced locomotor sensitization were investigated in Swiss Webster mice. METHODS: Sensitization to psychomotor stimulating effect of nicotine was rendered by seven injections of nicotine (1 mg/kg) on every other day. To investigate their effect on the development of sensitization to nicotine, L-NAME (15-60 mg/kg) and L-arginine (1 g/kg) were given before nicotine administration during the first seven sessions. To investigate the effect of these compounds on the expression of nicotine sensitization, after a 4-day drug-free period another group of mice received a challenge injection of nicotine on day 18. RESULTS: Nicotine (1 mg/kg) produced a robust locomotor sensitization in mice. The doses of 30 mg/kg and 60 mg/kg of L-NAME blocked the development of sensitization to nicotine; and, L-arginine (1 g/kg) pretreatment reversed this effect of L-NAME. Likewise, the doses of 30 mg/kg and 60 mg/kg of L-NAME inhibited the expression of sensitization to nicotine on day 18; and, L-arginine (1 g/kg) pretreatment reversed this inhibitory effect of L-NAME. CONCLUSIONS: Our results suggest that NO is implicated in the development and expression of nicotine-induced locomotor sensitization in mice.

Animals↗

CPP and amlodipine alter the decrease in basal acetylcholine and choline release by audiogenic stimulus in hippocampus of ethanol-withdrawn rats in vivo.

Effects of N-methyl-D-aspartate (NMDA) receptor and Ca2+ channel antagonists on extracellular acetylcholine and choline release in the hippocampus of ethanol-withdrawn rats were investigated by in vivo microdialysis. Ethanol was administered to Wistar rats in a liquid diet for 28 days. Basal acetylcholine and choline levels significantly increased at the 24th hour of ethanol withdrawal syndrome (EWS). Either an NMDA receptor antagonist (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) or a calcium channel antagonist amlodipine was administered, and 15 min later, an audiogenic stimulus (100 dB, 1 min) was applied to rats. While audiogenic stimulus increased acetylcholine and had no effect on choline release in control rats, it decreased acetylcholine and increased choline release in ethanol-withdrawn rats. CPP (15 mg/kg) and amlodipine (20 mg/kg) reversed the decrement in acetylcholine and increment in choline release in EW rats. Their effects on acetylcholine and choline release were not different from saline in control rats. Therefore, our findings suggest that, (a) because of adaptive changes in EWS, decrease of the acetylcholine release following audiogenic stimulus may play a role in the triggering of seizures, (b) hippocampal glutamatergic pathway may play a role in the audiogenic stimulus induced decrement of acetylcholine release in EWS, (c) inhibition of this pathway by NMDA receptor and calcium channel antagonists may prevent triggering of the seizures.

Acetylcholine↗

Effects of chronic ethanol administration and ethanol withdrawal on cyclic guanosine 3',5'-monophosphate (cGMP) levels in the rat brain.

The main objective of the present study is to investigate the possible effects of chronic ethanol consumption and ethanol withdrawal on cyclic guanosine 3', 5'-monophosphate (cGMP) levels in cerebral cortex, striatum, hippocampus and hypothalamus of rat brain. Ethanol was given to female Wistar rats (225-270g) by a liquid diet for 21 days. cGMP levels were measured in respective brain regions using an EIA kit at 7th, 14th and 21st days of ethanol ingestion and at 6th and 24th h of ethanol withdrawal. cGMP levels in cortex, striatum and hippocampus but not hypothalamus were found significantly increased at 14th and 21st days of ethanol consumption. The most prominent increase was observed in striatal tissues (approximately 350%). cGMP levels of striatum and hippocampus were still remaining significantly high at 6th h of ethanol withdrawal. Blood ethanol levels were found as 115.60, 50.0 and 7.0mg/dl just before and after 6 and 24h of ethanol withdrawal, respectively and audiogenic seizures also occurred at 6th h of ethanol withdrawal with an incidence of 75% in individual parallel groups. Our results suggest that changes of cGMP levels in cerebral cortex, striatum and hippocampus might participate in the mechanism of ethanol dependence and withdrawal in rats.

Animals↗

Effects of venlafaxine on ethanol withdrawal syndrome in rats.

The present study was designed to investigate the effects of venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRI), on ethanol withdrawal syndrome in rats. Adult male Wistar rats (187-319 g) were used for the study. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair-fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Venlafaxine (5, 10, 20 and 40 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After the 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behaviour and wet dog shakes were recorded or rated. A second series of injections was given at the 6th hour after the first one, and rats were then tested for audiogenic seizures. Venlafaxine produced some inhibitory effects on locomotor hyperactivity, stereotypic behaviours and wet dog shakes. However, a two-way anova of the data did not indicate any significant effect. It reduced the incidence of the audiogenic seizures at the 6th hour of ethanol withdrawal. Venlafaxine (20 mg/kg) also prolonged the latency of the seizures significantly. Our results suggest that acute venlafaxine treatment has limited beneficial effects on ethanol withdrawal syndrome in rats.

Analysis of Variance↗

Evidence for the role of nitric oxide in caffeine-induced locomotor activity in mice.

RATIONALE: Nitric oxide (NO) is implicated in the acute locomotor activating effects of some addictive drugs such as amphetamine and cocaine, but has not been investigated in the case of caffeine. OBJECTIVES: We investigated the effects of a nitric oxide synthase (NOS) inhibitor Nomega-Nitro- l-arginine methyl ester ( l-NAME) and a combination of l-arginine, a NO precursor, and l-NAME on caffeine induced locomotor activity in Swiss Webster mice. METHODS: Locomotor activity was recorded for 30 min immediately following caffeine (0.25-128 mg/kg) or saline administration. In a further study, l-NAME (15 and 30 mg/kg) was administered to another group of mice 30 min before caffeine (1 and 16 mg/kg) injections. Finally, l-arginine (1000 mg/kg), a nitric oxide precursor, was administered 20 min before the l-NAME (15 and 30 mg/kg) treatments and locomotor activities were again recorded immediately after caffeine (1 and 16 mg/kg) injections. RESULTS: Caffeine (0.5-16 mg/kg) significantly increased locomotor activity, while l-NAME (30 mg/kg) blocked caffeine (1 and 16 mg/kg)-induced locomotor activity. The low dose of l-NAME blocked only caffeine (1 mg/kg)-induced locomotor activity. l-Arginine reversed the inhibitory effects of l-NAME on caffeine-induced locomotor activity. l-NAME and l-arginine had no effect on the locomotor activity of the mice when given by themselves. CONCLUSIONS: The results suggest that caffeine-induced locomotor activity might be modulated by NO in mice.

Animals↗

Effects of harman and harmine on naloxone-precipitated withdrawal syndrome in morphine-dependent rats.

The effects of the beta-carbolines, harman and harmine, on naloxone-precipitated withdrawal syndrome in morphine-dependent rats were investigated. Two morphine pellets containing 75 mg morphine base were implanted subcutaneously in the scapular area of adult male Wistar rats (200-250 g) under light ether anesthesia. Rats were then assigned to several groups (n = 12 for each group). Seventy-two hours after morphine implantation, harman (5 and 10 mg/kg), harmine (5 and 10 mg/kg) or saline was injected to rats intraperitoneally (ip). After 45 min, a morphine withdrawal syndrome was precipitated by naloxone (2 mg/kg, ip), and morphine withdrawal signs were observed and evaluated for 15 min. Harmine (5 and 10 mg/kg) attenuated significantly the intensity of all signs of morphine withdrawal except for jumping. While jumping behaviour appearing in morphine withdrawal was intensified by harman (5 and 10 mg/kg) treatment, harmine administration did not produce any significant change in the intensity of this sign. Harman attenuated significantly the intensity of wet dog shakes, writhing, defecation, tremor and ptosis. However, it produced no significant changes in the intensity of teeth chattering and diarrhea. Our results suggest that harman and harmine, beta-carbolines, have some beneficial effects on naloxone-precipitated morphine withdrawal syndrome in rats. Findings from the present study also indicated that harmine was more effective than harman on morphine abstinence syndrome.

Animals↗

Bromocriptine and quinpirole, but not 7-OH-DPAT or SKF 38393, potentiate the inhibitory effect of L-NAME on ethanol-induced locomotor activity in mice.

The effects of N(G)-nitro- l-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, SKF 38393, bromocriptine (BRM), quinpirole (QPR) and 7-hydroxy-2-dipropylaminotetralin (7-OH-DPAT), dopamine receptor agonists, and combinations of the dopamine agonists and L-NAME on ethanol-induced locomotor activity in adult male Swiss-Webster mice were investigated. The mice were given ethanol (0.5-2 g/kg), L-NAME (15-60 mg/kg), SKF 38393 (5-20 mg/kg), BRM (2.5 and 5 mg/kg), QPR (0.25 and 0.5 mg/kg), 7-OH-DPAT (0.5 and 1.0 mg/kg), a combination of l-arginine (1 g/kg) and L-NAME (60 mg/kg), combinations of SKF 38393, BRM, QPR or 7-OH-DPAT with L-NAME (60 mg/kg) or ethanol (0.5 g/kg) and saline or vehicle by i.p. injection. Triple combinations (dopaminergic agonist, 60 mg/kg L-NAME and 0.5 g/kg ethanol) were also given. Locomotor activity was measured for 30 min immediately following ethanol injections. Ethanol (0.5 g/kg) significantly increased locomotor activity. L-NAME, BRM, QPR and 7-OH-DPAT blocked the ethanol (0.5 g/kg)-induced locomotor hyperactivity dose dependently and at doses that did not affect locomotor activity in naive mice when administered alone. The inhibitory effects of L-NAME (60 mg/kg) were not prevented by pretreatment with l-arginine. BRM and QPR, but not 7-OH-DPAT, significantly and dose-dependently potentiated the inhibitory effect of L-NAME. Our results suggest that L-NAME inhibits ethanol-induced locomotor hyperactivity in mice by a mechanism not involving NO. The inhibitory effect of L-NAME may be related to the activation of presynaptic dopamine D(2) receptors rather than dopamine D(3) receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Investigation of a possible sensitization development to a challenge dose of ethanol after 2 weeks following the single injection in mice.

In the present study, a possible sensitization development to a single injection of ethanol in mice was investigated. Subjects were adult male Swiss-Webster mice. Ethanol (0.5-4 g/kg) or saline (control) was intraperitoneally injected to mice. Horizontal, vertical and ambulatory locomotor activities were recorded for 30 min immediately following the ethanol or saline injections. After 2 weeks, each group of mice was randomly assigned to two groups. A single challenge dose of ethanol (1 g/kg) was administered to the first group, and saline was injected to the second group. Then, the locomotor activities were recorded for 30 min. In the first experiment, ethanol significantly increased the horizontal and ambulatory activities of the mice at the doses of 0.5 and 1 g/kg, but not at 2 g/kg, while they were decreased at the dose of 4 g/kg. Ethanol (0.5 g/kg) also significantly increased the vertical activity. After 2 weeks, the challenge injection of ethanol (1 g/kg) produced some significant increases in the horizontal and ambulatory activities of the group pretreated with ethanol (2 g/kg). It did not cause any significant change on the locomotor activities of the other three groups treated with lower (stimulant) or higher (depressant) doses of ethanol. In addition, there was no significant difference between locomotor activities of the groups challenged with saline. However, a two-way ANOVA of the data on the challenge injections did not indicate any sensitization development to the effects of ethanol on locomotor activities of the mice. Our results suggest that a locomotor sensitization did not develop to a single injection of ethanol after 2 weeks following the first injection in mice.

Analysis of Variance↗

Effects of fluoxetine on ethanol withdrawal syndrome in rats.

The present study was designed to investigate the effects of fluoxetine, a selective serotonin reuptake inhibitor, on ethanol withdrawal syndrome in rats. Adult male Wistar rats (218-255 g) were subjects. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Fluoxetine (2.5, 5 and 10 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes and tremor were recorded or rated. A second series of injections was given at 6 h after the first one, and subjects were then tested for audiogenic seizures. Fluoxetine produced some dose-dependent and significant inhibitory effects on all the signs of ethanol withdrawal during ethanol withdrawal period. Our results suggest that acute fluoxetine treatment has some beneficial effects on ethanol withdrawal in rats. Thus, this drug may be useful for treatment of ethanol withdrawal syndrome.

Administration, Oral↗