Dopamine D and acetylcholine M receptors might be related to post-operative cognitive dysfunction. The aim of the present study is to investigate whether several anesthetics which are used for general anesthesia and/or sedation, affect expression of dopamine D and acetylcholine M receptors in the rat brain. Thirty-six male rats aged 5-9 weeks old were divided into six groups (n = 6 in each group); five groups for anesthetics and one for control. The five groups were anesthetized with either dexmedetomidine 0.4 µg/kg/min, propofol 50 mg/kg/h, midazolam 25 mg/kg/h, sevoflurane 3.3%, or nitrous oxide 75% for 4 h. Then, the rats were decapitated, and the cerebral cortex, hippocampus, corpus striatum, brain stem, and cerebellum were collected from all rats. Then, real-time polymerase chain reaction was performed to examine the expression of Drd2 (cord dopamine D receptor) and Chrm1 (cord acetylcholine M receptor). There were no significant differences among the groups regarding Drd2 and Chrm1 mRNA expression of each region of the brain. Postsynaptic changes of dopamine D and acetylcholine M receptors due to administration of dexmedetomidine, propofol, midazolam, sevoflurane, and nitrous oxide are unlikely to occur at the doses of each anesthetic used in the present study.
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Neurol Int
December 2024
Natural and Humanities Sciences Center (CCNH), Experimental Morphophysiology Laboratory, Federal University of ABC (UFABC), São Bernardo do Campo 09606-070, Brazil.
Background/objectives: Antipsychotic medicines are used to treat several psychological disorders and some symptoms caused by dementia and schizophrenia. Haloperidol (Hal) is a typical antipsychotic usually used to treat psychosis; however, its use causes motor or extrapyramidal symptoms (EPS) such as catalepsy. Hal blocks the function of presynaptic D2 receptors on cholinergic interneurons, leading to the release of acetylcholine (ACh), which is hydrolyzed by the enzyme acetylcholinesterase (AChE).
View Article and Find Full Text PDFMajor depressive disorder (MDD) is one of the most common diseases affecting millions of people worldwide. The use of existing antidepressants in many cases does not allow achieving stable remission, probably due to insufficient understanding of pathological mechanisms. This indicates the need for the development of more effective drugs based on in-depth understanding of MDD's pathophysiology.
View Article and Find Full Text PDFRSC Adv
December 2024
Department of Pharmacognosy, Faculty of Pharmacy, Cairo University Cairo 11562 Egypt
Many plants are reported to enhance cognition in amnesic-animal models. The metabolite profile of fruit methanolic extract (CDFME) was characterized by LC-QTOF-MS/MS, and its total phenolics content (TPC) and total flavonoids content (TFC) were determined. In parallel, its cognitive-enhancing effect on scopolamine (SCOP)-induced AD in rats was evaluated.
View Article and Find Full Text PDFNeurobiol Dis
December 2024
Department of Psychiatry, Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, Canada. Electronic address:
Background: Altered balance between striatal direct and indirect pathways contributes to early motor, cognitive and psychiatric symptoms in Huntington disease (HD). While degeneration of striatal D2-type dopamine receptor (D2)-expressing indirect pathway medium spiny neurons (iMSNs) occurs prior to that of D1-type dopamine receptor (D1)-expressing direct pathway neurons, altered corticostriatal synaptic function precedes degeneration. D2-mediated signaling on iMSNs reduces their excitability and promotes endocannabinoid (eCB) synthesis, suppressing glutamate release from cortical afferents.
View Article and Find Full Text PDFNeurobiol Learn Mem
December 2024
Department of Psychology, The University of Texas at Austin, Austin TX 78712, United States; Department of Neurology, The University of Texas at Austin, Austin TX 78712, United States; Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin TX 78712, United States. Electronic address:
The ability to choose between options that differ in their risks and rewards depends on brain regions within the mesocorticolimbic circuit and regulation of their activity by neurotransmitter systems. Dopamine neurotransmission in particular plays a critical role in modulating such risk-taking behavior; however, the contribution of other major modulatory neurotransmitters, such as acetylcholine, is not as well-defined, especially for decision making in which the risk associated with more rewarding outcomes involves adverse consequences. Consequently, the goal of the current experiments was to examine how cholinergic signaling influences decision making involving risk of explicit punishment.
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