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pharmacologt test 1b
| Term | Definition |
|---|---|
| neurotransmitters | chemical messengers that enable neurons to send signals to other neurons |
| 4 criteria for classification of a chemical as a neurotransmitter | 1. synthesized in a presynaptic neuron 2. stored in presynaptic vesicles 3. released from presynaptic neuron axon terminal when an ap is fired 4. must affect postsynaptic neuron in same way way |
| neurotransmitter small molecules | amino acids, monoamines, acetylcholine |
| amino acids | glutamate, glycine, GABA |
| monoamines | serotonin, histamine, catecholamines. aka biogenic amines. one amino group connected by 2 carbons to aromatic ring |
| catecholamines | dopamine, norepinephrine, epinephrine |
| neuropeptides | neurotransmitters (ex endorphins, orexins, substance P) |
| glutamate | excitatory neurotransmitter in brain. |
| GABA | major inhibitory neurotransmitter. |
| inhibitory amino acid neurotransmitters | glycine and GABA |
| excitatory amino acid neurotransmitters | glutamate, aspartate |
| astrocyte key roles w/GABA and glutamate | 1. supply GABA and glut w/ glutamine (precurser for GABA and glut) 2. absorb glut and GABA form synapase via GABA-glutamine or glutamate-glutamine cycle |
| location and key roles of glutamate | sleep/wake, learning, prolonged exposure can be toxic (excitotoxicity) |
| glutamate synthesis | all over CNS, synthesized in presynaptic mitochondria by krebs cycle and from glutamine (from astrocytes via glutamate-glutamine) by glutaminase |
| how is glutamine removed from synapse? | active transport re uptake into presynaptic neuron and into astrocytes |
| location and key roles of GABA | all over CNS, roles in motor control, vision, anxiety |
| GABA synthesis | glutamate converted into GABA by GAD (L-glutamic acid-1-decarboxylase) |
| monamine degradation | typically MAO (enzyme monoamine oxidase) |
| Serotonin (5-HT) location and key roles | in enterochromaffin cells in GI tract (regulate intestine movement), in platelets (vasoconstrictor), in brain affects mood, appetite, sexuality, sleep |
| serotonin synthesis | Tryptophan converted to 5-hydroxytryptophan (5-HTP)--RATE LIMITING STEP-- then into 5-hydroxytryptamine (5-HT/serotonin) by aromatic amino acid decarboxylase |
| serotonin removal | reuptake into presynaptic neuron via Serotonin transporters (SERT) and enzymatic degradation (MAO) |
| histamine location and key roles | made by white blood cells. involved in immune response, itching, allergies. in brain hist. is made by small groups of neurons in hypothalamus and regulates sleep and circadian rhythms |
| histamine synthesis | L-histadine synthesized by histadine decarboxylase (HDC) and packaged into vesicles by VMAT-2 |
| histamine removal from synapse | enzymatic degradation by histamine-N-methyltransferase (HNMT) |
| catecholamines | monoamines with catechol group and side chain amine. DA, NE, EP. side group looks like cat head |
| how are catecholamines made? | all downstream products of amino acid tyrosine. |
| what drugs alter catecholamine levels? | COMT inhibitors |
| Dopamine (DA) location and key roles | all over the body. chemical messenger in kidney, pancreas, GI tact, blood vessels. in brain mediates movement, motivation, reward/addiction, and hormone release |
| Dopamine synthesis | made in cytoplasm from L-DOPA by dopa decarboxylase then packaged into vesicles my VMAT to prevent metabolism/degradation |
| Dopamine removal | degraded by enzymes monoamine oxidase (MAO), catechol-o-methyl transferase (COMT), or reuptaken into presynaptic neuron via dopamine transporter (DAT) |
| norepinephrine location and key roles | produced by adrenal glands, promotes fight or flight. in brain produced by small group or neurons for roles in alertness, memory, and attention |
| norepinephrine (NE) synthesis | Dopamine (DA) packaged into vesicles that also contain dopamine B hydroxylase (DBH) which converts DA into NE inside the vesicle |
| norepinephrine removal | mainly reuptake into presynaptic neuron via NE transporter NET, and degraded by enzymes MAO, COMT |
| Acetylcholine (ACh) location and key roles | at neuromuscular junctions (enables movement) and in specific circuits in the brain for motor control and memory. loss of ACh can lead to impaired memory. |
| Acetylcholine synthesis | made from acetyl CoA and choline by enzyme choline acetyltransferase (ChAT). put into vesicles by vesicular ACh transporter. cholinen availability is rate-limiting. |
| acetylcholine removal | degraded by acetylcholinesterase (AChE) into acetic acid and choline. choline (NOT ACh) is transported back into presynaptic neuron to make ACh. |
| neuropeptides | large molecules, made of 3 or more amino acids, made by many types of neurons, made in cell body, packaged into large dense core vesicles, modulate neuron function, metabotropic receptors. |
| neurotransmitter receptor | protein that receives chemical signal from outside the cell and generates cellular response |
| 4 kinds of receptors | 1. GPCR (metabotropic) 2. Channel linked receptors (ionotropic receptors) 3. enzyme linked receptors (kinase-linked) 4. nuclear receptors |
| what type of receptors can NT bind to activate? | ionotropic receptors and GPCRs |
| NT and receptors | NT activate receptor on postsynaptic neuron. |
| autoreceptors | regulate signaling levels. NT activates receptor on presynaptic neuron. enable neuron to sense how much NT is releasing. if activated too much can inhibit NT release or synthesis. |
| 5-HT1 mechanism & potential | serotonin, decrease cellular levels of cAMP, inhibitory |
| ionotropic receptors | ligand activated ion channels. multimeric protein complexes |
| multimeric protein complexes | outer regions have specific NT/chemical binding sites. membrane spanning segments form ion channel. NT binds to receptor, it opens, ions flow in or out down concentration gradient to cause EPSP or IPSP. rapid (1ms) |
| ion channels | selective for certain ion or ions |
| what ions do GABA receptors allow? | Cl- can enter |
| what ions do glutamate AMPA receptors allow? | Na+ and Ca2+ (if lacks GluR2 subunit), only. Ca2+ (if GluR2 subunit present) |
| homomeric ionotropic receptor | all subunits are the same |
| heteromeric ionotropic receptor | different combinations of subunits that dictate properties of receptor |
| drugs vs ionotropic receptor | 1. bind to specific subunit, change conformation of receptor which can alter rate/duration of ion flow or change ability of other chemicals to activate receptor 2.block channel to prevent ions from passing through |
| GPCR structure | 7 transmembrane alpha helices connected by extracellular and intracellular loops. metabotropic. takes longe to produce effects |
| metabotropic | GCPRs, produce effects indirectly. take longer to produce their effects but effects can last longer than ionotropic receptors. can produce excitatory or inhibitory responses. |
| G protein activation | 1. G protein floats around 2. G protein and NT bind to GPCR. g protein becomes activated exchanging GGDP for GTP 3. activate G protein splits into Ga and Gby complex 4. Ga breaks down GTP to GDP and inactivates Ga until meets another BGY |
| activated G proteins and effector proteins | -g protein gated ion channels or -g protein activated enzymes (activate downstream signaling molecules) |
| g protein gated ion channels | effectors that produce a faster, transient, more localized effect. excitatory or inhibitory, depending on channel triggers EPSP or IPSP |
| g protein activated enzymes | effectors that produce slower, more permanent/widespread effect. more complex than just EPSP Or IPSP |
| ga protein effectors | adenylyl cylcase (AC) and phospholipase c |
| GS a | stimulatory g protein, activates AC |
| Gi a | inhibitory G protein, inhibits AC |
| what is AC and what does it do in a g protein? | stimulates second messenger cyclicAMP, which activates PKA and transcriptions factors (CREB) |
| downstream effects of second messengers in GCPR? | altered protein activity, transcription rates, ion channel activity, etc |
| Gq a | stimulatory G protein, activates phospholipase c which splits PIP2 into DAG and IP3. DAG increases PKA. IP3 simulates release of CA2+ |
| what messenger does phospholipase C stimulate? | IP3 and DAG |
| opioid receptors | mew, gamma, kappa |
| acetylcholine receptors (even number) | M2 (inhibitory) GPCR M4 (inhibitory) GPCR (decrease adenylyl cyclase) |
| acetylcholine receptors (odd number) | M1 (excitatory) GPCR M3 (excitatory) GPCR M5 (excitatory) GPCR (stimulatory, coupled to Gq q) splits PIP2 into DAG and IP3. DAG increases PKA. IP3 simulates release of CA2+ |
Created by:
gillianfreeby