Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1997 Aug;132(4):366-74.
doi: 10.1007/s002130050357.

Potentiation of prepulse inhibition of the startle reflex in rats: pharmacological evaluation of the procedure as a model for detecting antipsychotic activity

Affiliations
Comparative Study

Potentiation of prepulse inhibition of the startle reflex in rats: pharmacological evaluation of the procedure as a model for detecting antipsychotic activity

R Depoortere et al. Psychopharmacology (Berl). 1997 Aug.

Abstract

Prepulse inhibition (PPI) of the startle reflex-whereby presentation of a weak prepulse preceding a startling pulse diminishes the amplitude of the startle reflex-is disrupted by dopamine (DA) agonists; this disruption can be reversed by antipsychotics. There are also some indications in the literature that a few antipsychotics (most notably clozapine and haloperidol) may, on their own, have effects opposite to those of DA agonists, i.e. may enhance PPI. In order to explore these antipsychotic-induced potentiations of PPI more thoroughly, we assessed, in Sprague-Dawley rats, the effects of IP administration of various clinically effective antipsychotics in a PPI procedure with levels of PPI (ranging from 5 to about 40%) low enough to facilitate detection of PPI-potentiating effects of drugs. Both clozapine (5-20 mg/kg) and haloperidol (0.25-1 mg/kg) robustly and dose-dependently potentiated PPI. A similar effect was not seen with risperidone (0.1-1 mg/kg) or with the three substituted benzamides amisulpride (10-60 mg/kg), raclopride (0.1-3 mg/kg) and remoxipride (1-10 mg/kg). As risperidone is known to have prominent 5-HT2 antagonistic activity, these results do not indicate a role for 5-HT2 receptors in the clozapine and haloperidol PPI-enhancing effects. The absence of effects with the benzamides and with risperidone, at doses with known anti-dopaminergic activity, suggests that DA antagonist activity is not involved. The demonstration that prazosin (3-20 mg/kg), a non-antipsychotic with alpha 1 adrenoceptor antagonistic properties, dose-dependently potentiated PPI indicates that alpha 1 receptors might mediate the clozapine and haloperidol PPI-enhancing activity. Additionally, the finding that diazepam (1-10 mg/kg) did not enhance, but on the contrary reduced PPI, argues against a sedation- or general depressant-mediated effect of clozapine, haloperidol and prazosin. The negative results with four clinically active antipsychotics (risperidone and the benzamides), and the positive result with the non-antipsychotic prazosin indicate that this PPI-enhancing procedure has poor predictive validity as a screening tool for potential antipsychotics.

PubMed Disclaimer

Publication types

LinkOut - more resources