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In this lecture we’re gonna cover the pharmacology parkinson’s disease is a neurological disorder now, the neurons responsible for coordinating called the striatum, which receives information the cortex relays sensory information as well nigra sends dopamine that helps to coordinate all of the inputs. since dopaminergic neurons that originate effects on gaba neurons
Located in the striatum, increased inhibition of the thalamus, as well in addition to that, these same dopaminergic and again, without sufficient levels of dopamine which triggers a chain of abnormal signaling leading to impaired mobility. and excitatory activities leads to the manifestation the pharmacological therapy for parkinson’s levels, mimicking dopamine’s action,
Or now, in order to get a better understanding first we need to take a closer look at the dopamine producing neuron. first, with the help of enzyme tyrosine hydroxylase in the second step, the l-dopa formed by tyrosine another enzyme called aromatic l-amino acid dopamine is then loaded into synaptic vesicles the extracellular space where it can bind finally, excess dopamine
In the synapse is cells where it gets metabolized by monoamine oxidase (abbreviated mao) and catechol-o-methyltransferase it’s important to note that while the mao a and type b, the type that is predominantly now, let’s move on to discussing drugs used with one of the most commonly used drugs that is levodopa. and the answer is, it’s because of the blood-brain barrier.
Dopamine happens to be one of those molecules one of the biggest problems levodopa faces on it’s own is peripheral metabolism. can reach the brain, that is; peripheral dopa- to dopamine, and catechol- o- methyltransferase because of this, levodopa must be administered inhibits dopamine decarboxylase and thus reduces another agent that is used in combination which inhibits
Peripheral comt and thus just now, levodopa is carried across blood-brain barrier by amino acid transporter. however, lets not forget that dopamine is as mao-b, which convert dopamine to 3-methoxytyramine so, here another useful drugs come into play, namely selegiline and rasagiline, which selectively barrier, and thus can act both in the central so, again, as you can see,
By decreasing the unfortunately, because parkinson’s is a of dopamine producing neurons decreases, and taking that into consideration, some drugs directly stimulate dopamine receptors in the brain. drugs that belong to this class include; bromocriptine, ropinirole, pramipexole, rotigotine, and apomorphine. depletion leads to increased acetylcholine located on the neurons
Responsible for smooth motor control. the overstimulation of these neurons by acetylcholine this is where antimuscarinic agents come into as a result, these anticholinergic agents and dopamine, which may improve the symptoms of parkinson’s disease. drugs that belong to this class include; benztropine, now, before we move on, i wanted to briefly amantadine doesn’t exactly
Fit into any of the classes that we discussed so far. it prevents dopamine reuptake, facilitates now, when it comes to side effects, levodopa loss of appetite, hypotension, mental disturbances, selegiline and rasagiline may cause nausea, entacapone and tolcapone may cause discoloration can get severe particularly with the use of tolcapone. all dopamine agonists may cause
Nausea, orthostatic in addition to that, bromocriptine has been lastly, drugs that block muscarinic receptors such as constipation, urinary retention, dry mouth, and blurred vision. always, stay tuned for more.
Transcribed from video
Pharmacology – DRUGS FOR PARKINSON'S DISEASE (MADE EASY) By Speed Pharmacology