Prazosin administered prior to inescapable stressor blocks subsequent exaggeration of acoustic startle response in rats

Manion, Sean T; Gamble, Eleanore H.; Li, He

doi:10.1016/j.pbb.2007.01.019

Cited by 29 publications

(30 citation statements)

References 36 publications

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“…Conversely, startle responsivity, general arousal, increases as the avoidance response is refined and can even persist into extinction sessions. This supports our and others' past work that found inescapable shock only increases startle reactivity after some period of time has passed since the acute exposure to the shock (in the range of days) (Manion et al, 2007;Servatius et al, 1995;Beck et al, 2002), unless the subject under study is female (Beck & Servatius, 2005;Beck et al, 2008). Thus, we also replicated that sex difference by failing to find any increases in startle responsivity in female rats following shock exposure (Beck & Servatius, 2005;Beck et al, 2008).…”

Section: Discussionsupporting

confidence: 91%

“…These data provide an interesting example of how startle reactivity can be enhanced by prior exposure to an escapable and avoidable stressor. Moreover, as was observed following inescapable stress (Servatius et al, 1995;Beck et al, 2002;Manion et al, 2007;Manion et al, 2010), the presentation of enhanced startle reactivity in male rats did not occur proximal to any period of significant shock exposure. This finding is important for 2 reasons.…”

Section: Extinction Of Active Avoidance Removal Of Avoidance Contextsupporting

confidence: 59%

“…this procedure increases startle magnitude in male rats several days following stressor exposure (Servatius et al, 1994;Servatius et al 1995;Beck et al, 2002;Manion et al, 2007;Manion et al, 2010); in other words, there is a delayed sensitization of the startle response (Beck et al, 2002). As shown in Figure 1, enhanced startle reactivity may then be observed up to several days later (Servatius et al, 1995;Beck et al, 2002;Manion et al, 2007;Manion et al, 2010).…”

mentioning

confidence: 87%

“…There are several examples of shock-induced changes in various behavioral indexes of anxiety-like reactions outside of the shock-exposure context (Servatius et al, 1994;Servatius et al, 1995;Beck et al, 2002;Cordero et al, 2003;Beck & Servatius, 2005;Manion et al, 2007;Daviu et al, 2010;Manion et al, 2010), which may lead one to assume that stressors which cause pain have a particularly significant role in causing context-independent changes in general arousal. However, in the case of acquiring behavior that is conducive to active avoidance of shock, the acute role of shock exposure in early acquisition can be contrasted with the expression of stimulus control during asymptotic performance levels.…”

Section: Acquisition Of Active Avoidance and Changes In Startle Reactmentioning

confidence: 99%

“…As shown in Figure 1, enhanced startle reactivity may then be observed up to several days later (Servatius et al, 1995;Beck et al, 2002;Manion et al, 2007;Manion et al, 2010). The delayed expression of this enhanced defensive response could be due to competing processes that are similarly elicited by inescapable shock.…”

mentioning

confidence: 91%

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Acquisition of Active Avoidance Behavior as a Precursor to Changes in General Arousal in an Animal Model of PTSD

Ricart¹,

Servatius²,

Beck³

2012

Post Traumatic Stress Disorders in a Global Context

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Section: Discussionsupporting

confidence: 91%

Section: Extinction Of Active Avoidance Removal Of Avoidance Contextsupporting

confidence: 59%

mentioning

confidence: 87%

Section: Acquisition Of Active Avoidance and Changes In Startle Reactmentioning

confidence: 99%

mentioning

confidence: 91%

See 3 more Smart Citations

Acquisition of Active Avoidance Behavior as a Precursor to Changes in General Arousal in an Animal Model of PTSD

Ricart¹,

Servatius²,

Beck³

2012

Post Traumatic Stress Disorders in a Global Context

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Effects of prazosin, clonidine, and propranolol on the elevations in brain reward thresholds and somatic signs associated with nicotine withdrawal in rats

et al. 2010

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Rationale-Tobacco withdrawal is characterized by a negative mood state and relatively mild somatic symptoms. Increased noradrenergic transmission has been reported to play an important role in opioid withdrawal, but little is known about the role of noradrenergic transmission in nicotine withdrawal.Objectives-The aim of these experiments was to investigate the effects of prazosin, clonidine, and propranolol on the negative mood state and somatic signs associated with nicotine withdrawal in rats.Methods-A discrete-trial intracranial self-stimulation procedure was used to assess the negative affective state of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function.Results-In all the experiments, the nicotinic acetylcholine receptor antagonist mecamylamine (3 mg/kg) elevated the brain reward thresholds of the nicotine-treated rats and did not affect those of the control rats. The α1-adrenergic receptor antagonist prazosin (0.0625 and 0.125 mg/kg) dosedependently attenuated the elevations in brain reward thresholds associated with precipitated nicotine withdrawal. The α2-adrenergic receptor agonist clonidine (10-40 μg/kg) and the nonselective β-adrenergic receptor antagonist propranolol (2.5-10 mg/kg) did not attenuate the elevations in brain reward thresholds associated with nicotine withdrawal. Mecamylamine (2 mg/ kg) induced more somatic signs in the nicotine-treated rats than in the control rats. Clonidine and propranolol, but not prazosin, decreased the total number of somatic signs associated with nicotine withdrawal.Conclusion-Blockade of α1-adrenergic receptors attenuates the deficit in brain reward function associated with nicotine withdrawal. Antagonism of β-adrenergic receptors or stimulation of α2-adrenergic receptors attenuates the somatic symptoms of nicotine withdrawal.

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Effect of prazosin and guanfacine on stress-induced reinstatement of alcohol and food seeking in rats

et al. 2011

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Rationale and Objectives Relapse to alcohol use during abstinence or maladaptive eating habits during dieting is often provoked by stress. The anxiogenic drug yohimbine, which causes stress-like responses in humans and nonhumans, reliably reinstates alcohol and food seeking in a rat relapse model. Yohimibine is a prototypical alpha-2 adrenoceptor antagonist but results from studies on noradrenaline's role in yohimbine-induced reinstatement of drug and food seeking are inconclusive. Here we further addressed this issue by studying the effect of the alpha-1 adrenoceptor antagonist prazosin and the alpha-2 adrenoceptor agonist guanfacine on yohimbine-induced reinstatement. Methods In Exp. 1, we trained rats to self-administer alcohol (12% w/v, 1-h/day) and after extinction of alcohol-reinforced lever-pressing, we tested prazosin's (0.5, 1.0, and 2.0 mg/kg, i.p.) or guanfacine's (0.125, 0.25, and 0.5 mg/kg, i.p.) effect on yohimbine (1.25 mg/kg, i.p.)-induced reinstatement; we also examined prazosin's effect on intermittent-footshock-stress-induced reinstatement. In Exp. 2, we trained food-restricted rats to self-administer 45 mg food pellets and first examined prazosin's or guanfacine's effects on food-reinforced responding, and then, after extinction of lever presses, on yohimibine-induced reinstatement. Results Prazosin (0.5-2.0 mg/kg) blocked yohimbine-induced reinstatement of food and alcohol seeking, as well as footshock-induced reinstatement of alcohol seeking. Guanfacine attenuated yohimbine-induced reinstatement of alcohol seeking at the highest dose (0.5 mg/kg) but its effect on yohimbine-induced reinstatement of food seeking was not significant. Neither prazosin nor guanfacine affected high rate food-reinforced responding. Conclusions Results demonstrate an important role of postsynaptic alpha-1 adrenoceptors in stress-induced reinstatement of alcohol and food seeking.

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Prazosin administered prior to inescapable stressor blocks subsequent exaggeration of acoustic startle response in rats

Cited by 29 publications

References 36 publications

Acquisition of Active Avoidance Behavior as a Precursor to Changes in General Arousal in an Animal Model of PTSD

Acquisition of Active Avoidance Behavior as a Precursor to Changes in General Arousal in an Animal Model of PTSD

Effects of prazosin, clonidine, and propranolol on the elevations in brain reward thresholds and somatic signs associated with nicotine withdrawal in rats

Effect of prazosin and guanfacine on stress-induced reinstatement of alcohol and food seeking in rats

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