Chlorpromazine, Reserpine and Meprobamate: Psychological Effects.

Starkweather, John A.

doi:10.1037/11259-034

Cited by 1 publication

(1 citation statement)

References 43 publications

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“…In rodents, reserpine causes hypoactivity (Williams and Pirch 1974), motor stereotypies (Neisewander et al 1991), akinesia (Dolphin et al 1976), lethargy (Sigg et al 1965) and anhedonia (Skalisz et al 2002), relevant to depression (Borison et al 1978; Lee et al 2012) and Parkinson’s disease (PD) (Duty and Jenner 2011). The drug also exerts conflicting action on clinical (Shamon and Perez 2009; Sarwer-Foner and Ogle 1956; Starkweather 1959) and animal anxiety, including no effects (Angrini et al 1998; Heslop and Curzon 1999), increased (Angrini et al 1998; Heslop and Curzon 1999; Haggendal and Lindqvist 1963; Ahlenius and Salmi 1994; LaBuda and Fuchs 2002) or reduced anxiety (Xu et al 1992) (also see tranquilizing effects is some fish species (Turner and Carl 1955; Cano 1959)).…”

Section: Introductionmentioning

confidence: 99%

Behavioral effects of bidirectional modulators of brain monoamines reserpine and d-amphetamine in zebrafish

Kyzar¹,

Stewart

Landsman³

et al. 2013

Brain Research

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Brain monoamines play a key role in the regulation of behavior. Reserpine depletes monoamines, and causes depression and hypoactivity in humans and rodents. In contrast, d-amphetamine increases brain monoamines’ levels, and evokes hyperactivity and anxiety. However, the effects of these agents on behavior and in relation to monoamine levels remain poorly understood, necessitating further experimental studies to understand their psychotropic action. Zebrafish (Danio rerio) are rapidly emerging as a promising model organism for drug screening and translational neuroscience research. Here, we have examined the acute and long-term effects of reserpine and d-amphetamine on zebrafish behavior in the novel tank test. Overall, d-amphetamine (5 and 10 mg/L) evokes anxiogenic-like effects in zebrafish acutely, but not 7 days later. In contrast, reserpine (20 and 40 mg/L) did not evoke overt acute behavioral effects, but markedly reduced activity 7 days later, resembling motor retardation observed in depression and/or Parkinson’s disease. Three-dimensional ‘temporal’ (X, Y, Time) reconstructions of zebrafish locomotion further supports these findings, confirming the utility of 3D-based video-tracking analyses in zebrafish models of drug action. Our results show that zebrafish are highly sensitive to drugs bi-directionally modulating brain monoamines, generally paralleling rodent and clinical findings. Collectively, this emphasizes the potential of zebrafish tests to model complex brain disorders associated with monoamine dysregulation.

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