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neuro pharmocology
Psychopharmacology terms and info for first exam
| Question | Answer |
|---|---|
| endocytosis | the transport of solid matter or liquid into a cell by means of coated vacuole or vesicle |
| exocytosis | the transport of material out of a cell by means of a vesicle that first engulfs the material and then is extruded through an opening in the cell membrane |
| diazepam | An Agonist used to treat anti anxiety |
| ionotropic receptors | transmitter or ligand gated ion channels |
| flumazenil | antagonist at gaba They can be used to reverse the actions of an agonist or inverse agonist. Can be used to treat overdose of diazepam, |
| depolarize | excitatory signals in the post synaptic cell cause the membrane to depolarize so that the postive charge can flow into the cell Depolarized is going towards zero |
| hyperpolarize | inhibitory signals in the post synaptic cell cause the membrane to hyperpolarize whereby positive charge flows out of the cell or negative charges flow into the cell Hyperpolarized is going away from zero |
| quantum | the amount of transmitter in the vesicle |
| Synapse | The key structure across which information is transferred via the use of chemical neurotransmitters in the synapse Can be electrical or chemical |
| Bioavailability | How well the drug gets into the brain and to its site of action. The extent to which a medication is used by the brain. The bioavailability of a drug determines how much of a drug thats administered actually reaches its target |
| Inverse Agonist | This drug produces the effect that's opposite the action of an agonist When an inverse agonist binds to a receptor it produces the opposite response of the neurotransmitter |
| Antipsychotic Drugs | Produce their main therapeutic effect by diminishing psychotic symptoms, like delusions and hallucinations All antipsychotic drugs are antagonists of D2 receptors |
| Buprenorphine | Partial agonist at opiod receptors Low does produce an analgesic and rewarding effect. Higher doses fail to yield a stronger effect. |
| Alkaloid | any of the various organic compound normally with basic chemical property and usually containing at least one nitrogen atom Some include Nicotine, cocaine and morpheine |
| Agonist | has the same effect as the neurotransmitter. Binds to the receptor and mimics the neurotransmitter action |
| ligand | a molecule ie: an antibody, hormone or drug that binds to a receptor |
| furosemide | a widely prescribed diuretic used to relieve oedema. Brand names: Lasix, Avandamet, Jalyn, Flomax, Aricept |
| Allosteric | pertaining to regulation of the rate of an enzymatic process |
| pharmakokinetic | the branch of pharmacology concerned with the way drugs are taken into, move around and are eliminated from the body |
| Prodrug | an inactive substance that is converted to a drug within the body by the action of enzymes or other chemicals |
| Psychotropic Drugs | Drugs that influence behavior, affect mood activity or perception as a mood altering drug. Brand Names: Thorazine, Clorazil, Lamictal, Asimia, Celexa |
| Monoamine | Any of various biogenic amine neurotransmitters having a single amino group: dopamine, epinephrine, norepinephrine |
| reserpine | an indole alkoloid antipsychotic and anti hypertensive drug that's been used to treat high blood pressure and relieve psychotic symptoms Has numerous side effects |
| quetiapine | brand name seroquel Oral anti psychotic drug used to treat schizophrenia and bipolar disorder. Inhibits communication between nerves of the brain. Blocks dopamine type 2 and serotonin type 2. Can increase the sedating effect of other drugs that sedate |
| efficacy | The biological effect exerted by the binding |
| Potency | The strength of the binding between a drug and its target. The drug is the ligand and the target is the receptor |
| Transodermal | When a drug or chemical is absorbed through the skin. |
| saturability | saturability occurs when all the receptors are occupied |
| selectivity | receptors are selected for certain drugs |
| Hydrophillic | likes water |
| Hydrophobic | doesn't like water |
| colchicine | stops neurotransport |
| soma or perikaryon | cell body |
| Dendrite | the primary sites of synaptic contact |
| endoplasmic reticulum | a network of tubular membranes within the cytoplasm of the cell where proteins are synthesized |
| mitochondria | an organelle in the cytoplasm of cells that functions in energy production |
| dendrite | the branching process of a neuron that conducts impulses towards the cell |
| golgi complex | a membranous complex of vesicles, vacuoles, and flattened sacs in the cytoplasm of most cells: involved in intracellular secretion and transport |
| tetrodotoxin | poison found mainly in the liver and ovaries of fish which are eaten. Binds to the outside of the Na+ channel |
| channelopathies | ion channel abnormalities that are responsible for many human diseases |
| phenytoin | an anti convulsant used in a wide variety of seizures. Has effects on ion channels, active transport and general membrane stabilization. Adverse effect and interactions with other drugs. |
| carbamazepine | an anti convulsant used to control grand mal and focal seizures. Has effects on ion channels, active transport and membrane stability. |
| lidocaine | a local anasthetic and cardiac depressant. Block Na+ (sodium)channels and prevent the conduction of nerve impulses that signal the occurrence of tissue damage and therefore pain. |
| action potential | A neuron will depolarize from -70mV to 50mV once a neuron undergoes significant depolarization it generates an action potential. An AP is an all or none depolarization or repolarization of the membrane potential releasing neurotransmitters to other cells |
| lipid bilayer | cell membrane |
| ATP Pump | The ATP (adenosine triphosphate) pump removes three Na+ (Sodium) ions from the cell and introduces two K+(potassium) ions. |
| ouabain | ouabain is an inhibitor of the Na+ pump, used like digitalis Can slowly reduce the resting potential of neurons to zero |
| digoxin | inhibitor of the Na+ pump. Can slowly reduce the resting potential of neurons to zero |
| deactivation | deactivation occurs when the ion channel returns to its resting state when the membrane voltage change subsides |
| norepinephrine | a neurotransmitter and hormone. Rapid increases cause panic attack. High doses make you happy, really high dose makes you euphoric. Meds used to raise levels are serotonin and adderall |
| Na+ | a sodium ion |
| K+ | a potassium ion |
| ataxia | a lack of muscle coordination which may affect gait, speech, eye movement May be from mutation in the K+ channels |
| acetylcholine | a neurotransmitter that is a derivative of choline; released at the ends of nerve fibers in the somatic and parasympathetic nervous systems |
| dihydropyridines | L-type channel blockers |
| L-Type Channel Blockers | The L-type calcium channel is a type of voltage-dependent calcium channel. "L" stands for long-lasting referring to the length of activation. |
| dihydropyridines | L-type channel blockers |
| L-Type Channel Blockers | The L-type calcium channel is a type of voltage-dependent calcium channel. "L" stands for long-lasting referring to the length of activation. Targets for antianginal and antihypertensive drugs. |
| nodes of Ranvier | small gaps in the myelin sheath of medullated axons |
| docking | Synaptic vesicles release neurotransmitter only at the active zone of a nerve terminal. Vesicles must be specifically targeted to this region through a process called docking |
| ligand bonding | 1.The bonding should be specific The ligand must bond to a specific target. Protein specific binding is saturable. 2. Binding should be saturable. Non specific binding is not saturable. 3. Binding should attain a steady state. |
| G Protein Coupled Receptors | A large protein family of transmembrane receptors that sense molecules outside the cell and activate inside signal transduction pathways |
| Receptor Potential | A receptor potential is produced by sensory transduction. It is a depolarizing event resulting from inward current flow. The influx of current brings the membrane potential of the sensory receptor towards the threshold for triggering an action potential. |
| Graded Potential | Graded potentials vary in size. They arise from the summation of the individual actions of ligand-gated ion channel proteins, and decrease over time and space. They are distinct from voltage-gated sodium and potassium channels. |
| Passive diffusion | Passive transport means moving biochemicals and atomic or molecular substances across the cell membrane. Unlike active transport, this process does not involve chemical energy. |
| Saltatory Conduction | Saltatory conduction meaning to hop or leap is the disbursement of action potentials along myelinated axons from one node of Ranvier to another, that increases the conduction speed of action potentials without needing to increase diameter of the axon. |
| Summation | Summation is a method of achieving or inhibiting action potential in the postsynaptic neuron, when one presynaptic neuron does not generate enough neurotransmitter. |
| Temporal Summation | Temporal summation is an effect generated by a single neuron as a way of achieving action potential. |
| Synaptic Cleft | A fluid filled space seperating the presynaptic and postsynaptic neurons. Prevents nerve impulses from directly passing from one neuron to the next. |
| Docking | The first step in the exocytotic cycle. Calcium dependent.Synaptic vesicles release neurotransmitter only at the active zone of a nerve terminal along the plasma membrane. Vesicles must be specifically targeted to this area. |
| Priming | The 2nd step in the exocytotic cycle. Priming requires ATP hydrolisis and is calcium dependent Primed vesicles release neurotransmitter within a millisecond of Ca2 influx into the cell. |
| Fusion | The third step in teh exocytotic cycle The release of neurotransmitter triggered by the influx of Ca2 through voltage gated channels in the plasma membrane |
| The 5 steps of Endocytosis | Docking, Priming, Fusion, Endocytosis and recycling |
| Psychopharmacology | The study of drugs given specifically to treat mental illness |
| neuropharmacology | the study of drug interactions with the nervous system |
| Clonidine | agonist Alpha 2 Originally used for its peripheral action to decrease hypertension PNS But it was noticed that it helped opiate withdrawal (CNS and PNS) helped with Tourettes (CNS) and ADD (CNS) |
| Protein Names | Large, small, alpha, beta, group1 and group2 |
| what are the monoamine neurotransmitters | dopamine, norepinephrine, epinephrine, serotonin and histamine |
| Where are the dopamine (DA) neurons cell bodies | in the mid brain within the substantia nigra |
| what does norepinephrine do? | it regulates arousal, attention, vigilance and memory |
| where is norepinephrine synthesized? | within the medulla and pons -the locus ceruleus provides all of the norepinephrine to the cerebral cortex |
| what do neurotransmitters do to the post synaptic membrane? | they either depolarize (excite) or Hyperpolarize (inhibit) the post synaptic membrane. |
| What are the two forms of synaptic transmission? | Fast Synaptic Transmission uses the ligand gated channel and slow uses a g protein binding |
| What are the chemical groupings for the neurotransmitters? | amino acid transmitters, peptides transmitters, monoamines transmitters, and nucleotides transmitters |
| What are some amino acid transmitters? | Glutamate and GABA are amino acid transmitters |
| What are some monoamine transmitters | dopamine, norepinephrine, serotonin and acetylcholine are all monoamine transmitters |
| What are peptide transmitters | enkephalin and diffusable gases |
| what is enkephalin? | •peptids known as the brain's endogenous opiates, they are important for pain relief and pleasure •enkephalins - One of the endogenous opioids that binds to opiate receptors and is used as a neurotransmitter. |
| What are the five steps of neurotransmitter release? | 1)Docking, 2)Priming, 3)Fusion, 4)endocytosis, and 5)recycling |
| What is docking? | binding to the plasma membrane |
| what is priming? | priming is an energy dependent step to get the vesicle ready for release |
| what is fusion? | release of neurotransmitter |
| what is endocytosis? | recovery of vesicle membrane by a protein coat |
| what is recycling? | the reuse of the vesicle membrane |
| what are snare proteins? | they are located on the vesicle as plasma membrane and function to target and bind the vesicle to the membrane for exocytosis |
| what are stereoisomers? | two forms of the same drug that are mirror images of one another |
| What is clonidine | Alpha2 (adrenergenic) agonist. Originally used for its peripheral action to decrease hypertension (PNS) Then it was found to help opiate withdrawal (CNS and PNS) and helped with Tourettes symptoms and ADD (CNS) |
| What is a dose response curve | the curve that shows the response between ED effective dose and FD Fatal dose. |
| what is high throughput screening | a technique in which computer modeling allows the analysis of large numbers of chemicals as to their abilities to bind to proteins. |
| What is the cell body | the site of protein synthesis and neurotransmitter synthesis in some systems. |
| What is the axon | the axon is 200 times the diameter of the cell body and usually covered with myelin |
| What is the cytoskeleton | the scaffold of a neuron is comprised of interconnected filaments called microtubules, intermediate filaments and actin fibers |
| what are microtubules | Microtubules are proteins that have structural and transport functions. They are sometimes called Microtubule associated proteins (MAP) and they are cross linked with intermediate filaments to make a "skeleton" down the length of a neuron. |
| what are actin filaments | actin filaments form an underlying structure over the whole surface of the neuron and are "contractile" involved in transport. They are also highly concentrated in dendritic spines suggesting that they have something to do with synaptic contact. |
| What drug can be used experimentally to study the role of microtubules | colchicine disrupts microtubule function and can be used to study the role of microtubules. |
| what drug disrupts actin filaments | cytochalasin disrupts actin filaments and can be used to study their role in cellular function. |
| what is glutamate | Glutamate is made in cells in the brain and does not cross the blood brain barrier. It increases the neural activity of almost every cell in the brain. There are glutamate receptors on nearly every cell in the brain. |
| what is the glutamate reuptake process? | After glutamate is released its taken up by glial cells where it is converted to glutamine.Glutamine is released from the glial cells and taken up by neurons through a transporter molecule we don't know very well. |
| What are the two glutamate reuptake transporters? | The glutamine reuptake transporters are EAAC (Excitatory amino acid carriers) and EAAT (Excitatory amino acid transporters) |
| what kind of receptor is on nearly every cell in the brain? | glutamate receptors |
| what happens with high levels of glutamate? | high levels of glutamate cause neuron death. Ischemia (like from a stroke) can cause high levels of glutamate and neuron death. |
| what are two classes of receptors? | Ionotropic and metabotropic |
| what do the excitatory amino acids do? | they make neurons fire |
| what is one of the most widely used neurotransmitters? | glutamate |
| which of the nerotransmitters doesn't cross the brain barrier so is therefore in the brain? | glutamate |
| what happens in the excitatory amino acids reuptake process | the inside of the glial cells is converted to glutamine because the glial cells become bags of glutamate |
| Why is too much glutamate toxic to neurons? | Because it actually stimulates the neuron to death. |
| what would happen if there was no reuptake of glutamate? | everything in the neurons and cells would be dead |
| What happens when the glial cells die? | their membrane breaks and spills the toxic glutamate which causes a wave of cell death in the brain-then there is a second wave of cell death and this is much more dangerous.Once the glial cell spills the glutamate you are in big trouble. |
| What are the three ionotropic receptors you should know? | Kainate (Kainic Acid) even really small amounts will kill neurons, this will destroy all the cells and leave the fibrous tubes NMDA (N-methyl-d-aspartate) there are three types and AMPA |
| what are glutamate and aspartate? | charged amino acids |
| why is the NMDA receptor unique among all of the neurotransmitters? | because it requires the simultaneous binding of two different agonists (glutamate and glycine) Neither of these agonists alone can open the ion channel |
| what are some of the drugs that bind at the ionotropic , NMDA glutamate receptors? | cycloserine, Phecyclidine (PCP) MK 801 and ketamine. These drugs bind at or near the Mg2+ binding site and they occlude the NMDA receptor channel |
| psychotomimetic | a drug or substance that produces symptoms like those of psychosis-hallucinations and delusions |
| what is one of the most important consequences of NMDA receptor activation? | the long lasting changes in synaptic functioning called synaptic plasticity which include LTP (long term potentiation and LTD (long term depression) of excitatory synaptic responses in the hippocampus |
| which drugs bind to the metabotropic site? | An Agonist LY35740 , an agonist on the presynapse side decreases glutamate. |
| what is synaptic plasticity? | long lasting changes in synaptic function |
| what is an excitatoy molecule? | Glutamate (Glu) |
| what is an inhibitory molecule? | GABA |
| what does el dopa do? | increases dopamine in the neurotransmitter |
| what are the biogenic Amines? | Dopamine DA (affects the Motor systems) Norepinephrine NE (affects the sensory systems) Serotonin 5HT (Affects emotion systems) Acetylcholine Ach (Affects neuromuscular system) |
| What are the amino amides? | Glutamate Glu (excitatory molecule) GABA (inhibitory molecule)There are actually a lot more excitatory molecules in the brain. |
| what is a nucleotide neurotransmitter? | Adenoside (ADD)(Inhibitory Molecule) There are a lot of these in the cortex. Caffeine comes in and blocks the inhibitory |
| What kind of drug is a precursor? | Antagonist |
| What kind of drug inhibits synthesis? | Agonist |
| What happens when there is too much up regulation on the receptor? | Up regulation of the receptors will increase the levels on one side but it won't equalize on the other side. Because its binding to the receptors- Down regulation has to occur and it may take several days which is what we call withdrawal. |
| What is quantal release? | neurotransmitters being released in waves or packets where the vesicles are clustered. Caused by electrical stimulation |
| what is el dopa? | El dopa is the precursor to the neurotransmitters dopamine, epinephrine (adrenaline) and norepinephrine. A psychoactive drug synthesized from the amino acid L-tyrosine El Dopa crosses the blood brain barrier- used to increase dopamine concentrations. |
| What are the catecholamines? | the neurotransmitters dopamine, norepinephrine (noradreniline) and epinephrine (adrenaline) |
| what are microtubules? | Microtubules are proteins that have structural and transport They are sometimes called membrane-associated proteins MAP and they are crosslinked with intermediate filaments to make a "skeleton" and they transport stuff up on down the length of an axon. |
| what are actin filaments? | actin filaments form an underlying structure over the whole surface of the neuron and are contractile They are also highly concentrated in dendritic spines suggesting they have something to do with synaptic contract. |
| What drug disrupts microtubule function? | Colchicine and Colchicine D can be used to study the role of microtubules |
| what is the function of the cytoskeleton? | The cytoskeleton functions to transport proteins made in the cell bodyto axonal and dendritic processes. |
| What is reversablity of receptor bindings? | binding is usually reversible, |
| what breaks during Alzheimers Dementia? | the microfilaments on the axon |
| how do you get a neurotransmitter into a cell | its placed into a vessel and released, (vescalized) |
| what are the names of the synapses? | axodendritic synapses, axosomatic synapses, axo axonal synapses, dendrodendritic synapses |
| what are axo axonal synapses? | they are some of the most effective ways of transport. |
| what are some dendodendritic synapses? | looking at two dendrites you see vesicles on both sides. When the action potential is fired it goes into the dendrite |
| what happens when the neuron fires? | the drug goes everywhere on the neuron |
| what is the terminal ending called | the bouton |
| what do glial cells do | they help neurons process information biochemically |
| what are the names of the glial cells? | astrocytes(they help with oxygen and nutritional stuff in the neuron), microglia-small cells that migrate through the brain and dispose of dead tissue, and oligodendrocytes the cells that comprise the myelin sheath around the axon along with schwann cells |
| what is the blood brain barrier | anything that passes through the brain has to go through the capillaries, it has to go through the walls of the membrane they have to be lipid soluble, very small and electrochemical. Molecules that are less polarized are more lipid soluble |
| what does amphetamine do to the brain | amphetamine you have to take a lot of it to get any past the blood brain barrier |
| how does methamphetamine get into the brain? | Because methamphetamine (when smoked) gets through the blood brain barrier much more quickly because its lipid soluble, it goes to the brain immediately and is very rewarding because of its speed and efficiency. |
| what happens to steroids in the brain? | Steroids bind to a cytoplasmic receptor and are translocated to the nucleus where they alter protein synthesis. |
| What happens if you block or deplete the calcium channel | you won't get any neurotransmitter |
| what happens to the membrane of the vesicle? | It is absorbed into the neurotransmitter |
| what happens to steroids in the brain? | Steroids bind to a cytoplasmic receptor and are translocated to the nucleus where they alter protein synthesis. |
| What happens if you block or deplete the calcium channel | you won't get any neurotransmitter |
| what happens to the membrane of the vesicle? | It is absorbed into the neurotransmitter |
| what is freeze fracture? | a study where cells are frozen with liquid nitrogen and then fractured or broken through the synaptic gap and the ice is removed and and you can look at the structure of the vesicle with a microscope. |
| What are snap proteins? | snap proteins attract one another, they are membrane bound proteins. There are two kinds of proteins they are snap and snare proteins. |
| what are receptors? | pieces of protein that form a long chain. |
| what are snare proteins? | they mediate vesicle fusion in exocytosis |
| what are snare proteins? | they mediate vesicle fusion in exocytosis |
| what are snare proteins? | they mediate vesicle fusion in exocytosis |
| What binds on the GABA receptor? | PCP binds to the GABA receptor as do alcohol and barbituates. Thats why its hard to determine if a person is intoxicated with barbituates or alcohol because they are binding to the same site. |
| what happens when the receptor is activated by the neurotransmitter? | the alpha subunit releases GDP, then GTP binds to the alpha subunit |
| what happens when a drug is polysynaptic? | it means that the drug is being controlled by many neurotransmitters. |
| what is retrograde transport? | movement of material to the cell body carrying it to the axon. retrograde goes down |
| What does an agonist do in the brain? | an agonist will mimic the action of the neurotransmitter and hyperpolarize the cell. |
| what does an antagonist do in the brain? | It has the opposite effect of the neurotransmitter and depolarizes the cell. |
| What is the history of the neurotransmitter? | The neurotransmitter begins with proteins that you take in with your diet which are synthesized into neurotransporters which are transported into vesicle packages and then released and deactivated and the cycle starts over again. |
| How can we affect the amount of dopamine in the brain. | by increasing El dopa |
| what is anterograde transport? | movement of the material to the cell body carrying it up the axon. |
| what does amphetamine do to the vesicles in the brain | a drug that breaks up vesicles. Amphetamine causes a depletion of dopamine and epinephrine, once a depletion of dopamine and epinephrine occur the neurotransmitter won't fire. |
| What mechanism in the brain stops the action of a drug? | deactivation of the enzyme or enzymatic deactivation-it stops the neurotransmission of the drug. |
| what is curare? | a poison derived from plants that used to be used on the ends of arrows to kill |
| what does nicotine do in the brain? | it stimulates the receptor and then blocks it. Nicotine can be very toxic there is 60 mg in bug spray and a cigar has 120 mg. if you eat a cigar you'll be dead. |
| what does black widow toxin do in the brain? | It pours Ach over the synapse and it kills almost instantly |
| If a drug is a precursor what does it do? | its an agonist |
| what is a drug that inhibits the synthesis? | its an agonist |
| what is a drug that breaks up the vesicle? | its an antagonist? |
| what if a drug prevents release? | its an antagonist |
| what is a drug that helps release? | its an agonist. |
| what is a drug that blocks the reuptake? | its an antagonist |
| what are g proteins? | they are the second messengers and are metabotrophic-they change the metabolism of the cell. |
| what are the four ways in which signals are transduced in the brain? | The four means of signal transduction in the brain are 1) neurotransmitter binding-binds to an ion channel (ionotropic), 2)neurotransmitter activation of a g protein and coupled ion channel 3)Neurotrophic factors activate a biochemical cascade 4)Steroids |
| what is a kinase | kinase is a molecule that changes another molecule. |
| what is the process of the g-proteins second messenger? | as soon as they are bound these g-proteins couple and then you get a second messenger. The second messengers start the phosophoration cascades. |
| what are the seven second messengers? | 1)cyclic nucleotides 2)adenylil cyclase 3) guanylil cyclase 4)phosphodiesterases (these degrade the cyclic)5)Calcium 6)Phospholipase C 7)Aracidonic Acid Metabolites |
| what does aspirin do in the brain? | Aspirin inhibits cox and is a Cox synthesizer which then produces prostaglandins |
| What is nociception? | A neurophysiological term that refers to our ability to detect noxious stimuli |
| what drug affects pain processing? | Opiates affect pain processing and there is a long list of them. Morphine. Codeine and Oxycodone(Percolone) are low potency mu agonists both can be combined with acetominophen (Percocet) Hydromorphone HCL (Dilaudid) and fentanyl(sublimaze) |
| name some nonsteroidal antiinflammatory drugs? NSAIDS) | Ibuprophen, aspirin, indomethacin (Indocin)These drugs block prostaglandin synthesis by blocking the enzyme cyclooxygenase. There are two kinds of cyclooxygenase COX1 COX2 |
| what is the phosphorylation cascade? | Takes a high energy molecule and phosphorylates it down into a low energy molecule and thats where the energy comes from. The regulation occurs by protein kinase. The kinases remove the phospate groups Protein Kinase A |
| what is rofecoxib? | Rofecoxib (Vioxx)COX 2 inhibitors-antagonist that provides pain relief for chronic pain.Blocking this enzyme impedes the production of the chemical messengers called prostaglandins that cause the pain and swelling of arthritis inflammation |
| what is celecoxib? | Celecoxib is (Celebrex) A type of drug that selectively blocks the enzyme cox-2 (cyclooxygenase-2). Blocking this enzyme impedes the production of the chemical messengers called prostaglandins that cause the pain and swelling of arthritis inflammation |
| what is the drug called sumatriptan? | Sumatriptan is (Imitrex)An agonist used to treat migraines and cluster headaches |
| what is hydromorphone HCL? | Hydromorphone is (Dilaudid)(hydromorphone hydrochloride), a hydrogenated ketone of morphine, is an opioid analgesic. A high potency agonist Usually used for treating the pain of terminally ill patients |
| what is fentanyl? | Fentanyl is (Sublimaze) a high potency agonist Used for treating pain Frequently Usually used for treating the pain of terminal patients |
| what is zolmitriptan? | zolmitriptan is (Zomig) a drug used to treat migraines This is a 5HT receptor agonist |
| how do opiates work in the brain? | opiates bind to c fibers and cause presynaptic inhibition |
| what is pentazocine? | pentazocine (Talwin) usually used to treat pain with pregnant women because it reduces the danger of depressing respiration in the baby These drugs bind to kappa receptors |
| what are some disorders caused by GABA | alcoholism ethanol binds to GABA, sleep disorders GABA is responsible for half the problems you could think of. Epilepsy, Huntingtons |
| what are the benzodiazepines? | Diazepam (Valium) Chloradiazedoxide (Librium) Lorazapan (Ativan) Alprazolam (Xanax) |
| what is Vigabatrin | Vigabatrin (Sabril) is used to treat epilepsy Its a GABA inhibitor and an anticonvulsant. |
| what does gabapentin do? | causes GABA to release which greatly increases inhibition. when its released its terminated by reuptake. |
| what is hydroxynipecotic acid? | it decreases gaba reuptake by blocking the transporter and blocking inhibitors |
| what kind of drugs work well with GABA | Tricyclic antidepressants like desimpramine and amyltriptyline |
| what is bicuculline? | Bicuculline (GABITRI) is a competitive antagonist at the GABA binding site. |
| what is RO15-4513 | this is the ultimate party drug it blocks all of the GABA and everything that binds to it. Its basically a sober up pill and it works |
| what does tyrosine hydroxolase do? | increases stress and adds more dopa and more norepinephrine in the brain. Think caffeine, nicotine and morpheine |
| what are the drugs that affect locus ceruleus activity? | drugs that affect locus ceruleus activity are opium, alcohol, nicotine, cocaine, amphetamine and benzodiazepaines |
| what is yohimbrine? | an adrenergenic antagonist active in the norepinephrine pathways and the locus ceruleus |
| where are the pathways for dopamine? | in the midbrain and the amygda. Substantia nigra to the amygdyla is the pathway synthesis |
| what is cocaine | cocaine is a dopamine transport blocker in the brain DAT |
| where is serotonin built in the brain? | serotonin is made down in the brain stem, the raphe nucleus |
| what is fenflouramine? | fenflouramine is an amphetamine molecule that causes long term damage because it breaks up vesicles so it can't be released. |
| what is MDMA | MDMA is ecstacy it binds to the serotonin transporters and to the receptor as well, ecstasy has been used in therapy and is conducive to the helping the patient to speak more freely |
| what do all the receptors for DA and NE belong to | G proteins |
| what is VMAT? | one of the transporters for serotonin |
| what is reserpine? | a drug used as an antipsychotic that bends to VMAT one of the side effects is that it greatly increases the salt content so one thing you would not want to do is prescribe ECT-you would kill them |
| what is fluoetine? | Fluoxetine (Prozac) it blocks sert |
| What are some partial agonists? | Buspirone (Anti Anxiety),Sumatriptin (Partial Agonist), all of the hallucinogens, Anti-psychotics, clozapine (clozaril) risperadone (Risperidal), Olanzapine (Zyprexa) |
| what are the two types of receptors for acetylcholine? | the 2 receptors for acetylcholine are muscarinic and nicotinic |
| what are the muscarinic agonists? | The muscarinic agonists are atropine and scopalomine |
| where is nicotine an agonist? | at the nicotinic receptor |
| what are the 3 receptors for histamine | The three receptors for histamine are all g-proteins and they do not cross the blood brain barrier |
| what is rate limiting | rate limiting is the enzyme that the drug works on |
| what happens to choline in the brain? | choline is not degraded it is excreted if the level of choline goes down in your diet you will die |
Created by:
julie livingston
Popular Psychology sets