The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

Byrnes, John

doi:10.1016/s0893-133x(99)00151-7

Cited by 25 publications

(26 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Acute cocaine administration disrupts PPI in rats (Martinez et al, 1999;Byrnes and Hammer, 2000) and mice (our unpublished data; Yamashita et al, 2006) at high doses. Other studies, however, have failed to show an acute effect of cocaine on PPI in rats (Varty and Higgins, 1998).…”

Section: Introductionmentioning

confidence: 82%

Contributions of Dopamine D1, D2, and D3 Receptor Subtypes to the Disruptive Effects of Cocaine on Prepulse Inhibition in Mice

Doherty

Masten

Powell

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Deficits in prepulse inhibition (PPI) of startle, an operational measure of sensorimotor gating, are characteristics of schizophrenia and related neuropsychiatric disorders. Previous studies in mice demonstrate a contribution of dopamine (DA) D 1 -family receptors in modulating PPI and DA D 2 receptors (D2R) in mediating the PPI-disruptive effects of amphetamine. To examine further the contributions of DA receptor subtypes in PPI, we used a combined pharmacological and genetic approach. In congenic C57BL/6 J wildtype mice, we tested whether the D1R antagonist SCH23390 or the D2/3R antagonist raclopride would attenuate the effects of the indirect DA agonist cocaine (40 mg/kg). Both the D1R and D2/3R antagonists attenuated the cocaine-induced PPI deficit. We also tested the effect of cocaine on PPI in wild-type and DA D1R, D2R, or D3R knockout mice. The cocaine-induced PPI deficit was influenced differently by the three DA receptor subtypes, being absent in D1R knockout mice, partially attenuated in D2R knockout mice, and exaggerated in D3R knockout mice. Thus, the D1R is necessary for the PPI-disruptive effects of cocaine, while the D2R partially contributes to these effects. Conversely, the D3R appears to inhibit the PPI-disruptive effects of cocaine. Uncovering neural mechanisms involved in PPI will further our understanding of substrates of sensorimotor gating and could lead to better therapeutics to treat complex cognitive disorders such as schizophrenia.

show abstract

Section: Introductionmentioning

confidence: 82%

Contributions of Dopamine D1, D2, and D3 Receptor Subtypes to the Disruptive Effects of Cocaine on Prepulse Inhibition in Mice

Doherty

Masten

Powell

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…BN rats had higher DA and DOPAC levels, as well as increased DA utilization, in the caudate putamen compared to WKY rats. Since DA receptor agonists (Mansbach et al, 1988;Swerdlow et al, 1991) and drugs that increase extracellular DA concentrations (Byrnes and Hammer, 2000;Martinez et al, 1999) decrease PPI, perhaps increased DA levels and utilization in the caudate putamen contribute to the reduced PPI observed in BN rats under basal conditions (Conti et al, 2002;Palmer et al, 2000). However, administration of haloperidol, a DA receptor antagonist, did not enhance PPI in BN rats .…”

Section: Discussionmentioning

confidence: 99%

The effect of corticotropin-releasing factor on prepulse inhibition is independent of serotonin in Brown Norway and Wistar-Kyoto rats

Sutherland

Page

Conti

2008

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

Prepulse inhibition (PPI), a form of sensorimotor gating, is reduced in a number of psychiatric disorders. Two experiments were conducted to determine whether corticotropin-releasing factor (CRF), which decreases PPI, does so via effects on serotonin (5-HT). Wistar Kyoto (WKY) and Brown Norway (BN) rats were used in both experiments in order to examine whether straindependent differences would be apparent in response to manipulations of the CRF and 5-HT systems. In the first experiment, WKY and BN rats received a subcutaneous injection of the 5-HT 2A/C receptor antagonist, ketanserin (2.0 mg/kg). Ten minutes later, rats received an intracerebroventricular (ICV) infusion of either 6.0 μl saline or CRF (0.3 μg or 3.0 μg). CRF decreased PPI despite blockade of 5-HT 2A/C receptors with ketanserin. In the second experiment, WKY and BN rats received an intraperitoneal injection of the 5-HT synthesis inhibitor, p-chlorophenylalanine (PCPA, 150 mg/kg), 48 and 24 hours prior to testing. On testing day, rats received an ICV infusion of either 6.0 μl saline or CRF (0.3 μg or 3.0 μg). CRF decreased PPI despite 5-HT depletion. These findings suggest that CRF does not decrease PPI via effects on 5-HT, since neither blockade of 5-HT 2A/C receptors nor 5-HT depletion attenuated this decrease.

show abstract

“…Repeated treatment with indirect dopamine agonists, such as cocaine or amphetamine, attenuates PPI disruption (Byrnes and Hammer, 2000;Feifel et al, 2002). Furthermore, PPI disruption induced by acute treatment with the D 2 -like receptor agonist, quinpirole, is completely reversed by longterm treatment (Culm and Hammer, 2004), but the putative substrates underlying such PPI tolerance are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Repeated Quinpirole Treatment Increases cAMP-Dependent Protein Kinase Activity and CREB Phosphorylation in Nucleus Accumbens and Reverses Quinpirole-Induced Sensorimotor Gating Deficits in Rats

Culm

Lugo‐Escobar

Hope

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

Sensorimotor gating, which is severely disrupted in schizophrenic patients, can be measured by assessing prepulse inhibition of the acoustic startle response (PPI). Acute administration of D 2 -like receptor agonists such as quinpirole reduces PPI, but tolerance occurs upon repeated administration. In the present study, PPI in rats was reduced by acute quinpirole (0.1 mg/kg, s.c.), but not following repeated quinpirole treatment once daily for 28 days. Repeated quinpirole treatment did not alter the levels of basal-, forskolin-(5 mM), or SKF 82958-(10 mM) stimulated adenylate cyclase activity in the nucleus accumbens (NAc), but significantly increased cAMPdependent protein kinase (PKA) activity. Phosphorylation of cAMP response element-binding protein (CREB) was significantly greater in the NAc after repeated quinpirole treatment than after repeated saline treatment with or without acute quinpirole challenge. Activation of PKA by intra-accumbens infusion of the cAMP analog, Sp-cAMPS, prevented acute quinpirole-induced PPI disruption, similar to the behavioral effect observed following repeated quinpirole treatment. Thus, repeated quinpirole treatment increases NAc PKA activity and CREB phosphorylation, and this neuroadaptive response might facilitate the recovery of sensorimotor gating in schizophrenia.

show abstract

The Disruptive Effect of Cocaine on Prepulse Inhibition Is Prevented by Repeated Administration in Rats

Cited by 25 publications

References 16 publications

Contributions of Dopamine D1, D2, and D3 Receptor Subtypes to the Disruptive Effects of Cocaine on Prepulse Inhibition in Mice

Contributions of Dopamine D1, D2, and D3 Receptor Subtypes to the Disruptive Effects of Cocaine on Prepulse Inhibition in Mice

The effect of corticotropin-releasing factor on prepulse inhibition is independent of serotonin in Brown Norway and Wistar-Kyoto rats

Repeated Quinpirole Treatment Increases cAMP-Dependent Protein Kinase Activity and CREB Phosphorylation in Nucleus Accumbens and Reverses Quinpirole-Induced Sensorimotor Gating Deficits in Rats

Contact Info

Product

Resources

About