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PSB 2000

Hersey 1 Psb2000 Exam 2 Highlighted stuff is on exam PPT. # 1 Resting Potential & Action Potential Study Questions: 1) What ions are important in the action potential? When the cell is at rest, which ions are most highly concentrated inside of the cell, and which ones are most highly concentrated outside of the cell? – (Na+ & Ca2+),( )K+, Cl-() – The inside of the neuron is more negatively charged than the outside of the neuron and the neuron is said to be polarized • Prepares neuron for action potential – Sodium is more than ten times more concentrated outside the neuron’s membrane than inside the neuron; Cl is more concentrated outside too! – K+ is more concentrated inside – At rest ions highly concentrated outside cell: Na+ & Cl-. Inside cell K+& negatively charged organic molecules. 2) Understand the forces working on the ions (electrical gradient and concentration gradient). – Cells have a concentration gradient- a difference in distribution of ions between the inside & outside of a membrane therefore the cell is polarized (at rest an electrical gradient , an electrical gradient is maintained across the plasma membrane (negative charge is greater inside the cell ~ (-70Mv)) – Concentration gradient: ions flow from areas of high concentration to low! (Sugar in water) – Electrical gradient: ions flow to areas of opposite charge (OPPOSITES ATTRACT) • Negative to positive, positive charge to negative. – The cell has a resting potential: difference in voltage across the membrane of a cell (- 70mV) @rest. 3) What is a voltage-gated channel? Where are they? – Proteins in the membrane that control the entry of sodium into the cell. – Depend on how permeable the membrane is and the voltage difference across the membrane (depends on if they are open or closed) – During resting potential vgc is closed – During action potential vgc is open & Na+ flows freely into cell. 4) Understand the steps of the action potential, and how one leads to the next. How is an action potential started and propagated? What ion enters first? Thru what type of channel does it enter? What forces drive it inside? Why does that channel close? What channel opens next? What ion moves thru that? What forces drive that ion? Etc etc. – Action Potential is how we send the electrical signal from 1 part of the Nervous System to a more distant part. When Na+ enters the cell, it flows down the axon, depolarizing the neighboring membrane and thus opening other VGNaC’s. 3 Na+ enter first, thru vgnac’s. – Threshold is reached at the axon hillock – VG Na+ channels open – Na+ enters cell – VG Na+ channels close and VGKC’s open – K+ leaves the cell – So much leaves it, it becomes hyperpolarized – When it reaches resting membrane potential again it can conduct another action potential – Period of hyperpolarization is called the REFRACTORY PERIOD. – Na+ in, K+ out, refractory period & repolarization – When Na+ entered the cell it flowed down the axon, depolarizing the neighboring membrane and thus opening other VGNa+channels. • Transmitter dependant Na+ channels open first • Voltage dependant Na+ channels open second • V dependant Na+ channels close • Voltage dependant K+ channels open Hersey 2 • ^then close • Na/K pumps repolarize – Propagation of action potential depends on • Diameter of axon • Insulation (myelin) 5) Terms to know and understand with regard to neurophysiology: polarized, depolarization, hyper polarization, repolarization, resting potential, threshold. With regard to those last 2 terms, what voltage is resting potential? What voltage is threshold? Where threshold must be reached for an action potential to occur? – Polarized: at rest, an electrical gradient is maintained across the plasma membrane (neg charge is greater inside the cell) – As the cell becomes less negative , it is depolarized (less polarized) – As cell becomes more negative, it is hyperpolarized (more polarized) – After/during refractory period repolarization; Na/K pump helps repolarize – Resting potential: difference in voltage across the membrane of a cell at rest ~-70mV – Threshold: the critical level of depolarization that must be achieved to trigger an action potential. • So threshold at the axon hillock…Na+ comes in & diffuses down axon & will bring next segment 5a. With regard to those last 2 terms, 5b. What voltage is resting potential? 5c. what voltage is threshold? 5d. where threshold must be reached for an action potential to occur? a. ~-70mV resting potential b. less negative than -70 is depolarized (threshold) c. more negative than -70 is hyperpolarized d. must happen in the membrane. (positive?) 6) What is the sodium/potassium pump? What does it do? What purpose does it serve? – Reduced voltage causes hundreds of sodium gates in that region of the membrane to open briefly, sodium ions flood into the cell depolarizing the membrane, which opens more voltage gated ion channels so wave of depolarization occurs for the action potential – Acts to maintain proper concentrations of Na+ and K+ – Needed for maintaining resting potential and for recovery from an action potential. – 3 Na+ out for every 2 K+ in, so more positive on outside – uses 70% all ATP in brain 7) What is the purpose of myelin? What happens at the nodes of Ranvier? What is saltatory conduction? – Myelin – “thick duct tape” holds Na+ inside. Insulation, effects propagation of AP • In myelinated axons, action potential can “jump” down axons, much faster. • Allows long distance rapid communication. • Nodes of ranvier where AP occurs; between segments of myelin • Voltage-gated Na+ channels are concentrated here. – Saltatory conduction- (speeds process up without having to increase diameter of axon) is the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials without needing to increase the diameter of an axon. 8) What does it mean that an action potential is “all or none”? – Action Potentials either happen or not. It’s like “flushing the toilet” it doesn’t get bigger or smaller. Not all action potentials are the same, each travel at certain speeds. – AP’s either fire entirely or not; NO MIDDLE GROUND – Action Potentials differ from Synaptic Potentials in the way that they are “all or none” Hersey 3 PPT. #2 Synaptic Potentials, Neurotransmitters Study Questions: 9) Know the different parts of a synapse (presynaptic cell, postsynaptic cell, synaptic cleft, neurotransmitters, receptors, vesicles) – vesicles contain neurotransmitter – 10) Know what happens at a synapse (chemical transmission). – Synapses are ligand gated channels 11) Understand different types of ion channels (ligand- and voltage-gated). Where are ligand-gated channels located? What is a “ligand”? VGC LGC Where? On axon Where? At synapses Open when cell reaches certain voltage Opens when a ligand (NT) binds Allows ions in or out Allows ions through -(changes voltage of cell) -(changes voltage of cell & may also start biochemical (during AP these open) cascade within cell) 12) What is an excitatory synapse? What is an inhibitory synapse? For each one, what ion enters the cell? What does that do to the cell? Does it make an action potential more or less likely? – Inhibitory neurotransmitters (IN) allow chloride (a negatively charged ion) into the postsynaptic cell and lead to an inhibitory postsynaptic potential. Cause Hyper polarization called (IPSP) – Excitatory neurotransmitters (EN) allow sodium and/or calcium (positively charged ions) into the postsynaptic cell and lead to an excitatory postsynaptic potential. Slight depolarization called EPSP. – Excitatory Synapse- we make post synaptic more likely to have action potential, Na+ comes into cell & depolarizes it. Hence makes cell less negative. – Inhibitory Synapse-Hyperpolarize cell so it’s less likely to have Action Potential • Cl- makes cell more negative, brings cell away from threshold bc more negative! 13) Know what EPSP and IPSP are. How do these differ from an action potential? Excitatory Postsynaptic Potentials (EPSP) – Excitatory ion channels are permeable to Na and K + – Because of the electrical and concentration gradient, more Na moves into the cell than K + – The inside of the cell becomes more positive, hence causing a local depolarization – If enough depolarization occurs (for example, because the neurotransmitter released caused nearby ion channels to open), an action potential is generated (GRADED not all or nothing) Inhibitory Postsynaptic Potentials (IPSP) – Inhibitory ion channels are permeable to Cl and K + – Because of the concentration gradient (not electrical), Cl moves into the cell and K moves out of the cell – The inside of the cell thus becomes more negative, hence causing a local hyperpolarization – The hyperpolarization will make it more difficult for the cell membrane potential to reach threshold, thereby making it less likely that an action potential will be generated • Graded NOT all or nothing – ON EXAM: difference between Action Potential & Synaptic Potential: • Action Potential is: VGC, down axons, & all or nothing. • Synaptic Potentials: LGC, at synapses, & graded. 14) What are temporal and spatial summation? – Temporal summation: several impulses from 1 neuron over time. – Spatial summation: Impulses from several neurons at the same time. 2 or more locations are brought together. Hersey 4 15) What causes neurotransmitter release from the axon terminal? – The vesicle merges with the presynaptic membrane. – exocytosis 16) What is the difference between ionotropic and metabotropic receptors? Ionotropic – A type of synaptic receptor. The receptor and effector functions of gating are carried out by different domains of a single macromolecule – Gates are almost immediately opened for an ion to flow into cell Metabotropic – A type of synaptic receptor. The receptor and effector functions of gating are carried out by separate molecules. Compare ionotropic. – a sequence of metabolic actions that are slower and longer lasting 17) Where are neurotransmitters made? – Synthesized by neurons, packaged in vesicles – Large : made in soma (cell body) – Small: made in terminal 18) What happens to neurotransmitters when they are released, and how are they cleared from a synapse?  Released into synapse &binds to receptor on postsynaptic cell; ion channels opened &ions enter postsynaptic cell; change in activity of postsynaptic cell  Made in soma or terminal (depending on the NT)  1-100 mm/day  Removed from synapse by reuptake by presynaptic neuron, absorption by glia, or enzymatic degradation 19) Can a neuron release more than 1 neurotransmitter? Can you think of an example of this? – Yes, Motor neuron in spinal cord release acetylcholine (Ach) onto muscle fibers, and other branches of the same axon release both Ach and glutamate onto other spinal cord neurons. PPT. #3 Neurotransmitters & Hormones 20) What is the difference between ionotropic and metabotropic receptors? 21) Know the common neurotransmitters. What is the most common excitatory neurotransmitter? What is the most common inhibitory neurotransmitter? – glutamate: excitatory – GABA: inhibitory – ACh: voluntary muscles, autonomic NS – Dopamine: pleasure, movement, learning, decrease in depression, anxiety, parkinsons disease, raise in schizo – Serotonin: sleep, calm, eating, lower in depression, anxiety, aggression – Norepinephrine: autonomic NS Hersey 5 22) Where are neurotransmitters made? What neurotransmitters share a pathway of synthesis? What are the initial precursors (the first thing in the synthesis pathway) for dopamine, norepinepherine, epinepherine, serotonin and acetylcholine? – Large : made in soma – Small: made in terminal 23) What happens to neurotransmitters when they are released, and how are they cleared from a synapse? – Inhibitory or excitatory – Removed by: reuptake by presynaptic neuron – Absorption by glia – Or enzynamatic degradation – After released diffuse across synaptic cleft – What are initial precursors? o Dopamine: tyrosine o Norepinephrine: dopamine  Epinephrine: norepinepherine o Serotonin: tryptophan o ACh: choline 24) Can a neuron release more than 1 neurotransmitter? Can you think of an example of this? – Yes, some from same terminal, some different terminals • Motor neuron in spinal cord release Ach onto muscle fiber, other branches of same axon release both Ach and glutamate onto other spinal cord neurons – 25) For dopamine and serotonin: what are they involved in? – dopamine • 1. Reward – NUCLEUS ACCUMBENS • a. natural (food and sex) • b. artificial (drugs of abuse) • 2. Movement – Parkinson’s Disease • 3. Disorders: ADHD, Depression, – Schizophrenia, etc • *on exam asked adhd, depression, & schizophrenia all lack what? • agonist: : amphetamine, cocaine, antidepressants, Ritalin – serotonin • •Sleep, calm, eating; ↓ in depression, anxiety, aggression • agonist: SSRIs (prozac, paxil, etc); MDMA (Ecstasy); BuSpar (anti-anxiety) 26) Know the terms agonist and antagonist. – Agonist: a drug that mimics or increases effects of neurotransmitter – Antagonist: drug that blocks effects of a neurotransmitter 27) How are hormones transported around the body? What types of receptors do hormones use? – Blood – metabotropic 28) What brain region controls hormone release from the pituitary gland? – hypothalamus 29) What is different between the anterior and posterior pituitary, including what hormones are released from each lobe? – The anterior pituitary is glandular tissue, meaning that it makes and secretes hormones. This hormone production/release is controlled by the hypothalamus which is directly above the pituitary. • Adrenocorticotropic hormone (ACTH) Hersey 6 • Thyroid stimulating hormone • Prolactin (mammary glands) • Growth hormone; somatropin • Gonadotropins: follicle stimulating hormone – The posterior pituitary is neural tissue. It contains hormone-secreting terminal buttons of axons whose cell bodies lie within the hypothalamus. SO the hypothalamus makes these hormones, they are sent down the axons to the posterior pituitary, and released from the post pit into the bloodstream. • Oxytocin and vasopressin 30) What are some other glands in the body that pituitary hormones influence? – Thyroid – Mammary – Gonads- fsh and lh – Growth in general – *on exam answer was all of above 31) Understand the principle of negative feedback in hormone release. - One of the most important features of the endocrine system is its regulation (control) by negative feedback. This means that the glands within the endocrine system that stimulate the release of a hormone (for example, the pituitary) from another gland (for example, the thyroid) are eventually shut off, in a sense, so that too much hormone is not produced and a hormone imbalance is avoided. PPT #4 Drug Actions and Substance Abuse 32) In general, all drugs of abuse cause dopamine release in the nucleus accumbens. Okay, not a question, but KNOW THAT! 33) Stimulants: know some examples of stimulant drugs. What neurotransmitters do they increase? What are some behavioral effects? o Amphetamine (AMPH), cocaine, Ritalin (for ADHD), ecstasy o Increase dopamine, especially in nucleus accumbens o raise serotonin and nor epinephrine release o raise excitement, activity, alertness, mood o lower fatigue –Cocaine: what is its method of action (ie, what does it do at a synapse)? o Cocaine blocks reuptake of serotonin, dopamine, and nor epinephrine o Binds to DAT (dopamine transporter) blocking reuptake of dopamine o DAT maintains proper dopamine levels by removing excess dopamine from synapse o End effect is increase dopamine in synapse – “high” o Stored dopamine is depleted somewhat “crash” and depression –What does Ritalin do at the synapse? How is it different from cocaine? o Ritalin has same effect as cocaine on dopamine, but different time-course and dose (Ritalin increases and decreases slower; take less Ritalin at a time as compared to cocaine) o Different from cocaine bc of o Dose o Oral administration o Slow release formulas o More gradual effect: no sudden high –What does ecstasy do at the synapse? What are the effects of long-term use neurons? What are some psychological/cognitive effects? Know examples of hormones that ecstasy affects and the behavioral result. o Ecstasy (MDMA) increases the release…at high doses it also increases serotonin release. o At high doses stimulates serotonin release (reverses serotonin transporter) hallucinogenic effects, decrease in depression, and anxiety Hersey 7 o Large injections destroys dopamine and serotonin neurons thinner cell layers in some brain areas o Neurons may recover after few months of not using o Human users: more depression, anxiety, sleep problems, memory deficits, attention problems, and impulsiveness; even after 1-2 years of quitting o Hormones o Increase in oxytocin release  Social attachment stuff o Increase in vasopressin release  Antidiuretic; stimulates you to drink water •What is serotonin syndrome? Understand why drug interactions could cause it. o Serotonin syndrome: too much serotonin released into body bc of too much of a serotonin agonist or bc mixing drugs that act in come capacity as serotonin agonists •What type of receptor does nicotine use? What is the effect of long-term nicotine use on dopamine cells? o Increases dopamine release in nucleus accumbens o Stimulates nicotinic Ach receptor on VTA neurons, exciting them o Cells become less responsive than usual after repeated nicotine use (tolerance)  other pleasures (including nicotine itself) become less reinforcing •Opiates: know some example. What receptor do they use? What is the endogenous ligand of those receptors (in other words, we don’t have those receptors so we can use heroine…why do we have them)? How do opioids increase dopamine in n. accumbens? What is methadone, how does it work and why is it used clinically? o Examples: Morphine, heroine, methadone o Receptor: opioid receptors (aka endorphin receptors) o Why do you even have those?? So you can appreciate the effects of heroin?? Hint: Endorphins= endogenous morphines You have opioid/endorphin receptors b/c your brain makes its own opioids (called endorphins) that are helpful in pain control o On GABA neurons in VTA (GABA usually inhibits dopamine neurons in VTA that project to NA; inhibit the GABA neurons = disinhibition of dopamine neurons) o Methadone taken for heroin a
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