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191 Cards in this Set
- Front
- Back
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Where is dopamine produced?
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in the brainstem area. pars compacta of substantial nigra to basal ganglia, ventral tegmental area to the rest of the forebrain
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synthesis of dopamine
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tyrosine is acted upon by TH (rate limiting enzyme) to produce DOPA(precursor). DD/AAADC converts DOPA into dopamine
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synthesis of norepinephrine
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DBH(dopamine beta hydroxylase) converts dopamine into norepinephrine
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synthesis of epinephrine
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in the adrenal medulla, the enzyme PNMT converts norepinephrine into epinephrine
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false transmitters - catecholamines
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alpha-methyl DOPA, acted upon by DD/AAADC to produce the false transmitter alpha-methyl-DA, can be acted upon by DBH to produce alpha-methyl-NE
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DA degradation
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two pathways COMT and MAO, both begin with dopamine and end with homovanillate acid
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COMT DA degradation pathway
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DA stripped of carboxyl group and methyl group added, end with intermediate acted upon by MAO which takes amine group off and adds a carboxyl group, produces HVA. Preferred pathway bc no aldehydes are produced
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MAO DA degradation pathway
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DA converted into an aldehyde by MAO, broken down by COMT to produce HVA
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uses/abuses of DA ligands
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appetite suppression, antidepressants, antipsychotics, fatigue suppression, enhanced attention, treatment of motor dysfunction, pressure effects, mania mimicry, mild hallucinations
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hypothesis of affect/psychosis
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in depression there is a lack of DA in the frontal cortex. in psychosis tere may be too many producers of DA in the nucleus accumbens
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vesicular DA transporters
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12 transmembrane segment proteins, proton dependent. for every molecule of DA, one proton comes out, proton pump is an ATPase. blocked by reserpine and tetrahydrobenazine
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synaptic DAT
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12 transmembrane proteins, Na and Cl dependent. Transports to the side with lower concentration, oubain inhibits transport bc it blocks Na and K ATPases
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amphetamines and analogs
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increase DA in synapse, re-released by neuron, quick and persistent action, increase synpatic DA levels and later see an increase in HVA. include dextroamphetamine, methamphetamine, methylphenidate, cocaine, phenmetrazine
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What causes Parkinson's diease?
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taking synthetic opiates, a byproduct is MPTP that is converted to MPP by glial cells that is taken into mitochondria where it blocks the CREB cycle and kills DA neurons
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DA receptors
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metabotropic, have 7 transmembrane segments, bind g-protein, 5 classes of DA receptors. D1 and D5 called D1-like, tied to Gs alpha subunit, considered excitatory DA receptor. D2-D4, D2-like, tied to Gi's
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D2 dopamine receptors
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beta gamma decrease VDCC and VDKC and CDKC. D2 receptors are often autoreceptors, prevent the release of DA when stimulated by actiating the Gi, decreasing the phosphorylation of TH, D2s found postsynaptically
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DA agonists, all five receptors
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dopamine, lisuride, apomorphine
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DA agonists, D1 and D5
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dihydrexidine
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DA agonist D1 only
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fenoldpam
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DA agonist D2 and D3 only
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quinpirole
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DA agonist,D2-D4
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bromocriptine, pergolide
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DA agonist D2 and D3
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pramipexole, ropinirole, both for RLS
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DAR antagonist, all five
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spiperone
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DAR antagonist, D1 and D5
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ecopipam
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DAR antagonist, D2-D4
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domoperidone
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DAR antagonist D2 and D3
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amisulpride, antipsychotic
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DAR antagonist D2-D4
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chloripromazine, triflupenazine, piperazine, respiridone
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DAR antagonist, D4 only
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clozapine
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DA autoreceptor
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D2 receptor on presynaptic side, tied to Gi, inhibit AC, inhibit cAMP, less PKA and less TH, less production of DOPA, less DA. D2 provide negative feelback, drugs that block D2 increase DA
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lithium
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hypothesized to interact with PI turnover, has effects on phosphorylation, PIP2, IP2 and Ca. It is known to decrease the amount of substrates released by PIP2
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Where are the most D2 receptors found?
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in the striatum with D1 recpetors
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Tardive dyskinesia
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DA blocked with antipsychotic meds, the NS makes more DA receptors to compensate, increase the dose of antipsychotics, eventually DA stops being produced endogenously, start to see Parkinson's like symptoms. If patein stops taking drug they will be supersensitive to DA , more psychotic
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VNET blockers
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proton dependent transporter, ATPase are Mg dependent. Guanethedine and bretylium and guandrel prevent NE from being packed into vesicles, all used to control pressure
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What drug blocks NE, DAT, and 5-HT reuptake?
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indatraline and cocane
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What drug blocks NE and DAT reuptake only?
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bupropion
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What drugs block Ne and 5-HT reuptake?
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venlafaxine, clomipramine
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What drugs block NE reuptake only?
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tricyclics, imipramin, amitriptyline, viloxazine, atomaxetine
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Which NT is affected by A-specific MAO inhibitor?
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NE and 5-HT
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Which Nt is affected by b-specific MAO inhibitors?
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DA and histamine
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What is a reversible a-specific MAO inhibitor?
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befloxatone
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What is an irreversible a-specific MAO inhibitor
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clorgyline, harmaline
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What is a nonspecific MAO inhibitor?
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iproniazid (irreversible)
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What is an irreversible B-specific MAO ihibitor?
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deprenyl, selegiline
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What is an irreversible COMT inhibitor?
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tolcapone
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What are the reversible MAO=b inhibitors?
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there are none
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Why are MAO inhibitors dangerous?
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eating red wine, aged cheese or turkey while taking MAO-I's can cause heart attack bc they contain amino acid precursors for the biosynthesis of the transmitters
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What are the classes of adrenoceptors (NE and EPI)?
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alpha1-Gi. Alpha2-Gi. beta-Gs
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Alpha 1A adrenoceptors nonselective agonists
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DA, NE, EPI, phenylephrine, ephedrine
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alpha 1A adrenoceptors selective agonists
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tetrahydrazoline
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alpha1A adrenoceptors selective antagonist
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niguldipine
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alpha 1A adrenoceptors nonselective antagonist
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phentolamine, prozosin
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alpha1A adrenoceptors suicide antagonist
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phenoxbenzamine
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alpha1B adrenoceptors selective antagonist
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cyclozasin
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alpha1B nonselective antagonist
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phentolamine, prazosin
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alpha1B suicide antagonist
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phenoxbenzamine
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alpha1D
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decongestants, interacts with alpha1 receptors, ephedrine, pseudoephedrine, phenylephrine, tetrahydrozoline
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alpha2A adrenoceptors nonselective agonist
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NE, EPI, clonidine
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Alpha2a adrenoceptors selective partial agonist
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oxymetazoline, LSD-25
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alpha2a nonselective antagonist adrenoceptor
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phentolamine, prazosin, yohimbine
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What does the beta gamma subunit of alpha2a adrenoceptor do?
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inactivates VDCC and activates CDKC
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What is the function of the alpha2B adrenoceptor
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vasoconstriction
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alpha2B adrenoceptor nonselective agonist
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NE, EPI, clonidine
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alpha2B adrenoceptor selective antagonist
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imiloxon
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alpha2b adrenoceptor nonselective antagonist
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phentolamine, prazosin, yohimbine
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alpha2C adrenoceptor selective antagonist
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rauwolscine
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antihypertensive vasodilators
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phentolamine, natural treatment for erectile dysfunction, has to be directly injected into organ
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hallucinogenic relatives of NE
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phenylethylamine, cathine, ephedrine, LSD-25, yohimbine, 5-HT, mescaline, elimicin, MDMA
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steroid hormone effector mechanism
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steroids are lipophilic, bind to receptors in the cell, translocation event, bind to DNA, transcription of genes/interference of transcription, RNA through ER, translation of new proteins
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heat shock proteins
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important for regulating intracellular receptors, forms a complex with proteins, ligand binds to receptor, uncoupling/unbinding from heat shock protein, free receptor ligand complex. Translocation event, receptor dimerizes in nucleus, interacts with DNA, transcription changes
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Type 1 intracellular steroid receptors
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n-terminal(amino acid) and carboxy-terminal. dimerize at hinge region and carboxy terminal end is responsible for binding the hormone
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gonadal steroids
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estrogen, androgen, progesterone
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adrenal steroids
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glucocorticoid, mineralocorticoid
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estrogen antagonists
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clomiphene, tamoxifen, used in treatment of breast cancer to block proliferation of estrogen sensitive tumor cells
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estrogen agonist effects
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regulate hormone secretion, regulate cholesterol metabolism, increase lipid protein synthesis,maintenece of neural plasticity
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endogenous estrogen agonists
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estradiol, estiol, estrone
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androgen endogenous agonists
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testosterone, DHT
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androgen antagonist
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flutamide
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androgen agonist effects
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maintenance of sex drive, enhance bone Ca retention, increase lipid, protein synthesis, maintain neural plasticity
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progesterone antagonist
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mifepristone, used as abortifactant to disrupt maintenance of uterine endometrial lining and block fertilized egg implantation, used for various adrenal disorders
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progesterone agonist effects
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enhance bone Ca retention, stabilize uterine proliferation, stabilize lipid metabolism
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glucocorticoid endogenous agonist
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cortisol, corticosterone
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clucocorticoid antagonist
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mefipristone
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glucocorticoid agonist effect
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increase hepatic gluconeogenesis, increase protein anabolism, glycolysis, increase BP, increase HR, immunosuppression, glucose is primary fuel for production of ATP
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mineralocorticoid endogenous agonist
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aldosterone
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mineralocorticoid antagonist
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spirvolctone
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mineralocorticoid agonist effects
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Na retention
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gonadal steroid biosynthesis
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cholesterol, produces progesterone, produces testosterone, most of the female's testosterone is converted to estradiol
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testosterone
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primary male sex hormone, can be converted into DHT by alpha-reductase. DHT is three times more potent at activating androgen receptors, causes baldness
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estrogen
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potent in regulating structure and function of neurons, more dense dendritic spikes
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Which portion of the pituitary is known as the neural lobe?
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posterior pituitary
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hormonal regulation of estrus
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FSH and LH released from pituitary, production of other hormones. 2 monthly surges in estradiol, one that preceeds LH and FSH surge and one that follows. After the larger of the two peaks is an increase in progesterone productin
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FSH and LH
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FSH begins maturation of follicles. LH stimulates corpus luteum/spermatogenesis. FSH plays a smaller role than LH in males. Both released by anterior pituitary, Gs signaling.
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estrogen receptors
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dimeric receptors, two gene families, ER-alpha, ER-beta, heterodimers with both alpha and beta present.
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gonadotropin hormones
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GnRH, FSH, LH, prolactin
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prolactin
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considered a cytokine receptor, single transmembrane segment coupled to JAK/STAT pathway. released by anterior pituitary, receptors in mammary glands stimulate lactation.
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JAK/STAT
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janus kinases, signal transduction and activator of transcription, ligand binding occurs at extracellular face of receptors, dimer formed, two JAKs bound. STAT phosphorylated, bind to one another and translocate across the nuclear membrane and activate transcription
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GnRH
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inhibits production of LH and stimulates production of testosterone
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What are anti-androgens used for?
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treatment of sex offenders, treatment of prostate cancer, treatment of male pattern baldness
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biosythesis of adrenal steroids
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cholesterol precursor, produces progesterone, in adrenal produces either corticosteroid into aldosterone, or other cells nearby produce cortisol, the primary glucocorticoid
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steroid synthesis inhibitors
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ketoconazol, metyrapone
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CRF
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corticotropin releasing factor, released through portal circulation of hypothalamus into anterior pituitary from posterior, causes the release of ACTH, causes the release of glucocorticoids from the adrenal cortex.
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corticosteroids
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short and long term effects on immune and cardiac systems. cross BBB, detected by receptors in hippocampus, pyramidal CA1 neurons that project back to hypothalamus, inhibiting production of CRF. Typically takes 40 minutes for the effect to take place
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stimulants
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cocaine, amphetamines
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depressants/narcotics
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opiates, barbiturates, BDZs
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hallucinogenics/psychoactives
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marijuana, peyote, designer drugs (ecstasy), PCP, hashish, psilocybin, LSD, ketamine
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federal drug schedules
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1.heroine, LSD, marijuana, designer drugs 2. morphine, cocaine, methadone, methamphetamine 3.anabolic steroids, codeine/hydrocodone, most barbiturates 4.darvon, BDZs, anxiolytics 5. cough medicine with codeine
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health risks of stimulants
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sudden arrythmias, cardiac failure, risk of acute psychosis, perceived subjective superiority in performance, risk of physical dependence strong
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health risks of hallucinogens
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mental health problems, bad trips/flashbacks, erroneous substances, psychological dependence mostly only with PCP or ketamine
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health risks of opiates
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overdose, coma, respiratory depression, emesis, HIV from needle sharing, malnutrition, contaminants in drug, strong risk of dependence
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health risks of depressants
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overdose, respiratory depression, emesis, contaminants, strong risk for physical dependence
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health risk of cannabis
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smoking related respiratory problems (higher tar content than cigarettes), mild immunosupression, problems with adulterants, herbicides
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potential clinical uses of cannabis
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antiemetic/nausea suppressant, relief of ocular pressure in glaucoma, anxiolytic
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cannabinoid receptors
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CB1 and CB2, role in neural plasticity, both tied to Gs. CB1, the beta gamma subunit inhibits N and P type VDCC and increase activity of Ia channels and rectifier channels
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health risks of anabolic steroids
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immunosupression, cardiac hypertrophy, cardiac failure, acceleration of male balding, induction of prostate cancer and other tumors, risk of acute psychosis
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HHPA axis and stress hormone regulation
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circulation of CRF to anterior pituitary, release of ACTH, adrenals release glucocorticoids, circulate to hippocampus, inhibited, shuts down pathway that allows the release of hormone
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ACTH
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signal for production of corticosteroids, comes from a longer peptide sequence POMC
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adrenal cortex
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outermost layer detects angiotensinII. zona glomerulosa respond to AII signal, detect ACTH and release glucocorticoids
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Where is epinephrine released?
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from the adrenal medulla
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steroid binding and release
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corticosteroids are released at a high rate, gonadal steroids released in small amounts. Corticoisteroids are mostly bound to plasma proteins, so have no effect. cortisol binds to receptors for other adrenal hormone, mineralocorticoids
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clinical corticosteroids
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betamethasone, cortisol, dexamethasone, prednison
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clinical corticosteroid uses
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replaces endogenous ligands (Addison's disease), supress inflammation and immune response (arthritis, asthma, lupus, IBS, hepatitis, dermatitis) prevent immune reaction in chemotherapies
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COX inhibitor
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aspirin
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NSAIDs
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acetaminophen, ibuprofen, naproxen
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COX1
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required for gastric function
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COX2 inhibitor
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more specific and avoid gastrointestinal side effects. Celecoxib (celebrex), may cause heart attack
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uses/abuses of opiate peptides
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analgesia, cough supressant, prevention of withdrawal, sedation, other psychotropic effects
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categories of opiate receptors
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Mu, delta, kappa, ORL1. All Gi/Go
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Mu opiate receptor endogenous agonist
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beta-endorphin
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mu opiate receptor selective exogenous agonist
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morphine
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mu opiate receptor selective anatgonist
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cyprodime
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delta opiate receptor endogenous agonist
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leu-enkephalin, met-enkephalin, deltorphin
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kappa opiate receptor endogenous agonist
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dynorphin A
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ORL1 opiate receptor endogenous agonist
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nociceptin/orphanin
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Where do enkephalin's come from?
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hypothalamus
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nonspecific antagonist for opiate receptors
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naloxone, naltrexone, dprenorphine
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organic opium alkaloids
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narcotine, papaverine, thebaine, morphine, codeine
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modified opiates
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oxycodone(percodan, oxycontin), diacetylmorphine(heroin), hydromorphine(dilaudid), hydrocodone(vicodin)
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synthetic opiates
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fentanyl, meperidine, propoxyphene, bprenophrine, methadone
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opiate anatgonist
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naloxone, naltrexone
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addiction/dependence
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upregulation of AC leads to increased cAMP production leads to increase in PKA activity. Increase in PLC activity
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withdrawal symptoms of opiates
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early symptoms: greater increase in AC activity, yawning, loss of appetite, restlessness, irritability, runny nose.
Longer duration: tremors, panic, chills, sweating, cramps, nausea, vomiting |
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overdose symptoms of opiates
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initial: slow shallow breathing, restricted pupils, severe drowsiness, cold, clammy skin.
life threatening: convulsion, vomiting, severe respiratory depression, loss of consciousness, coma |
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sigma opiate receptors
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not actually opiates, part of the amino acid sequence for NMDA receptor. Not an independent type of receptor, part of the sequence for most types of ion channel. Include haloperidol, ketamine, PCP, pentazocine, DTG, ifenprodil
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degradation of ethanol
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acted upon by alcohol dehydrogenase to an aldehyde, which is transported nto the mitochondria, acted upon by aldehyde dehydrogenase (rate limiting enzyme) to end with acetic acid
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THP
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tetrahydropapaveroline, formed after alcohol degradation processes are exhausted, made of aldehyde intermediate and dopamine. It is an opiate analog that counteracts the feeling of the aldehyde
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volatile anesthetics
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nitrous oxide, diethyl ether, chloroform, isoflurane, sevoflurane
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Where does serotonin come from?
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raphe nucleus, dorsal has projections to many sites, median has a very specific pattern of innervation
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serotonin synthesis
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L-tryptophan acted upon by tryptophan hydroxylase to produce tryptomine(substrate) acted upon by AAADC to produce serotonin
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serotonin degradation
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broken down by MAO or COMT end with aldehyde, broken down by aldehyde dehydrogenase to produce 5-HIAA
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MAO inhibitors
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carbidopa, fenfluromine(blocks TryOHase), disulfrem (blocks AD)
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serotonin receptor transporters
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two types, vesicular and synaptic. both blocked by fenfluramine. vesicular is proton dependent with aTPase. Synaptic is Na and Cl dependent
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SSRI
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fluoxetine(prozac), sertraline(zoloft), citalpram(celexa), paroxetine(paxil), fluvoxamine(luvox)
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serotonin receptors
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5HT1a,1b,1d,1e,1f, use Gi/Go. 5HT2a,b,c, use Gq. 5HT3, not metabotropic, A and B are heteropentameric ion channel. 5HT4-like receptors include 5HT4,6,7 , use Gs.
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ubiquitous serotonin agonists 5HT1
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serotonin, quipazine
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selective serotonin partial agonist 5HT1
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LSD, psilocybin (psilocin: active metabolite)
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selective full agonist 5HT1a
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buspirone, DPAT, bufotenin, DMT
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selective full agonist 5HT1b and 5HT1d
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ergotamine, methysergide, sumatripan
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selective antagonist 5HT1a
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spiperone
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selective antagonist 5HT1b and 5HT1d
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isomoltane
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selective antagonist 5HT1e and 5HT1f
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methiothepin
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nonselective serotonin antagonist 5HT1
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pindolol
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nonselective serotonin agonist 5HT2
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serotonin, quipazine, alpha-me-5HT
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partial agonist 5HT2a
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LSD-25, psilocybin, phenlethylamine, mescaline
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5HT2a selective agonists
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DMT, DOI, DOB, DOM
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5HT2c selective agonist
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agonelatine, stimulates sateity
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5HT2a selective antagonist
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ketaserin, antischizophrenia
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5HT2b selective antagonist
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metergoline
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5HT2c selective antagonist
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ritonserin, methysergide
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nonselective antagonist 5HT2
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mesulergin, dibenzyline
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At which 5HT receptors are psychedelic drug effects mediated?
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5HT2a receptors
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5HT3 nonselective agonist
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serotonin, quipazine
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5HT2 selective agonist
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CBG, 2-me-5HT
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5HT3 selective antagonist
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ondansetron(zofran), zacopride, antiemetics
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nonselective 5HT4-like receptor agonist
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serotonin, quipazine
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5HT6 partial agonist
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LSD, methysergide
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5HT7 partial agonist
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8-OH-DPAT, psilocin, psilocybin, methysergide
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5HT6 selective agonist
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EMDT, CTST
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5HT7 selective agonist
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COAT
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5HT6 selective antagonist
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amoxipine
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5HT6 and 7 nonselective antagonist
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clozapine
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melatonin
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metabolite of serotonin, serotonin broken down by 5HT N-acetylase into n-acetyl-5HT which is broken down by 5-OH-indol-OMT into melatonin. This occurs in the pineal gland
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HA biosynthesis
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l-histadine, enzyme histamine decarboxylase product is histamine. Brocresine will block HD and histmine synthesis
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HA degradation
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start with histamine, broken down by methyltransfersase. Can be blocked by tacrine and metoprine. MAO-b produces aldehyde, aldehydehehydrogenase produces acetate. ALD-DH blocked by disulfram. Peripherally start with diamine oxidase creates an aldehyde intermediate
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peripheral HA
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H1Rs, inflammation(mast cells).
H2Rs, digestion |
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Origins of CNS HAminergeic projections
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HA produced in hypothalamus, tuberomammillary neurons.E1-E5 synthesize and release histamine.
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HA receptors
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H1:Gq, post-synaptic, multiple peripheral cells responsible for allergic/inflammatory responses.
H2:post-synaptic, gastric parietal cells. H3: pre and post-synaptic H4: pre and post-synaptic, leukocytes |
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Uses/potentials of HA ligands
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peripheral H1 antagonists: anti-inflammatory, allergy treatment, anti-congestive
peripheral H2 antagonist: antacids central H1 antagonist: anti-emetics/antidizziness peripheral H1 agonist: antihypertensive H3 agonist: role in hibernation Central H3 antagonists: AD, nootropics, ADD therapy, anti-obesity treatment |
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HA agonists
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histamine(1-4), histaprodifen(H1), dimaprit(2), imetit(3 and 4), proxyfan(3), clobenprofit(4)
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H1 competitive antagonists (antihistamines)
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chlorpheniramine, diphenhydramine(benadryl), cetirizine(zyrtec), cyclizine, loratadine(claratin), fexofenadine(allegra), dimenhydrinate(dramamine), mecilzine, promethazine, triprolidine
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competitive antagonist HA (not H1)
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cimetidine(tagamet H2), ranitidine(zantac H2), clobenpropit(H3), thioperamide(H3 and H4)
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inverse agonist
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tiotidine(H2) decrease in acid signal
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