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41b - March 19 2013 DOPAMINE AND DOPAMINE DRUGS(1).docx

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Mac Burnham

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[After watching video]  Funny thing about schizophrenia is that you’re blocking D2 in treatment, which you thing about these basal ganglia disorders.nesia, but often you get both. This is a strange DOPAMINE AND DOPAMINE DRUGS Metabolic Pathway Tyrosine (tyrosine hydroxylase) L-DOPA (DOPA decarboxylase) Dopamine (MAO, COMT) HVA Dopamine Drugs Toxin: 6 OHDA  6 OHDA, a toxin. You know another toxin, MPTP. It’s a toxin that was accidentally produced in designer drugs and it caused a lot of Parkinsonian symptoms in a lot of young people.  6 OHDA has to be taken up by neurons and metabolized into something, and metabolite kills them. Some doses get both DA and NE neurons, but can protect the NE neurons with tricyclic antidepressant like ???imiprimine??? Check this. Would only kill DA neurons. Synthesis:  With extrapyramidal disorders, often trying to increase dopamine or decrease dopamine levels. L-DOPA (increases)  With parkisonsons disease, the problem is too little dopamine, and want to increase it. So they give l-dopa, which is the precursor. Get good relief in initial few years of treatment. AMPT (blocks tyrosine)  This would be something that would send down synthetic pathway for DA and NE. so it would lower them both together. It’s a tyrosine hydroxylase inhibitor. benserazide (blocks peripheral DOPA decarboxylase) carbidopa (blocks peripheral) DOPA decarboxylase)  The BG disorders are usually treated with DA agonists, like l-dopa, but the dopamine agonists tend to make you nauseous. Remember in floor of fourth ventricle you have area prostrema, the chemical trigger zonepoison vomit centre (few areas without bbb). When activated you’ll throw up. Your body is detecting poisons in blood, and then it will empty stomach and stop absorption. You also get this with DA agonists, for some reason it will make you throw up because it actives the CTZ. One thing that is a problem with l- dopa therapy is it produces DA in blood stream as well as in brain and it goes to chemical trigger zone and makes you throw up  So they will give l-dopa in presence of benserazide and carbidopa. These are peripheral decarboxylase inhibitors. They stop transition of l-dopa to dopamine in blood stream, but not in your brain. Storage: reserpine, tetrabenazine (block)  We talked about resperine already, derived from Indian folk medicine used to lower blood pressure. Interest to us because 15% of patients got depressed.  Another drug is tetrabenazine, and they block storage.  DA would be stored in vesicles, and once it is stored in vesicles, it’s ready for release. So reserpine makes DA leak out of vesicles where its broken down by MAOs in the cytoplasm, tetrabenazine does the same thing. Both these drugs are not specific for dopamine, block storage in all monoamines  L-DOPA would improve parkinson’s, reserpine would make it worse Release: amphetamine, amantadine (?) (increase)  AMPH releases DA and NE.  Another drug we get onto is Amantadine. It was an antiviral drug which was found to help parkinsons patients. Now used as antiparkinsonian drug. With amantadine, story that originally came out was that it was a dopamine releaser. Re-uptake: cocaine, methylphenidate (block)  Cocaine and methylphenidate are blockers of reuptake of DA and NE Metabolism MAOI (block MAO A and B)) isocarboxacid,pargyline, phenylzine, tranylcypromine  MAOIs are drugs we used traditionally to block metabolism of DA. Of course would also block NE, DA, and 5HT. Listed here are the old ones. They’re also irreversible: bind
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