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  • Fear-potentiated startle response  (2)
  • 5-HT1D receptor  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Reduction of guinea pig pup isolation calls by anxiolytic and antidepressant drugs (1996)
    Springer
    Psychopharmacology 128 (1996), S. 31-38 
    Details
    ISSN: 1432-2072
    Keywords: Key words Distress vocalizations ; Guinea pig pup ; Anxiolytics ; Antidepressants ; Benzodiazepines ; 5-HT1A receptor ligands ; 5-HT uptake inhibitors ; NA uptake inhibitor ; 5-CT ; 5-HT1D receptor ; Alcohol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Guinea pigs possess central 5-HT1D receptors similar to humans but different from rats and mice. In order to study the role of this receptor on animal behaviour, it may be of interest to develop a paradigm measuring affective states in the guinea pig. Therefore we assessed the effects of a variety of psychotropic drugs on guinea pig pup isolation calls. Anxiolytic compounds such as the benzodiazepine receptor agonists diazepam and alprazolam, the full 5-HT1A receptor agonists 8-OH-DPAT and flesinoxan, and alcohol reduced isolation calling by the guinea pig pup. Moreover, mixed antidepressant/anxiolytic compounds like the 5-HT uptake inhibitors fluvoxamine and clomipramine or the MAO-inhibitor clorgyline as well as the antidepressant NA uptake inhibitors desipramine and maprotiline suppressed vocalizations. The 5-HT1D/1A receptor agonist 5-CT was also very effective in reducing separation calls. Remarkably, the partial 5-HT1A receptor agonists buspirone and BMY 7378 did not affect calling. The neuroleptic haloperidol, the psychostimulant d-amphetamine, the putative anxiogenics DMCM and m-CPP and the putative anxiolytics ondansetron and CI-988 had no effect on isolation calls of guinea pig pups. We propose this paradigm could be helpful to assess behavioural effects of anxiolytic and antidepressant drugs in a species different from rat or mouse, and in which the effects of 5-HT1D receptor ligands may possibly be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050106
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The effects of 5-HT1A receptor agonists, 5-HT1A receptor antagonists and their interaction on the fear-potentiated startle response (1998)
    Springer
    Psychopharmacology 139 (1998), S. 383-390 
    Details
    ISSN: 1432-2072
    Keywords: Key words Anxiety ; Fear-potentiated startle response ; 8-OH-DPAT ; Flesinoxan ; WAY 100 ; 635 ; (±)-Pindolol ; DU 125 ; 530 ; Lower lip retraction ; 5-HT1A receptor agonist ; 5-HT1A receptor antagonist ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study investigated whether the anxiolytic effect of 5-HT1A receptor agonists on the fear-potentiated startle response could be antagonized by 5-HT1A receptor antagonists. Therefore, control and fear-potentiated startle amplitudes were measured after co-administration of vehicle, flesinoxan (10 mg/kg PO) or 8-OH-DPAT (0.3 mg/kg SC) and DU 125,530 (0, 1, 3 and 10 mg/kg SC), (±)-pindolol (0, 3, 10 and 30 mg/kg SC) or WAY 100,635 (0, 0.1, 0.3 and 1 mg/kg SC). Unexpectedly, the three antagonists themselves as measured in the vehicle-pretreatment groups dose-dependently decreased startle potentiation. Further, DU 125,530 and WAY 100,635 were able to reverse the attenuating effect of 8-OH-DPAT, while no antagonism of the flesinoxan effect on startle potentiation was found. In contrast, both the flesinoxan- and 8-OH-DPAT-induced lower lip retraction were antagonized by DU 125,530 and WAY 100,635, but not by (±)-pindolol. The findings of the present study suggest that drugs acting on 5-HT1A receptors differentially affect lower lip retraction and startle potentiation probably mediated by different neuronal populations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050729
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Fear-potentiated startle response is remarkably similar in two laboratories (1996)
    Springer
    Psychopharmacology 126 (1996), S. 104-109 
    Details
    ISSN: 1432-2072
    Keywords: Anxiety ; Fear-potentiated startle response ; Predictive validity ; Reliability ; Oxazepam ; Flesinoxan ; Fluvoxamine ; Strychnine-potentiated startle response
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The fear-potentiated startle response paradigm is used to investigate anxiolytic properties of drugs. The first objective of the present study was to further investigate the predictive validity of this paradigm. The anxiolytics chlordiazepoxide (2.5–10 mg/kg IP) and oxazepam (1–10 mg/kg PO) and the putative anxiolytic flesinoxan (1–10 mg/kg PO) decreased startle potentiation dose-dependently, indicating an anxiolytic effect. The antidepressant fluvoxamine (5–20 mg/kg PO) did not affect startle potentiation. Ideally, anxiolytic drugs attenuate startle potentiation without affecting control startle levels, although some studies report altered control startle amplitudes. The second objective was to investigate whether different effects on control startle amplitudes are related to different startle devices. Therefore, the drugs were tested in two laboratories. Results showed no significant differences between laboratories, indicating that equipment is not a critical factor in the drug-induced alteration of control startle levels. In an additional experiment, it was shown that flesinoxan (10 mg/kg PO) did not affect strychnine-induced startle potentiation, supporting the idea that the attenuating effect of flesinoxan on the fear-potentiated startle response is due to its anxiolytic properties. Thus, the fear-potentiated startle response paradigm appears a valid and reliable model for anxiolytic properties of drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246344
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    Paper (German National Licenses)
    Fulltext
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