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ElecChemSigPt2
ElectricalChemicalSignaling_Part2
| Question | Answer |
|---|---|
| What are characteristics of graded potentials? | 1. NOT all or none 2. Graded: may increase/decrease in size 3. decremental 4. summable/cancelable 5. local 6. may be excitatory or inhibitory |
| What are characteristics of graded potentials? | 1. NOT all or none 2. Graded: may increase/decrease in size 3. decremental 4. summable/cancelable 5. local 6. may be excitatory or inhibitory |
| Graded potentials can be decremental, what does that mean? | Over a period of distance on cell membrane, they will dissipate |
| Graded potentials are summable/cancelable, what does that mean? | The net result is we either get an action potential or we don't |
| What's the big deal about graded potentials? | They're important in processing information |
| What are the functions of graded potentials? | 1. integration 2. transduction |
| How do graded potentials function in integration? | 1. decision making at the cellular level (neurons) 2. called post-synaptic potentials (the process of forming charges happens here) |
| How do graded potentials function in transduction? | 1. conversion of stimulus into action potential (adding up all the + & -) 2. called receptor potentials 3. stimulus modality: chemical/mechanical/light(photons)/heat,cold/pain 4. receptors: chemo/mechano/photo/thermo(receptors)/nociceptors |
| Where is the location of graded potentials? | neuronal cell bodies & dendrites |
| How is the post-synaptic potentials created? | 1. neurotrans. binds 2 neurotrans. (chem. gated channel) 2. chem. gated chan opens allowing a. Na+ / Ca2+ influx creates excitatory post-synaptic potentials (EPSPs) OR b. K+ efflux or Cl- influx creates inhibitory post-synaptic potentials (IPSPs) |
| What happens when inhibitory post-synaptic potentials (IPSPs) are created? | membrane becomes MORE negative further away from threshold point at axon hillock |
| What does INFLUX mean? | brings in more POSITIVE, causing DEPOLARIZATION, membrane becomes LESS negative |
| What does EFFLUX mean? | brings in less POSITIVE, causing HYPERPOLARIZATION, membrane becomes MORE negative |
| Explain excitatory post-synaptic potentials (EPSPs) | 1. cause localized DEPOLARIZATION events (due to influx of Na+ or Ca2+ ions) 2. individually, unless they occur very close to axon hillock, nothing happens 3. may be summed |
| Explain inhibitory post-synaptic potentials (IPSPs) | 1. cause localized HYPERPOLARIZATION events (due to influx of Cl- or efflux of K+ ions) 2. may be summed to create greater hyperpolarization |
| How can summation be categorized? | 1. Temporal (over time) 2. Spatial (over space) |
| Describe Post Synaptic Potentials | 1. may be EPSPs or IPSPs 2. sum of all post-synaptic events is called the GRAND POST SYNAPTIC POTENTIAL (GPSP) |
| Explain GRAND POST SYNAPTIC POTENTIAL (GPSP) | 1. It's an ON or OFF event 2. If GPSP allows axon hillock to REACH THRESHOLD, an action potential OCCURS 3. If GPSP is NOT GREAT ENOUGH to reach threshold, or moves axon hillock membrane potential AWAY from threshold, NO action potential occurs |
| Refresh my memory, what are GAP JUNCTIONS again? | 1. direct flow via CONNEXONS btw cells (ions, cAMP) 2. found to some extent in most cells of body (exceptions: freely mobile cells - RBC's, sperm) |
| What role do connexons play in gap junctions? | 1. Connexons (formed by connexins) create a connection btw cell membranes of adjacent cells 2. Rate of flow depends on density of gap junctions |
| Why are gap junctions useful? | 1. for creating unified response in cardiac/smooth tissue 2. for modulating neuron activity in retina 3. communication btw glial cells in Central Nervous System |
| How do you alter the rate of movement in gap junctions? | Add more connexons |
| What is a chemical synapse? | The process that occurs between electrical synapses |
| Summarize the overall structure of a chemical synapse | 1. Transfers action potential to target cell/membrane via neurocrines/neurotransmitters 2. presynaptic neurons 3. postsynaptic cell 4. synaptic cleft |
| What is a presynaptic neuron? | In a chemical synapse, it's the neuron secreting CHEMICAL SIGNALS |
| What is a post synaptic cell? | In a chemical synapse, it's the cells receiving (with receptors on the postsynaptic membrane) the chemicals |
| What is a synaptic cleft? | The small space that the neurotransmitters diffuse |
| Describe chemical synapses PHYSIOLOGICALLY | Process of converting act. pot. (ELECTRICAL) at synaptic bulb to a MECHANICAL event that causes the release of neurotransmitters (CHEMICAL) that then creates a membrane potential (ELECTRICAL) event on the post synpatic membrane |
| Describe the process of synaptic transmission | 1. action potential DEPOLARIZES AXON TERMINAL 2. Voltage gated Ca2+ chans activated by DEPOLARIZATION, allows Ca2+ influx into SYNAPTIC BULB 3. Ca2+ triggers 2ndary msgr sys 4. neurotrans. bind to receptors on postsynaptic membrane |
| When Ca2+ triggers secondary messenger system during synaptic transmission, what happens? | 1. motor proteins attach to vesicles and move along cytoskeletal 'tracks' to docking proteins in presynaptic membrane 2. vesicle binds and release neurotransmitters into synaptic cleft |
| When neurotransmitter binds to receptors on the postsynaptic membrane during synaptic transmission, what happens? | A response is initiated (EPSP or IPSP) |
| Graded potentials can be decremental, what does that mean? | Over a period of distance on cell membrane, they will dissipate |
| Graded potentials are summable/cancelable, what does that mean? | The net result is we either get an action potential or we don't |
| What's the big deal about graded potentials? | They're important in processing information |
| hat are the functions of graded potentials? | 1. integration 2. transduction |
| How do graded potentials function in integration? | 1. decision making at the cellular level (neurons) 2. called post-synaptic potentials (the process of forming charges happens here) |
| How do graded potentials function in transduction? | 1. conversion of stimulus into action potential (adding up all the + & -) 2. called receptor potentials 3. stimulus modality: chemical/mechanical/light(photons)/heat,cold/pain 4. receptors: chemo/mechano/photo/thermo(receptors)/nociceptors |
| Where is the location of graded potentials? | neuronal cell bodies & dendrites |
| How is the post-synaptic potentials created? | 1. neurotrans. binds 2 neurotrans. (chem. gated channel) 2. chem. gated chan opens allowing a. Na+ / Ca2+ influx creates excitatory post-synaptic potentials (EPSPs) OR b. K+ efflux or Cl- influx creates inhibitory post-synaptic potentials (IPSPs) |
| What happens when inhibitory post-synaptic potentials (IPSPs) are created? | membrane becomes MORE negative further away from threshold point at axon hillock |
| What does INFLUX mean? | brings in more POSITIVE, causing DEPOLARIZATION, membrane becomes LESS negative |
| What does EFFLUX mean? | brings in less POSITIVE, causing HYPERPOLARIZATION, membrane becomes MORE negative |
| Explain excitatory post-synaptic potentials (EPSPs) | 1. cause localized DEPOLARIZATION events (due to influx of Na+ or Ca2+ ions) 2. individually, unless they occur very close to axon hillock, nothing happens 3. may be summed |
| Explain inhibitory post-synaptic potentials (IPSPs) | 1. cause localized HYPERPOLARIZATION events (due to influx of Cl- or efflux of K+ ions) 2. may be summed to create greater hyperpolarization |
| How can summation be categorized? | 1. Temporal (over time) 2. Spatial (over space) |
| Describe Post Synaptic Potentials | 1. may be EPSPs or IPSPs 2. sum of all post-synaptic events is called the GRAND POST SYNAPTIC POTENTIAL (GPSP) |
| Explain GRAND POST SYNAPTIC POTENTIAL (GPSP) | 1. It's an ON or OFF event 2. If GPSP allows axon hillock to REACH THRESHOLD, an action potential OCCURS 3. If GPSP is NOT GREAT ENOUGH to reach threshold, or moves axon hillock membrane potential AWAY from threshold, NO action potential occurs |
| Refresh my memory, what are GAP JUNCTIONS again? | 1. direct flow via CONNEXONS btw cells (ions, cAMP) 2. found to some extent in most cells of body (exceptions: freely mobile cells - RBC's, sperm) |
| What role do connexons play in gap junctions? | 1. Connexons (formed by connexins) create a connection btw cell membranes of adjacent cells 2. Rate of flow depends on density of gap junctions |
| Why are gap junctions useful? | 1. for creating unified response in cardiac/smooth tissue 2. for modulating neuron activity in retina 3. communication btw glial cells in Central Nervous System |
| How do you alter the rate of movement in gap junctions? | Add more connexons |
| What is a chemical synapse? | The process that occurs between electrical synapses |
| Summarize the overall structure of a chemical synapse | 1. Transfers action potential to target cell/membrane via neurocrines/neurotransmitters 2. presynaptic neurons 3. postsynaptic cell 4. synaptic cleft |
| What is a presynaptic neuron? | In a chemical synapse, it's the neuron secreting CHEMICAL SIGNALS |
| What is a post synaptic cell? | In a chemical synapse, it's the cells receiving (with receptors on the postsynaptic membrane) the chemicals |
| What is a synaptic cleft? | The small space that the neurotransmitters diffuse |
| Describe chemical synapses PHYSIOLOGICALLY | Process of converting act. pot. (ELECTRICAL) at synaptic bulb to a MECHANICAL event that causes the release of neurotransmitters (CHEMICAL) that then creates a membrane potential (ELECTRICAL) event on the post synpatic membrane |
| Describe the process of synaptic transmission | 1. action potential DEPOLARIZES AXON TERMINAL 2. Voltage gated Ca2+ chans activated by DEPOLARIZATION, allows Ca2+ influx into SYNAPTIC BULB 3. Ca2+ triggers 2ndary msgr sys4. neurotrans. bind to receptors on postsynaptic membrane |
| When Ca2+ triggers secondary messenger system during synaptic transmission, what happens? | 1. motor proteins attach to vesicles and move along cytoskeletal 'tracks' to docking proteins in presynaptic membrane 2. vesicle binds and release neurotransmitters into synaptic cleft |
| When neurotransmitter binds to receptors on the postsynaptic membrane during synaptic transmission, what happens? | A response is initiated (EPSP or IPSP) |
| What do neurocrines consist of? | Neurotransmitters, neuromodulators |
| List the NEUROTRANSMITTERS | (AAAPPGL) 1. Acetylcholine 2. Amines 3. Amino Acids 4. Peptides 5. Purines 6. Gases 7. Lipids |
| Describe Acetylcholine | 1. derived from choline & acetyl CoA 2. binds to cholinergic class of receptor which may be a. nicotine b. muscarinic 3. used widely a. by all preganglionic neurons in ANS b. by all postganglionic neurons of the PARASYMPATHETIC sys of ANS |
| What is NICOTINIC? | 1. Excitatory 2. Ion Channel Receptor (ICR) - Na+/K+ 3. Agonist = nicotine 4. Antagonist = curare & beta-bungarotoxin (causes paralysis) |
| What is MUSCARINIC? | 1. GPCR (G-protein channel receptors) 2. Mainly in smooth/cardiac muscle 3. Receptors also in CNS & glands (both exo/endocrine) 4. Agonist = muscarine 5. Antagonist = atropine |
| Describe AMINES | 1. derived from single amino acid TYROSINE 2. function as neurohormones |
| What are the 5 different neurohormones? | (DopeassNiggazEatinSeriousHistamine) 1. DOPAMINE 2. NOREPINEPHRINE 3. EPINEPHRINE 4. SERATONIN 5. HISTAMINE |
| Describe DOPAMINE | 1. produced in brain (substantia nigra, ventral tegmental area & hypothalamus) where it inhibits release of PROLACTIN 2. binds to dopamine receptors (at least 5) 3. GPCR 4. Targets the CNS |
| What is DOPAMINE's role in the substania nigra? | 1. Involved in reward/recognition as well as major player in muscle control (death of dopamine producing neurons in the substantia nigra is responsible for Parkinson's disease) 2. In the VTA, it is implicated in reward/cognition/motivation/addiction |
| What happens when DOPAMINE is given orally? | It will act as a SYMPATHOMIMETRIC, increasing heart rate and blood pressure, but will NOT affect CNS as it does NOT cross the blood brain barrier |
| Describe norepinephrine & epinephrine | 1. both produced in adrenal medulla 2. bind to ADRENERGIC RECEPTORS (alpha, beta) 3. GPCR 4. affects smooth/cardiac muscle tissue as well as exo/endocrine glands |
| Describe SERATONIN | 1. from TRYPTOPHAN (aa) 2. binds to SEROTONERGIC RECEPTORS (at least 20 diff ones) 3. activates ICR that regulate Na+/K+ |
| What is the function of SERATONIN in the CNS? | In CNS, functions include regulation of mood, appetite, sleep, muscle contraction, and some cognitive fx including memory and learning |
| Where is most SERATONIN produced? | By the enteroendocrine system (gut) in regulation of digestive function |
| Describe HISTAMINE | 1. From Histidine (aa) 2. Binds to Histamine receptors (GPCRs) in the CNS/PNS & system-wide (in CNS - modulates sleep) 3. 4 Receptors to date 4. Antagonists in CNS will induce sleepiness (ANTIHISTAMINES) |
| What are the FOUR major amino acids that function as NEUROTRANSMITTERS in the Central Nervous System? | 1. Glutamate 2. Aspartate 3. GABA 4. Glycine |
| Describe the amino acid GLUTAMATE (NT = neurotransmitters) | 1. most abundant/excitatory NT in CNS 2. involved in LONG TERM POTENTIATION (LTP) or synaptic plasticity 3. Binds to Glutaminergic ionotropic (iGluR) class of receptors: AMPA & NMDA 4. LTP - binding 2 NMDA cause cell 2 increase density of AMPA recep |
| Describe the amino acid ASPARTATE | Binds to NMDA receptors, but can also be an EXCITOTOXIN (increase excitatory nature of tissue) |
| Describe the amino acid GABA (NT = neurotransmitters) | 1. main INHIBITORY NT of BRAIN 2. bind 2 GABA receptors (ICRs that control Cl-) 3. Antagonist: PICROTOXIN: it is non-competitive, strong convulsive effects 4. Potentiators: alcohol, benzodiazapene & barbituates (also block AMPA recep. for glutamate) |
| Describe the amino acid GLYCINE (NT = neurotransmitters) | 1. main inhibitory NT of the SPINAL CORD 2. A CO-AGONIST with glutamate on NMDA receptors (in an excitatory role) 3. An ANTAGONIST is STRYCHNINE (causing convulsions, possibly death due to ASPHYXIATION) |
| What is BENZODIAZAPENES used for? | Over 80 drugs utilize it with most being ANTIANXIETY, ANTICONVULSIVE, HYPNOTIC in effect |
| Describe PEPTIDES | 1. Usu. 2 amino acids 2. may function as NT as well as NEUROHORMONES 3. may be involved with NEUROMODULATION in pain/analgesic pathways |
| What are some of the PEPTIDE NEUROHORMONES? | 1. CCK (Cholecystokinin) - secreted when gall bladder empties into duodenum 2. Vasopressin - controls blood pressure via kidney function 3. Atrial Natriuretic Peptide (ANP) - secreted by heart when atria stretched, increase urination |
| Peptides are involved in neuromodulation in pain/analgesic pathways such as... | 1. Substance P - Pain 2. Enkephalins 3. Endorphins 4. #2 & #3 are for PAIN REMEDIATION |
| List the 3 types of PURINES | They all bind to PURINERGIC RECEPTORS 1. adenosine 2. AMP 3. ATP |
| What is the purine ADENOSINE involved with? | 1. Sleep - levels of adenosine rise continuously after awaking, eventually shutting u down 2. Bind to adenosine receptors (A.R) which are GPCRs & modulate activity of adenylyl cyclase (A.C.) a. 2 AR's INHIBIT A.C activity b. 2 AR's INCREASE A.C. acti |
| Describe the purines AMP & ATP | 1. bind to receptor (GPCRs) and modulate intracellular levels of Ca2+ and cAMP 2. as adenosine depending on receptor, may have + or - effect 3. energy intermediaries |
| Which GASES act as neurotransmitters? | 1. NO - Nitric oxide 2. CO - Carbon Monoxide 3. H2S - Hydrogen Sulfide |
| T/F There is relatively little known about the gases as neurotransmitters | TRUE |
| What do we know about the gas Nitric oxide as a neurotransmitter? | 1. stimulates GUANYLATE CYCLASE, which forms cyclic GMP (cGMP) 2. cGMP activate protein kinase G, causing phosphorylation of myosin light chain phosphatase, which then activate myosin light-chain kinase 3. cause smooth muscle relaxation |
| Describe LIPIDS as neurotransmitters | 1. Eiconsoid neurocrines that bind to CANNABINOID receptors 2. There are 2 receptors |
| What are the TWO lipid cannabinoid receptors? | 1. CB1 - in brain & linked to psychoactive anture of marijuana 2. CB2 - mostly peripheral & associated with immune system a. pain/inflammation remediation b. CB2 don't cause psychoactive issues 3. can't activate CB2 w/o activating CB1 |
| What are the TWO basic receptor types? | 1. Ionotropic (ion channel-receptors) 2. Metabotropic (G-protein coupled receptors) |
| T/F There are multiple subtypes (isoforms) of receptors for each neurotransmitter (except gases) | TRUE |
| T/F Having two basic types of receptors allows for ONE NEUROTRANSMITTER to have MULTIPLE effects | TRUE |
| T/F Serotonin has 20 different receptor types identified | TRUE |
| Describe physiology of CHOLINERGIC & ADRENERGIC receptors | 1. Cholinergic may be nicotinic or muscarinic a. both bind acetylcholine b. binding events differ vastly |
| Where are NICOTINIC receptors found? | 1. They're ICR (Na+/K+) and found mainly in skeletal muscle, ANS of the PNS, and the CNS 2. Excitatory as DEPOLARIZATION occurs upon binding (influx Na+, efflux of Ca2+) |
| Where are MUSCARINIC receptors found? | 1. They're GPCR and found in CNS & ANS 2. reaction varies with receptor subtype & affect 2ndary messenger pathways |
| What are the TWO GLUTAMINERGIC RECEPTORS? | 1. AMPA 2. NMDA |
| Describe the GLUTAMINERGIC receptor AMPA | 1. ICR that cause DEPOLARIZATION (Na+ influx - excitatory) upon binding of glutamate 2. Does NOT bind to acetylcholine |
| Describe the GLUTAMINERGIC receptor NMDA | ICR (ion channel receptors) that are TRIVALENT CATION CHANNELS |
| What does it mean to be a TRIVALENT CATION CHANNEL? | Na+, K+, Ca2+ can pass thru BUT a. coactivation by glutamate & depolarizing event are required b. glutamate PARTIALLY opens channel c. depolarization causes Mg2+ to be REMOVED, OPENING channel COMPLETELY d. aspartate also bind to NMDA receptors |
| How is the rate of response for ICRs? | Ion flow is typically FAST (due to ion channels & GAP JUNCTIONS) 1. ligand binds to protein, channel opens 2. typical EPSPs and IPSPs |
| What is the rate of response for GPCRs? | Intracellular change is SLOWER 1. if the change is an electrical change, it is a SLOW synatpic potential 2. can be used for long term changes in potentiation |
| What are steps 1-3 to LONG TERM POTENTIATION? | 1. glutamate binds 2 AMPA/NMDA chans 2. Net Na+ entry thru AMPA channels depolarizes postsynaptic cell 3. depolarization ejects Mg2+ from NMDA receptor-channel and opens channel |
| What are steps 4-6 to LONG TERM POTENTIATION? | 4. Ca2+ enters cytoplasm thru NMDA channel 5. Ca2+ activates 2ndary messenger pathways 6. paracrine from postsynaptic cell enhances glutamate release |
| T/F FOREVER is bad when it comes to Neurotransmitter binding | TRUE |
| What kind of rules do neurotransmitter binding follow? | 1. reversible 2. equilibrium - if presynaptic neuron reuptakes its NT, the NT bound to the receptor has to leave to maintain equilibrium |
| How does on remove a neurotransmitter from binding? | 1. diffusion - uptake in synaptic bulb (requires ligand that can detach easily) 2. enzymatic activity in synaptic cleft 3. removal of receptors by ENDOCYTOSIS will limit the effect as well |
| T/F Neurotransmitters can be returned to axon terminals for reuse or transported into glial cells | TRUE |
| T/F Enzymes inactivate neurotransmitters | TRUE |
| T/F Presynaptic modulation take place at the AXON TERMINAL near the SYNAPTIC BULB | TRUE |
| Why does presynaptic modulation take place near the synaptic bulb? | allows for local/specific control of that synaptic bulb and associated post-synaptic receptors (may be inhibitory or excitatory) |
| T/F Postsynaptic modulation takes place at the cell and controls the axon hillock | TRUE |
| T/F Post synaptic modulations are less specific | TRUE, if EXCITATORY, ALL synapses are effected. if INHIBITORY, ALL synapses are affected |
| Give example of presynaptic modulation | 1. an excitatory neuron fires 2. an action potential is generated 3. an INHIBITORY neuron fires, blocking neurotransmitter relase at ONE synapse |
| Give example of postsynpatic modulation | 1. One excitatory and one inhibitory presynaptic neuron fires 2. modulated signal in postsynpatic neuron below threshold 3. no action pot. initiated at trigger zone 4. no response in ANY target cell |
Created by:
lophung