Search results
Results from the WOW.Com Content Network
The reinforcing effects of alcohol consumption are mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P-4502E1 in the brain. [60] Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic ...
Acamprosate has been successfully used to control tinnitus, hyperacusis, ear pain, and inner ear pressure during alcohol use due to spasms of the tensor tympani muscle. [medical citation needed] In addition, alcohol also inhibits the activity of N-methyl-D-aspartate receptors (NMDARs).
Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% ...
α 2 agonist: inhibits adenylyl cyclase activity, reduces brainstem vasomotor center-mediated CNS activation; used as antihypertensive, sedative & treatment of opiate dependence and alcohol withdrawal symptoms). Selected examples are: Brimonidine; Clonidine (mixed alpha2-adrenergic and imidazoline-I1 receptor agonist) Dexmedetomidine; Fadolmidine
Bethanechol is a muscarinic agonist.It is included in the therapy for underactive bladder with poor contraction of detrusor muscle. [2] Since contraction of detrusor muscle in the bladder is controlled by the parasympathetic nervous system, Bethanechol can bind to muscarinic receptors to stimulate activation of the parasympathetic nervous system and restore contraction of detrusor muscle.
The level of ethanol consumption that minimizes the risk of disease, injury, and death is subject to some controversy. [16] Several studies have found a J-shaped relationship between alcohol consumption and health, [17] [18] [2] [19] meaning that risk is minimized at a certain (non-zero) consumption level, and drinking below or above this level increases risk, with the risk level of drinking a ...
Alcohol education is the practice of disseminating information about the effects of alcohol on health, as well as society and the family unit. [72] It was introduced into the public schools by temperance organizations such as the Woman's Christian Temperance Union in the late 19th century. [ 72 ]
A competitive antagonist does not affect the Emax of the agonist. This is because the effect of an agonist can be maximized by adding the dose of the agonist as the action of the antagonist is reversible. The maximum effect of the agonist can be achieved by adding the concentration of the agonist. [6] [31]