{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T23:34:25Z","timestamp":1772926465939,"version":"3.50.1"},"reference-count":64,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,8,31]],"date-time":"2015-08-31T00:00:00Z","timestamp":1440979200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIH","award":["DA027580 (to S.H.M.)"],"award-info":[{"award-number":["DA027580 (to S.H.M.)"]}]},{"name":"NIH","award":["AA10760 (to SHM)"],"award-info":[{"award-number":["AA10760 (to SHM)"]}]},{"name":"NIH","award":["DA018165 (to S.H.M.)"],"award-info":[{"award-number":["DA018165 (to S.H.M.)"]}]},{"name":"U.S. Department of Veterans Affairs Biomedical Laboratory Research and Development","award":["1BX 001643 (to C.K.M.)"],"award-info":[{"award-number":["1BX 001643 (to C.K.M.)"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:p>Changes in executive function are at the root of most cognitive problems associated with Parkinson's disease. Because dopaminergic treatment does not necessarily alleviate deficits in executive function, it has been hypothesized that dysfunction of neurotransmitters\/systems other than dopamine (DA) may be associated with this decrease in cognitive function. We have reported decreases in motor function and dopaminergic\/glutamatergic biomarkers in a progressive 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) Parkinson's mouse model. Assessment of executive function and dopaminergic\/glutamatergic biomarkers within the limbic circuit has not previously been explored in our model. Our results show progressive behavioral decline in a cued response task (a rodent model for frontal cortex cognitive function) with increasing weekly doses of MPTP. Although within the dorsolateral (DL) striatum mice that had been given MPTP showed a 63% and 83% loss of tyrosine hydroxylase and dopamine transporter expression, respectively, there were no changes in the nucleus accumbens or medial prefrontal cortex (mPFC). Furthermore, dopamine\u20101 receptor and vesicular glutamate transporter (VGLUT)\u22121 expression increased in the mPFC following DA loss. There were significant MPTP\u2010induced decreases and increases in VGLUT\u20101 and VGLUT\u20102 expression, respectively, within the DL striatum. We propose that the behavioral decline following MPTP treatment may be associated with a change not only in cortical\u2013cortical (VGLUT\u20101) glutamate function but also in striatal DA and glutamate (VGLUT\u20101\/VGLUT\u20102) input. \u00a9 2015 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.23638","type":"journal-article","created":{"date-parts":[[2015,9,2]],"date-time":"2015-09-02T17:47:01Z","timestamp":1441216021000},"page":"1849-1864","source":"Crossref","is-referenced-by-count":19,"title":["Executive function deficits and glutamatergic protein alterations in a progressive 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine mouse model of Parkinson's disease"],"prefix":"10.1002","volume":"93","author":[{"given":"Lacey","family":"Pflibsen","sequence":"first","affiliation":[{"name":"Research Services, VA Medical Center\/Portland Portland Oregon"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine 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