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  • 1
    Electronic Resource
    Electronic Resource
    Functional behavioral homology between rat 5-HT1B and guinea pig 5-HT1D receptors in the modulation of prepulse inhibition of startle (1996)
    Springer
    Psychopharmacology 125 (1996), S. 231-237 
    Details
    ISSN: 1432-2072
    Keywords: 5-HT1B ; 5-HT1D ; Guinea pig ; Rat ; Locomotor activity ; Prepulse inhibition ; Startle ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The serotonin (5-HT) 1B receptor in rats and mice appears to be homologous to the 5-HT1D receptor found in other mammals, such as guinea pigs and humans. The present series of experiments explored the functional similarity between the rat 5-HT1B receptor and the guinea pig 5-HT1D receptor on two behavioral measures known to be influenced by 5-HT1B receptor manipulations in rats: prepulse inhibition of the startle response (PPI) and locomotor activity. Because the 5-HT1B agonist RU 24969 disrupts PPI and stimulates locomotor behavior in rats, it was predicted that the 5-HT1D agonist, SDZ 219–964, would demonstrate a similar behavioral profile in guinea pigs. In support of this hypothesis, SDZ 219–964 was found to disrupt PPI dose-dependently (1.0 and 2.0 mg/kg) without significantly affecting startle amplitude and to increase locomotor activity (0.5–2.0 mg/kg) in guinea pigs. In guinea pigs, RU 24969 failed to affect PPI, although it did increase locomotor activity, indicating that RU 24969 may have activity at the 5-HT1D receptor. As expected, RU 24969 in rats disrupted PPI (2.5 and 5.0 mg/kg) and significantly increased locomotor activity (1.25–5.0 mg/kg). In rats, however, SDZ 219–964 had generalized, stimulatory effects on startle reactivity, without independent effects on PPI or locomotor activity. The spatial patterns of locomotion exhibited by guinea pigs treated with SDZ 219–964 versus those of rats treated with RU 24969 demonstrate important qualitative differences in structure, indicating that the neural substrates subserving these effects may be different. It is concluded that a functional similarity exists between 5-HT1D and 5-HT1B receptors with regard to the modulation of sensorimotor inhibition and, to a lesser extent, locomotor activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02247333
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Lack of sensitization to the effects of d-amphetamine and apomorphine on sensorimotor gating in rats (1998)
    Springer
    Psychopharmacology 135 (1998), S. 296-304 
    Details
    ISSN: 1432-2072
    Keywords: Key words Prepulse inhibition ; Sensorimotor gating ; Sensitization ; Locomotor activity ; Amphetamine ; Apomorphine ; Schizophrenia ; Startle ; Dopamine ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This study assessed whether repeated injections of d-amphetamine or apomorphine could induce sensitization to the disruptive effects of these psychomotor stimulants on sensorimotor gating in rats. In the first experiment, rats were given six pre-exposures to either 2.0 mg/kg d-amphetamine or saline before being tested for the effects of d-amphetamine (0.0, 0.5, 1.0, 2.0 or 4.0 mg/kg, IP) on prepulse inhibition of acoustic startle (PPI) and locomotor activity. The tests for PPI confirmed that sensorimotor gating could be disrupted by a high dose of d-amphetamine (4.0 mg/kg). However, comparison of the dose-response curves for the drug and saline pre-exposed groups did not reveal evidence for sensitization to this d-amphetamine effect in drug-pre-exposed rats, despite indications that sensitization had developed to the locomotor stimulant effects of d-amphetamine. A similar pattern of results was obtained in a second experiment that examined the effects of apomorphine (0.0, 0.1, 0.2, 0.4 and 0.8 mg/kg, SC) on PPI and locomotion in rats pre-exposed to 2.0 mg/kg of this drug or its vehicle. These findings demonstrate that treatments which induce sensitization to the behavioral activating effects of psychomotor stimulants do not necessarily produce sensitization to the disruptive effects of stimulants on sensorimotor gating. The implications of these results for hypotheses linking sensitization-like processes to the etiology of schizophrenia are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050513
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  • 3
    Electronic Resource
    Electronic Resource
    Opposite effects of 3,4-methylenedioxymethamphetamine (MDMA) on sensorimotor gating in rats versus healthy humans (1999)
    Springer
    Psychopharmacology 143 (1999), S. 365-372 
    Details
    ISSN: 1432-2072
    Keywords: Key words MDMA (3 ; 4-methylenedioxymethamphetamine) ; Serotonin ; Psychopathology ; Human ; Rat ; Prepulse inhibition ; Habituation ; Schizophrenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rationale: Prepulse inhibition of acoustic startle refers to the reduction in the startle response when the startling stimulus is preceded by a weak prepulse stimulus. This phenomenon provides an operational measure of sensorimotor gating that has been found to be reduced in patients with schizophrenia and rats treated with serotonin agonists or serotonin releasers. Objective: In this study, we compared the effects of a serotonin releaser, MDMA, on prepulse inhibition in laboratory rats and healthy human volunteers. In particular, we investigated whether MDMA disrupts PPI in humans as observed in animal studies. Methods: Rats were tested after placebo and MDMA in a counterbalanced order at an interval of 1 week, with separate groups of rats being used for each dose of MDMA (1.7, 5.4 and 17.0 mg/kg). On each test day, rats were first tested after no injections and retested 2 h later, 10 min after a subcutaneous injection of placebo or MDMA. For the human study, a placebo-controlled within-subject design and double-blind procedures were used. Subjects were examined twice at a 2 to 4 week interval after either placebo or drug administration (order being counterbalanced). On each test day, subjects underwent baseline testing including psychological and PPI measures. Ninety minutes later, subjects received placebo or MDMA (1.7 mg/kg PO) and were retested after 75 min during the peak of behavioral effects of MDMA. Results: As expected, MDMA decreased prepulse inhibition in a dose-related fashion in rats. In contrast, a typical recreational dose of MDMA (1.7 mg/kg, orally) increased prepulse inhibition in subjects experiencing robust psychological effects. Conclusions: This surprising disparity between the effects of the drug in rats and humans may reflect a species-specific difference in the mechanism of action of MDMA or in the behavioral expression of a similar pharmacological effect, or both.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050960
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Corticotropin-releasing factor potentiates acoustic startle in rats: Blockade by chlordiazepoxide (1986)
    Springer
    Psychopharmacology 88 (1986), S. 147-152 
    Details
    ISSN: 1432-2072
    Keywords: Corticotropin-releasing factor ; Startle ; Chlordiazepoxide ; Anxiety ; Strychnine ; Amphetamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A series of experiments was performed to investigate the effects of corticotropin-releasing factor (CRF) on the amplitude of the acoustic startle response (ASR) in rats. Intracerebroventricular (ICV) administration of 1 μg rat CRF significantly potentiated acoustic startle amplitude; these effects were reversed in a dose-dependent manner by pretreatment with the benzodiazepine chlordiazepoxide (CDP). Doses of CDP that anatgonized CRF-potentiated ASR did not lower startle baseline or antagonize amphetamine-or strychnine-potentiated ASR. These results suggest that CRF has “anxiogenic” properties and may serve as a neuroendocrine modulator of stress-enhanced behaviors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00652231
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    Paper (German National Licenses)
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