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Previously, we created mice that are unable to synthesize NE and epinephrine due to targeted disruption of the dopamine-beta-hydroxylase gearard (Dbh).

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Ziprasidone was tested as

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a positive control. These included the NE reuptake inhibitors desipramine and reboxetine, the monoamine oxidase inhibitor pargyline, and the atypical antidepressant Bupropion ( Wellbutrin SR ). However, the effect active ingredient valtrex in contrast to ziprasidone, reversed PCP-disrupted PPI in rats. PCP-disrupted PPI in rats was less sensitive to false positives than the d-amphetamine-disrupted

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PPI model, based on the antidepressants tested in this study. However, the Dbh(-/-) mice failed to demonstrate antidepressant-like behavioral effects following the administration of several classes of antidepressants.

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Both desipramine and ziprasidone normalised d-amphetamine-disrupted PPI, while Citalopram ( Celexa ) and Bupropion ( Wellbutrin SR ) were inactive. Taken together, these data show that the use of mice that lack endogenous NE

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may be an important strategy for unraveling the role of NE in tests sensitive to the effects of various psychotherapeutic agents.. In addition, desipramine significantly reduced immobility

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in the Dbh(-/-) mice following pretreatment with the synthetic NE precursor L-threo-3,4-dihydroxyphenylserine,

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but not saline. To specifically test the role of NE in mediating behavioral changes elicited by antidepressants, these

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mice were examined in the forced swim test. Schizophrenic patients have a deficit in prepulse inhibition (PPI) which can be modelled in rats by administration of direct or indirect dopamine

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(DA) receptor agonists and N-methyl-D-aspartate (NMDA) receptor antagonists. Effects of acute treatment with antidepressant drugs on sensorimotor gating deficits in rats.RATIONALE. There was no difference in baseline immobility scores in the forced swim test between Dbh( /-) mice, which have normal levels of NE, and Dbh(-/-) mice. To investigate

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the effects of three antidepressant compounds, a serotonin reuptake inhibitor, a dopamine reuptake inhibitor, and a noradrenaline reuptake inhibitor in the rat PPI model. Moreover, antipsychotics reverse the disruptive effect of DA agonists and NMDA

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receptor antagonists in this rat model. Antidepressants have been suggested not to affect PPI in humans. Use of dopamine-beta-hydroxylase-deficient mice to determine the role of norepinephrine in the mechanism of action of antidepressant drugs.Norepinephrine (NE) is thought to play an important role in the pathophysiology of depression, and in the mechanism of action of antidepressant compounds. The effect

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of acute treatment with Citalopram ( Celexa ), Bupropion ( Wellbutrin SR ) and desipramine on d-amphetamine-disrupted and phencyclidine (PCP)-disrupted PPI in rats was investigated.

Biochemical studies sho that there was no significant difference in the regional brain levels of NE transporter immunoreactivity or monoamine oxidase activity, the primary targets for most of the compounds examined. Thus, antidepressants are not expected to antagonise PPI disruption in rats, and should normally be used as negative controls in this model. Consequently, this model is considered as predictive of antipsychotic action in the clinic.