Role of dopamine in prepulse inhibition of acoustic startle
Prepulse inhibition of acoustic startle is the reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Prepulse inhibition occurs normally in humans and experimental animals, but schizophrenic persons often exhibit a marked im...
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| Veröffentlicht in: | Psychopharmacologia 2000-04, Vol.149 (2), p.181-188 |
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| description | Prepulse inhibition of acoustic startle is the reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Prepulse inhibition occurs normally in humans and experimental animals, but schizophrenic persons often exhibit a marked impairment in this measure. Previous studies have shown that dopamine (DA)-dependent neuronal mechanisms are involved in the modulation of prepulse inhibition.
Experiments were conducted in rats to elucidate further the involvement of DA-ergic mechanisms in prepulse inhibition.
In line with previous studies, the indirect DA agonist, amphetamine, was shown to decrease prepulse inhibition. A close reverse relationship over time between DA overflow in the nucleus accumbens and prepulse inhibition was obtained using a technique allowing concomitant measurement of these parameters in awake, freely moving rats. This effect was more pronounced in amphetamine-treated rats compared to rats treated with equimolar doses of cocaine, which increased DA overflow without affecting prepulse inhibition. In other experiments, the combined treatment with subthreshold doses of the selective DA D1 agonist, SKF 38393, and the selective DA D2 agonist, quinpirole, was also shown to decrease prepulse inhibition. Finally, the selective DA D2 antagonist, raclopride, was shown to enhance prepulse inhibition.
In line with previous studies, it is concluded that DA neurotransmission is involved in the modulation of prepulse inhibition and that the ventral part of the mesostriatal DA system may serve an important role in this modulation. Furthermore, the possibility is discussed that the discrepant results on prepulse inhibition obtained with amphetamine and cocaine may disclose functionally relevant differences in their mechanisms of action, and that the enhancement of prepulse inhibition induced by some antipsychotics in rats may reflect their propensity to induce adverse mental effects in humans. |
| doi_str_mv | 10.1007/s002130000369 |
| format | Article |
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Experiments were conducted in rats to elucidate further the involvement of DA-ergic mechanisms in prepulse inhibition.
In line with previous studies, the indirect DA agonist, amphetamine, was shown to decrease prepulse inhibition. A close reverse relationship over time between DA overflow in the nucleus accumbens and prepulse inhibition was obtained using a technique allowing concomitant measurement of these parameters in awake, freely moving rats. This effect was more pronounced in amphetamine-treated rats compared to rats treated with equimolar doses of cocaine, which increased DA overflow without affecting prepulse inhibition. In other experiments, the combined treatment with subthreshold doses of the selective DA D1 agonist, SKF 38393, and the selective DA D2 agonist, quinpirole, was also shown to decrease prepulse inhibition. Finally, the selective DA D2 antagonist, raclopride, was shown to enhance prepulse inhibition.
In line with previous studies, it is concluded that DA neurotransmission is involved in the modulation of prepulse inhibition and that the ventral part of the mesostriatal DA system may serve an important role in this modulation. Furthermore, the possibility is discussed that the discrepant results on prepulse inhibition obtained with amphetamine and cocaine may disclose functionally relevant differences in their mechanisms of action, and that the enhancement of prepulse inhibition induced by some antipsychotics in rats may reflect their propensity to induce adverse mental effects in humans.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s002130000369</identifier><identifier>PMID: 10805614</identifier><identifier>CODEN: PSYPAG</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology ; Acoustic Stimulation ; Agonists ; Amphetamine - pharmacology ; Amphetamines ; Analysis of Variance ; Animals ; Antipsychotics ; Biological and medical sciences ; Catecholaminergic system ; Cocaine ; Cocaine - pharmacology ; Dopamine ; Dopamine - physiology ; Dopamine Agonists - pharmacology ; Dopamine Antagonists - pharmacology ; Dopamine D1 receptors ; Dopamine D2 Receptor Antagonists ; Dopamine D2 receptors ; Male ; Medical sciences ; Neuromodulation ; Neuropharmacology ; Neurotransmission ; Neurotransmitters. Neurotransmission. Receptors ; Noise ; Nucleus accumbens ; Pharmacology. Drug treatments ; Quinpirole ; Quinpirole - pharmacology ; Raclopride ; Raclopride - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Dopamine D1 - agonists ; Receptors, Dopamine D1 - metabolism ; Receptors, Dopamine D2 - agonists ; Receptors, Dopamine D2 - metabolism ; Reflex, Startle - drug effects ; Reflex, Startle - physiology ; Startle response</subject><ispartof>Psychopharmacologia, 2000-04, Vol.149 (2), p.181-188</ispartof><rights>2000 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 2000.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c377t-bbaa770f088465aad6440791962a1956a78b9195b5c760cb3ee2f9b6cf15da2d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1346381$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10805614$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JIANHUA ZHANG</creatorcontrib><creatorcontrib>FORKSTAM, C</creatorcontrib><creatorcontrib>ENGEL, J. A</creatorcontrib><creatorcontrib>SVENSSON, L</creatorcontrib><title>Role of dopamine in prepulse inhibition of acoustic startle</title><title>Psychopharmacologia</title><addtitle>Psychopharmacology (Berl)</addtitle><description>Prepulse inhibition of acoustic startle is the reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Prepulse inhibition occurs normally in humans and experimental animals, but schizophrenic persons often exhibit a marked impairment in this measure. Previous studies have shown that dopamine (DA)-dependent neuronal mechanisms are involved in the modulation of prepulse inhibition.
Experiments were conducted in rats to elucidate further the involvement of DA-ergic mechanisms in prepulse inhibition.
In line with previous studies, the indirect DA agonist, amphetamine, was shown to decrease prepulse inhibition. A close reverse relationship over time between DA overflow in the nucleus accumbens and prepulse inhibition was obtained using a technique allowing concomitant measurement of these parameters in awake, freely moving rats. This effect was more pronounced in amphetamine-treated rats compared to rats treated with equimolar doses of cocaine, which increased DA overflow without affecting prepulse inhibition. In other experiments, the combined treatment with subthreshold doses of the selective DA D1 agonist, SKF 38393, and the selective DA D2 agonist, quinpirole, was also shown to decrease prepulse inhibition. Finally, the selective DA D2 antagonist, raclopride, was shown to enhance prepulse inhibition.
In line with previous studies, it is concluded that DA neurotransmission is involved in the modulation of prepulse inhibition and that the ventral part of the mesostriatal DA system may serve an important role in this modulation. Furthermore, the possibility is discussed that the discrepant results on prepulse inhibition obtained with amphetamine and cocaine may disclose functionally relevant differences in their mechanisms of action, and that the enhancement of prepulse inhibition induced by some antipsychotics in rats may reflect their propensity to induce adverse mental effects in humans.</description><subject>2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology</subject><subject>Acoustic Stimulation</subject><subject>Agonists</subject><subject>Amphetamine - pharmacology</subject><subject>Amphetamines</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Antipsychotics</subject><subject>Biological and medical sciences</subject><subject>Catecholaminergic system</subject><subject>Cocaine</subject><subject>Cocaine - pharmacology</subject><subject>Dopamine</subject><subject>Dopamine - physiology</subject><subject>Dopamine Agonists - pharmacology</subject><subject>Dopamine Antagonists - pharmacology</subject><subject>Dopamine D1 receptors</subject><subject>Dopamine D2 Receptor Antagonists</subject><subject>Dopamine D2 receptors</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuromodulation</subject><subject>Neuropharmacology</subject><subject>Neurotransmission</subject><subject>Neurotransmitters. 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Neurotransmission. Receptors</topic><topic>Noise</topic><topic>Nucleus accumbens</topic><topic>Pharmacology. Drug treatments</topic><topic>Quinpirole</topic><topic>Quinpirole - pharmacology</topic><topic>Raclopride</topic><topic>Raclopride - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Dopamine D1 - agonists</topic><topic>Receptors, Dopamine D1 - metabolism</topic><topic>Receptors, Dopamine D2 - agonists</topic><topic>Receptors, Dopamine D2 - metabolism</topic><topic>Reflex, Startle - drug effects</topic><topic>Reflex, Startle - physiology</topic><topic>Startle response</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JIANHUA ZHANG</creatorcontrib><creatorcontrib>FORKSTAM, C</creatorcontrib><creatorcontrib>ENGEL, J. 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A</au><au>SVENSSON, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of dopamine in prepulse inhibition of acoustic startle</atitle><jtitle>Psychopharmacologia</jtitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2000-04-01</date><risdate>2000</risdate><volume>149</volume><issue>2</issue><spage>181</spage><epage>188</epage><pages>181-188</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><coden>PSYPAG</coden><abstract>Prepulse inhibition of acoustic startle is the reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Prepulse inhibition occurs normally in humans and experimental animals, but schizophrenic persons often exhibit a marked impairment in this measure. Previous studies have shown that dopamine (DA)-dependent neuronal mechanisms are involved in the modulation of prepulse inhibition.
Experiments were conducted in rats to elucidate further the involvement of DA-ergic mechanisms in prepulse inhibition.
In line with previous studies, the indirect DA agonist, amphetamine, was shown to decrease prepulse inhibition. A close reverse relationship over time between DA overflow in the nucleus accumbens and prepulse inhibition was obtained using a technique allowing concomitant measurement of these parameters in awake, freely moving rats. This effect was more pronounced in amphetamine-treated rats compared to rats treated with equimolar doses of cocaine, which increased DA overflow without affecting prepulse inhibition. In other experiments, the combined treatment with subthreshold doses of the selective DA D1 agonist, SKF 38393, and the selective DA D2 agonist, quinpirole, was also shown to decrease prepulse inhibition. Finally, the selective DA D2 antagonist, raclopride, was shown to enhance prepulse inhibition.
In line with previous studies, it is concluded that DA neurotransmission is involved in the modulation of prepulse inhibition and that the ventral part of the mesostriatal DA system may serve an important role in this modulation. Furthermore, the possibility is discussed that the discrepant results on prepulse inhibition obtained with amphetamine and cocaine may disclose functionally relevant differences in their mechanisms of action, and that the enhancement of prepulse inhibition induced by some antipsychotics in rats may reflect their propensity to induce adverse mental effects in humans.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>10805614</pmid><doi>10.1007/s002130000369</doi><tpages>8</tpages></addata></record> |
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| subjects | 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology Acoustic Stimulation Agonists Amphetamine - pharmacology Amphetamines Analysis of Variance Animals Antipsychotics Biological and medical sciences Catecholaminergic system Cocaine Cocaine - pharmacology Dopamine Dopamine - physiology Dopamine Agonists - pharmacology Dopamine Antagonists - pharmacology Dopamine D1 receptors Dopamine D2 Receptor Antagonists Dopamine D2 receptors Male Medical sciences Neuromodulation Neuropharmacology Neurotransmission Neurotransmitters. Neurotransmission. Receptors Noise Nucleus accumbens Pharmacology. Drug treatments Quinpirole Quinpirole - pharmacology Raclopride Raclopride - pharmacology Rats Rats, Sprague-Dawley Receptors, Dopamine D1 - agonists Receptors, Dopamine D1 - metabolism Receptors, Dopamine D2 - agonists Receptors, Dopamine D2 - metabolism Reflex, Startle - drug effects Reflex, Startle - physiology Startle response |
| title | Role of dopamine in prepulse inhibition of acoustic startle |
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