<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chesworth R</submitter><funding>Western Sydney University</funding><funding>National Health and Medical Research Council</funding><funding>Rebecca L. Cooper Medical Research Foundation</funding><funding>Dementia Australia Research Foundation</funding><pagination>1531-1546</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10271887</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>240(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Individuals with schizophrenia have high rates of comorbid substance use problems. One potential explanation for this comorbidity is similar neuropathophysiology in substance use and schizophrenia, which may arise from shared genetic risk factors between the two disorders. Here we investigated if genetic risk for schizophrenia could affect drug reward and reinforcement for cocaine in an established mouse model of genetic risk for schizophrenia, the neuregulin 1 transmembrane domain heterozygous (Nrg1 TM HET) mouse.&lt;h4>Methods&lt;/h4>We examined drug-induced locomotor sensitization and conditioned place preference for several cocaine doses (5, 10, 20, 30 mg/kg) in male adult Nrg1 TM HET and wild-type-like (WT) littermates. We also investigated intravenous self-administration</pubmed_abstract><journal>Psychopharmacology</journal><pubmed_title>Impaired extinction of operant cocaine in a genetic mouse model of schizophrenia risk.</pubmed_title><pmcid>PMC10271887</pmcid><funding_grant_id>Project Grant 2022</funding_grant_id><funding_grant_id>1102012</funding_grant_id><funding_grant_id>1141789</funding_grant_id><funding_grant_id>1095215</funding_grant_id><funding_grant_id>PG2020883</funding_grant_id><pubmed_authors>Visini G</pubmed_authors><pubmed_authors>Karl T</pubmed_authors><pubmed_authors>Chesworth R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impaired extinction of operant cocaine in a genetic mouse model of schizophrenia risk.</name><description>&lt;h4>Background&lt;/h4>Individuals with schizophrenia have high rates of comorbid substance use problems. One potential explanation for this comorbidity is similar neuropathophysiology in substance use and schizophrenia, which may arise from shared genetic risk factors between the two disorders. Here we investigated if genetic risk for schizophrenia could affect drug reward and reinforcement for cocaine in an established mouse model of genetic risk for schizophrenia, the neuregulin 1 transmembrane domain heterozygous (Nrg1 TM HET) mouse.&lt;h4>Methods&lt;/h4>We examined drug-induced locomotor sensitization and conditioned place preference for several cocaine doses (5, 10, 20, 30 mg/kg) in male adult Nrg1 TM HET and wild-type-like (WT) littermates. We also investigated intravenous self-administration</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jul</publication><modification>2025-04-18T20:35:47.865Z</modification><creation>2025-02-19T00:50:04.415Z</creation></dates><accession>S-EPMC10271887</accession><cross_references><pubmed>37233814</pubmed><doi>10.1007/s00213-023-06386-8</doi></cross_references></HashMap>