Role of basolateral amygdala dopamine in modulating prepulse inhibition and latent inhibition in the rat

The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modu...

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Published inPsychopharmacologia Vol. 176; no. 2; pp. 139 - 145
Main Authors STEVENSON, C. W, GRATTON, Alain
Format Journal Article
LanguageEnglish
Published Berlin Springer 01.11.2004
Springer Nature B.V
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Abstract The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI). The effects of BLA D1 (SCH 23390) and D2/D3 (raclopride) receptor blockade on PPI and LI were examined. Separate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 microg/0.5 microl per side), raclopride (2.5 or 5.0 microg/0.5 microl per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing. Intra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI. These results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.
AbstractList Rationale: The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI). Objective: The effects of BLA D sub(1) (SCH 23390) and D sub(2)/D sub(3) (raclopride) receptor blockade on PPI and LI were examined. Methods: Separate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 mu g/0.5 mu l per side), raclopride (2.5 or 5.0 mu g/0.5 mu l per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing. Results: Intra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI. Conclusions: These results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.
The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI). The effects of BLA D1 (SCH 23390) and D2/D3 (raclopride) receptor blockade on PPI and LI were examined. Separate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 microg/0.5 microl per side), raclopride (2.5 or 5.0 microg/0.5 microl per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing. Intra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI. These results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.
The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI). The effects of BLA D1 (SCH 23390) and D2/D3 (raclopride) receptor blockade on PPI and LI were examined. Separate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 microg/0.5 microl per side), raclopride (2.5 or 5.0 microg/0.5 microl per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing. Intra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI. These results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.
RATIONALEThe dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI).OBJECTIVEThe effects of BLA D1 (SCH 23390) and D2/D3 (raclopride) receptor blockade on PPI and LI were examined.METHODSSeparate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 microg/0.5 microl per side), raclopride (2.5 or 5.0 microg/0.5 microl per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing.RESULTSIntra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI.CONCLUSIONSThese results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.
Author GRATTON, Alain
STEVENSON, C. W
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Keywords Conditioned taste aversion
Amygdala
Rat
Neuroleptic
D3 Dopamine receptor
SCH 23390
Acquisition process
Acoustic startle response
Gating
Amygdaloid nucleus
Raclopride
Dopamine
D1 receptor
Dopamine antagonist
Rodentia
D1 Dopamine receptor
Catecholamine
D2/D3 receptor
Sensorimotor gating
Vertebrata
Mammalia
D2 Dopamine receptor
Animal
Neurotransmitter
Perception
Taste
Conditioned aversion
Latent inhibition
Prepulse inhibition
Language English
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Snippet The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the...
Rationale: The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA...
RATIONALEThe dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission....
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crossref
pubmed
pascalfrancis
SourceType Aggregation Database
Index Database
StartPage 139
SubjectTerms Amygdala - drug effects
Amygdala - physiology
Animals
Biological and medical sciences
Dopamine - physiology
Dopamine Antagonists - pharmacology
Dose-Response Relationship, Drug
Male
Medical sciences
Neural Inhibition - drug effects
Neural Inhibition - physiology
Neuropharmacology
Pharmacology. Drug treatments
Rats
Rats, Long-Evans
Receptors, Dopamine - physiology
Reflex, Startle - drug effects
Reflex, Startle - physiology
Title Role of basolateral amygdala dopamine in modulating prepulse inhibition and latent inhibition in the rat
URI https://www.ncbi.nlm.nih.gov/pubmed/15114433
https://www.proquest.com/docview/218971291
https://search.proquest.com/docview/17603365
https://search.proquest.com/docview/67005498
Volume 176
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