The Ca2+ channel blockade changes the behavioral and biochemical effects of immobilization stress. (1/314)

We investigated how the effects of chronic immobilization stress in rats are modified by Ca2+ channel blockade preceding restraint sessions. The application of nifedipine (5 mg/kg) shortly before each of seven daily 2 h restraint sessions prevented the development of sensitized response to amphetamine as well as the stress-induced elevation of the densities of L-type Ca2+ channel in the hippocampus and significantly reduced the elevation of the densities of [3H]nitrendipine binding sites in the cortex and D1 dopamine receptors in the limbic forebrain. Neither stress, nor nifedipine affected the density of alpha 1-adrenoceptors and D1 receptors in the cerebral cortex nor D2 dopamine receptors in the striatum. A single restraint session caused an elevation of blood corticosterone level that remained unaffected by nifedipine pretreatment, but the reduction of this response during the eighth session was significantly less expressed in nifedipine-treated rats. We conclude that L-type calcium channel blockade prevents development of several stress-induced adaptive responses.  (+info)

Effects of the 5-HT2C/2B antagonist SB 206553 on hyperactivity induced by cocaine. (2/314)

Serotonin (5-HT) appears to play a modulatory role in the behavioral effects of cocaine, although the impact of 5-HT2C receptors in this control has not been fully established. The aim of the present study was to establish whether acute pretreatment with the selective 5-HT2C/2B antagonist SB 206553 (1, 2, and 4 mg/kg i.p.) altered hyperactivity induced by cocaine (15 mg/kg, i.p.) using an open field activity system which recorded central, peripheral, and rearing activity. Pretreatment with 1 and 2 mg/kg of SB 206553 attenuated cocaine-induced central and peripheral activity, respectively; rearing was also attenuated by the latter dose. However, the 4-mg/kg dose of SB 206553 significantly enhanced the effects of cocaine on peripheral activity. Based upon the present observations and an interpretation of previous research to implicate 5-HT2C receptor control of the dopamine (DA) mesoaccumbens pathways in behavior, a thorough and systematic analysis of the role of 5-HT2C (and 5-HT2B) receptors in psychostimulant-induced behaviors is warranted.  (+info)

Absence of hyperactivity in lead-exposed developing rats. (3/314)

It has been reported that postnatal lead treatment produces hyperactivity in rodents. Using rats, we attempted to extend these findings. Locomotor activity of offspring of lead-intubated and pair-fed control mothers was measured at 24-27 days of age, and no significant differences in reactivity or basal activity were found. Observational scoring of the animals at 28-29 and 35-36 days of age indicated that active behaviors were slightly reduced in the lead-treated rats. The brain lead concentrations of experimental animals were slightly reduced in the lead-treated rats. The brain lead concentrations of experimental animals were significantly elevated over controls. Estimates of statistical power indicated that behavioral effects of the magnitude reported in the literature would likely have been detected. The present results indicate that low-level lead exposure may not reliably produce hyperactivity in rodents. A review of the literature suggests that other data provide little support for a recently proposed rodent model of hyperactivity in children.  (+info)

Pharmacological properties of some xanthone derivatives. (4/314)

A series of aminoalkanolic derivatives of xanthone were examined in some experimental models of epilepsia, i.e., pilocarpine, aminophylline and pentetrazole-induced seizures. A final objective of this research was to examine the action of these compounds on the central nervous system, namely on spontaneous locomotor activity, amphetamine-induced hyperactivity and narcotic sleep induced by hexobarbital, as well as their influence on the gamma-aminobutyric acid (GABA) level and glutamic acid decarboxylase (GAD) activity in mice brain. The most interesting were the pharmacological results of (R)-2-N-methylamino-1-butanol derivative of 7-chloro-2-methylxanthone [Id], which displayed protective activity against the seizures induced by maximum electroshock and pentetrazole induced seizures; moreover, this compound had a relatively low toxicity and did not exhibit a neurotoxic effect. The influence on the locomotor activity as well as on the amphetamine-induced locomotor hyperactivity in mice was also seen for Id. Compound Id did not decrease the GABA level in mice brain.  (+info)

The effects of the 5-hydroxytryptamine(1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin on spontaneous activity, cocaine-induced hyperactivity and behavioral sensitization: a microanalysis of locomotor activity. (5/314)

The influence of the 5-hydroxytryptamine(1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin (DPAT) on locomotor hyperactivity induced by the acute and chronic administration of cocaine was assessed. Horizontal activity was measured in the periphery and center of an open field test enclosure equipped with photobeams; vertical activity was also recorded. Peripheral hyperactivity induced by an acute administration of cocaine (10 or 20 mg/kg) was significantly enhanced by 0.2 mg/kg DPAT. In contrast, central and vertical activities were reduced in a dose-related manner by DPAT (0.1 and 0.2 mg/kg); DPAT also suppressed central (0.2 mg/kg) and vertical (0.1 and 0.2 mg/kg) activities when administered alone. Similar observations were made on day 1 of chronic treatment with DPAT (0, 0.1, or 0.2 mg/kg) injected 15 min before an injection of cocaine (0, 10, or 15 mg/kg) administered twice daily for 7 days. By day 7 of repeated DPAT treatment, sensitization of DPAT-evoked peripheral activity developed, which contrasted with tolerance to the central and vertical hypoactivity evoked by DPAT. Sensitization developed to the repeated treatment with 15 mg/kg cocaine but not 10 mg/kg cocaine. Interestingly, enhancements of all activity measures were observed between days 1 and 7 in rats cotreated with DPAT plus either dose of cocaine. This sensitization to DPAT plus cocaine was expressed on challenge with DPAT and cocaine but not with cocaine alone. The present study implies that the stimulation of 5-hydroxytryptamine(1A) receptors is capable of modulating the hyperactivity evoked by cocaine, possibly via modulation of the mesoaccumbens dopamine circuit thought to mediate the behavioral effects of cocaine.  (+info)

Transient neuromotor phenotype in transgenic spastic mice expressing low levels of glycine receptor beta-subunit: an animal model of startle disease. (6/314)

Startle disease or hereditary hyperekplexia has been shown to result from mutations in the alpha1-subunit gene of the inhibitory glycine receptor (GlyR). In hyperekplexia patients, neuromotor symptoms generally become apparent at birth, improve with age, and often disappear in adulthood. Loss-of-function mutations of GlyR alpha or beta-subunits in mice show rather severe neuromotor phenotypes. Here, we generated mutant mice with a transient neuromotor deficiency by introducing a GlyR beta transgene into the spastic mouse (spa/spa), a recessive mutant carrying a transposon insertion within the GlyR beta-subunit gene. In spa/spa TG456 mice, one of three strains generated with this construct, which expressed very low levels of GlyR beta transgene-dependent mRNA and protein, the spastic phenotype was found to depend upon the transgene copy number. Notably, mice carrying two copies of the transgene showed an age-dependent sensitivity to tremor induction, which peaked at approximately 3-4 weeks postnatally. This closely resembles the development of symptoms in human hyperekplexia patients, where motor coordination significantly improves after adolescence. The spa/spa TG456 line thus may serve as an animal model of human startle disease.  (+info)

Increased hyperkinesis in noninfarcted areas during short-term follow-up in patients with first anterior acute myocardial infarction treated by direct percutaneous transluminal coronary angioplasty. (7/314)

The time course and clinical significance of hyperkinetic wall motion (HWM) in a noninfarcted area in direct percutaneous transluminal coronary angioplasty (PTCA) has not been clearly demonstrated in patients with acute myocardial infarction (AMI). The objectives of this study were to examine the change in HWM during one-month follow-up after direct PTCA and determine its impact on the recovery of global left ventricular function. A total of 61 patients with first anteroseptal AMI and one vessel disease were evaluated. The paired left ventriculograms in the 30 degrees right anterior oblique view taken both at baseline and follow-up were analyzed by the centerline and area length methods. The severity of hypokinesis was expressed by mean regional wall motion (standard deviation/chord) in most hypocontractile 50% of chords respondable to left anterior descending coronary artery area and HWM by mean regional wall motion in most hypercontractile 50% of chords of noninfarcted area. HWM increased from 0.18 +/- 1.07 to 0.48 +/- 1.30 (p = 0.0608). The delta global ejection fraction (global ejection fraction at follow-up minus global ejection fraction at baseline) was correlated with both delta infarcted wall motion (infarcted wall motion at follow-up minus infarcted wall motion at baseline) and delta HWM (HWM at follow-up minus HWM at baseline) (r = 0.576, p < 0.0001, r= 0.383, p = 0.0036, respectively) during follow-up. Further, the delta global ejection fraction showed better correlation with delta (HWM + infarcted wall motion) [(HWM plus infarcted wall motion at follow-up) minus (HWM plus infarcted wall motion at baseline)] (r= 0.593, p < 0.0001). Direct PTCA resulted in the enhancement of HWVM, which contributed to the increase in the global ejection fraction with the recovery of infarcted wall motion.  (+info)

Latency to paroxetine-induced anxiolysis in the rat is reduced by co-administration of the 5-HT(1A) receptor antagonist WAY100635. (8/314)

We report here the use of rat high-light social interaction to model the temporal anxiolytic/antidepressant effects of SSRIs seen in the clinic. Compared to vehicle controls, 21, but not 14, days of paroxetine treatment (3 mg kg(-1), p.o., daily) produced a marked increase in rat social interaction (Vehicle=71.3+/-7.3 s; Paroxetine=116.7+/-14.7 s; P<0.01) with no concurrent effect on locomotor activity, consistent with anxiolysis. To assess whether concurrent 5-HT(1A) receptor blockade reduces the time to onset of anxiolysis seen with paroxetine alone (21 days), rats were implanted with osmotic minipumps to continuously infuse the 5-HT(1A) receptor antagonist WAY100635 (1 mg kg(-1) day(-1), s.c., 7 days) alone or in combination with paroxetine (3 mg kg(-1), p.o., daily, 7 days), prior to anxiety testing. Paroxetine (Veh/Par=61.9+/-7.9 s) or WAY100635 (WAY/Veh=71.6+/-4.7 s) alone, had no effect on social interaction time compared to vehicle treated controls (Veh/Veh=76.4+/-4.9 s), whilst coadministration of WAY100635 with paroxetine, produced a marked elevation in social interaction (WAY/Par=149.3+/-16.8 s; P<0.01) relative to all other groups with no concurrent change in locomotor activity. In contrast, acute administration of WAY100635 (0.03 mg kg(-1), s.c.) with paroxetine (3 mg kg(-1), p.o.) did not alter any behavioural measure, suggesting that the anxiolysis induced by the combination after 7 days is attributable to a CNS adaptive response. This data demonstrates that coadministration of a 5-HT(1A) receptor antagonist with paroxetine markedly reduces the latency to anxiolysis, in the rat. This study supports the use of the rat social interaction test to further delineate adaptive changes in the CNS responsible for the anxiolytic/antidepressant action of SSRIs seen in humans.  (+info)

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