Here’s a lil’ dose of pharmocology
Presentation i’ll be briefly discussing methylphenidate methylphenidate now is a common drug which was first synthesized in 1944 in hopes that it would treat disruptive behavior and children after showing some early promise in the pipeline stage three clinical trials began in the 50s so that it could be brought to the american market after its patenting in the
60s it was used to reverse the sedation caused by a perpetuate drugs although over time the usage would evolve methylphenidate crosses the blood-brain barrier begins to interact with gray matter its main action is binding at the dopamine and norepinephrine transporters where the molecules block the reuptake of the neurotransmitters from the synapse into their
Respective presynaptic neurons it interacts with these transporters throughout the dopamine and norepinephrine neurotransmitter systems in the frontal lobes basal ganglia and cerebellum where it modulates the inhibitory control methylphenidate exists in four forms due to having two chiral centers although it is only the d3r isomer that has high binding affinity
And thus it is the only forum with significant clinical efficacy to the right we can see the affinity of the d3o compared to the l3o form with respect to the different targets the lower the disassociation constant and half maximal inhibitory concentration is the higher the affinity is to the target when someone takes muscle finity they can expect to have a three to
Four times increase in dopamine and norepinephrine levels in the striatum and prefrontal cortex as well as an increase in neuronal firing rate for the neurons the molecule interacts with a more recently discovered mechanism of mental affinity is as an indirect cholinergic agonist which is achieves by binding to the sigma 1 receptor here is a schematic showing how
Methylphenidate binds to the sigma 1 g-protein coupled receptor thereby activating phospholipase c which activates in acetal triphosphate calcium release from the endoplasmic reticulum and protein kinase c leading to ndma receptor phosphorylation this phosphorylating event causes an increase in mdma mediated activity side-effects the most prominent methylphenidate
Use is for controlling symptoms of adhd like hyperactivity and inattention it achieves us through the mechanism stated previously by stimulating the areas of the brain in charge of inhibiting reflexive behavior and focusing attention narcolepsy and major depressive disorder otherwise known as nbd are also sometimes treated with methylphenidate in the case of
Narcolepsy it promotes wakefulness which counteracts the daytime drowsiness people experience with the condition methylphenidate is also used in md d patients if other first-line treatments don’t work methylphenidate may actually protect neurons from the toxic effects of parkinson’s disease and methamphetamine abuse by hypothetically reducing the cytosolic levels
Of dopamine and thus fewer reactive oxygen ee metabolites are created downstream which aren’t neurotoxic methylphenidate induces sympathy mimetic effects sympathomimetic effects as it increases nurp in different levels throughout the brain and body increases of dopamine by mental affinity action in the striatum have also been correlated with higher epinephrine
Levels in the blood so the typical sympathic of effects are seen like tachycardia loss of appetite et cetera methylphenidate can also induce a stronger psychosis and those who are already psychotic or bipolar and has been reported to induce immune system hypersensitivity
Transcribed from video
Methylphenidate Presentation By Cole Corbett