REM sleep deprivation alters dopamine D2 receptor binding in the rat frontal cortex
| Autor: | Anwar Hamdi, Chandan Prasad, Jeffery W. Brock, Keith D. Ross, Shorye Payne |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Clinical Biochemistry Central nervous system Rapid eye movement sleep Sleep REM Motor Activity Toxicology Biochemistry Rats Sprague-Dawley Radioligand Assay Behavioral Neuroscience Internal medicine Dopamine receptor D2 medicine Animals Receptor Biological Psychiatry Pharmacology Receptors Dopamine D2 Chemistry Dopaminergic Frontal Lobe Rats Cortex (botany) Kinetics Endocrinology medicine.anatomical_structure Cerebral cortex Dopamine receptor Benzamides Dopamine Antagonists Sleep Deprivation |
| Zdroj: | Pharmacology Biochemistry and Behavior. 52:43-48 |
| ISSN: | 0091-3057 |
| DOI: | 10.1016/0091-3057(94)00411-b |
| Popis: | REM sleep deprivation (RSD) of rats results in facilitation of dopaminergic behavior and an increase in striatal D2 receptor density. To determine whether RSD results in changes in D2 receptor in other brain regions, receptor affinity (Kd) and density (Bmax) were measured in the anteromediofrontal (AM), cingulate (CN), and sulcal cortex (SL) in four groups of rats: 1), RSD96 group (RSD for 96 h; small pedestal/water tank method), 2) RSD24 group (large pedestals for 72 h then small pedestals for 24 h), 3) tank control group (TC; large pedestals for 96 h), and 4) cage control group. In separate groups, ambulation was recorded for 30 min following treatments. Group RSD96 showed an increase in activity compared to TC, and TC was increased compared to CC (p < 0.05 for all). In group RSD24, the AM showed an increase in Bmax and Kd (p < 0.05), but there were no effects by RSD96. In the CN, Bmax and Kd were decreased by RSD96 (p < 0.05) but not RSD24. In the SL, Bmax was increased by RSD96, but not RSD24, whereas Kd was increased in both RSD groups (p < 0.05). |
| Databáze: | OpenAIRE |
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