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65 Cards in this Set
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Describe the criteria that influence the choice of model systems used for studying physiology (5) |
1. Convenience - easy to rear and manipulate, cheap, short life cycle; easy repitition 2. Biomedical or economic importance - mosquitos, corn, pathogens; malaria, food source 3. Exhibit extreme adaptations - barn owl hearing, electric eel sensory systems 4. Phylogenetically important - can gleam information about modern species based on evolutionary similarities; hagfish and lamprey - preceeded neural development in modern species 5. Interactions among criteria |
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Explain why the cell membrane is selectively permeable, based on the structure and function of membrane transport proteins |
Transporter proteins selectively bind ligands based on charge and size and move them in at different rates Ion channels are fastest, permeases are medium, ATP-powered pumps are slowest Channels have protein domain arranged in a ring to form a pore, a wide area called the vestibule and a narrow area called the selectivity filter Filter lets substances in based on charge and size - Lined with regions of specific charge to let in one and repel the other - Selectivity filter is small so large ions cant go througb - Selectivity filter removes hydration shell by favourably binding (outcompeting) using its electronegative regions to small ions of a specific size to only let in one (eg. K+ instead of Na+ even though Na+ is smaller) Gated ion channels can be opened and closed by changes in voltage, binding of ligands and changes in mechanical force |
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Predict how modifications to the selectivity filters of membrane channels will affect movement of molecules across the membrane |
If the K+ selectivity filter became smaller, the electronegative amino acids in the filter wouldn't be arranged in a way that outcompetes water in binding to K+ and so it would no longer remove the hydration shell. Since K+ with the shell is too big to fit through the filter, K+ permeability would decrease However since the Na+ ion is smaller than K+, the amino acids could now outcompete water for binding to Na+ and thus may be able to remove its hydration shell. This would increase the permeability of Na+ instead across the membrane. |
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Use the Nernst equation to calculate the equilibrium potential (Eion) |
Equilibrium potential: potential at which there is no net movement of an ion across a membrane that is permeable to that ion (refers only to one ion) |
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Use the Goldman equation to calculate the membrane potential (Vm) |
Ions that influence the membrane potential must have a concentration gradient across the membrane and be able to move across the membrane. The more permeable, the more influence the ion would have Charge, concentration and permeability are factors |
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Explain how electrical and chemical gradients and changes in membrane permeability affect Vm |
Permeability: the more permeable an ion, the more influence it has on the membrane potential Chemical gradients: ions move down their chemical gradient in general, changing Vm requires very little ion movement and so no measurable change in concentration gradient Electrical gradient: Na+/K+ pump (3 Na+ out, 2K+ in) help establish resting potential by moving ions against their gradient to counteract the movement through leak pathways at the cost of ATP |
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Calculate the energy required to move a molecule against its concentration gradient to determine the feasibility of secondary active transport |
Free energy change is due to movement along a concentration gradient as well as changes in charge distribution Free energy in total is dGconc + dGvolt (cal/mol or J/mol) At equilibrium dGtotal = 0 |
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Compare and contrast the four functional zones of a neuron |
1. Reception - dendrites and cell body (soma) Incoming signals are received and changed to a membrane potential 2. Integration - axon hillock Converts Vm changes into action potentials 3. Conduction - axon AP travels along the axon 4. Transmission - axon terminals Transmission via gap junction (electrical) or conversion to chemical signal (NT) |
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Analyze factors that affect the magnitude and direction (depolarizing or hyperpolarizing) of a graded potential stimulated by an incoming signal |
Signals arriving at dendrites/soma open gated ion channels increasing permeability to that ion changing the potential of the cell Strength of stimulus - larger stimulus causes more NT release allowing more channels to open with channels opening for longer |
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Analyze factors that affect the relative magnitude of a graded potential as it travels from the signal reception site to the axon hillock |
Conduction with decrement - graded potential magnitude decreases with distance from the opened ion channel 1. Leakage of ions across membrane 2. Electrical resistance of the cytoplasm 3. Electrical properties of the membrane |
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Explain the chemical and electrical mechanisms involved in each of the three phases of a neuron action potential. |
1. Depolarization - temporal and spatial summation of graded potentials reaching the axon hillock If this change in Vm reaches threshold, voltage-gated Na+ channels open allowing a large influx of Na+, depolarizing the cell while voltage-gated K+ channels open more slowly after the Na+ channels open 2. Repolarization - Inactivation gate of VG Na+ channels close after some time of the activation gate being open while the K+ channels remain open, repolarizing the cell. VG Na+ activation gate also closes quickly during this time 3. After-hyperpolarization - K+ channels slowly close, hyperpolarizing the cell. The Na+/K+ ATPase then returns the cell to resting Vm. Excess K+ near the outside membrane diffuses away |
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Analyze how different factors affect the direction and frequency of action potentials as they are conducted along an axon. |
Direction AP generation relies on the positive feedback loop of depolarization --> VG Na+ opens --> more depolarization --> more VG Na+ open The density of VG Na+ channels need to be high in order for this to happen, only present at high density in the axon and so can open propagate from dendrite --> cell body --> axon AP travels by electrotonic current spread, VG Na+ channels that had just opened now have the inactivation gate closed so even though current spreads that way, it can't generate an AP after just generating it Frequency VG Na+ channels inactivation gate opens up after a certain amount of time and with Vm moving towards resting potential - while it is closed; absolute refractory period Strong enough stimulus after the VG Na+ inactivation gate is open, even if the cell is hyperpolarized of below resting potential can still stimulate an AP; relative refractory period |
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Compare and contrast neuron types based on their function and structure |
Function Efferent neurons - sends signals from brain to the body Interneurons - forms connections between neurons Afferent neurons - sends sensory signal from body to the brain Structure Multipolar: many processes (many dendrites, one axon) Bipolar: two processes (one dendrite one axon) Unipolar: one cell body, many axons |
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Infer the strength of a transmitted signal based on action potential frequency Neurotransmitter diversity |
Action potential frequency increases with stronger stimuli Stronger stimuli will send an AP during the relative refractory period while weaker stimuli will not K+ efflux and remaining inactivated Na+ channels contribute to the relative refractory period Absolute RP limits max frequency to 500-1000 AP per second (lasts 1-2ms) Many types released at different neurons - receptors are such that the same NT can be excitatory on one neuron and inhibitory on another |
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Analyze the influence of other types of voltage-gated ion channels (for example, Ca2+ or Cl-) on action potential shape |
VG Ca2+ channels depolarize the cell (Ca2+ influx) - sometimes used with VG Na+ channels, sometimes used instead of VG Na+ channels Influx of Ca2+ is often slower and more prolonged than Na+ influx - slower rate of AP due to longer refractory period Ligand-gated Cl- channels hyperpolarize the membrane |
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Types of glial cells with structures |
Schwann cells - myelinate cells in the PNS Oligodendrocytes - myelinate cells in the CNS Astrocytes - transport nutrients, remove debris in the CNS Microglia - remove debris and dead cells from CNS Ependymal cells - line the fluid-filled cavities of CNS |
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Predict how changes in the isoform and/or density of voltage-gated ion channels (Na+ and/or K+) in a cell membrane will affect action potential shape |
K+ channel isoforms - Activation threshold voltage of the channel to change - Speed of activation - Time channel remains open Na+ channel density - Higher density means lowered threshold voltage, increasing excitability |
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Predict how changes in capacitance and resistance will affect the conduction within an axon |
Intracellular resistance: as Ri increases, conduction decrement increases Extracellular resistance: as Re increases, decrement increases Membrane resistance: as Rm increases, decrement decreases More resistance = less K+ leak channels = less charge leaking out = less current decrement |
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Analyze how the cable properties of an axon determine the signal conduction speed of neurons |
Length constant (lambda) = distance over which the membrane potential will decrease to 37% of its original value Larger lambda = more distance covered Higher with increased membrane resistance and decreased intracellular resistance; ECF resistance is low and constant and so isn't factored in Higher lambda = faster speed of conduction due to more electrotonic flow (fast) relative to AP generation (slow) |
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Predict how changes in axon diameter will affect conduction speed Disadvantages of large axons |
Rm decreases with increased surface area More SA = more leak channels = less resistance Larger axon diameter = decreased Rm = decreased lambda Rm -proportional to r (SA of cylinder) Ri decreases with increased volume Larger axon diameter = decreased Ri = increased lambda Ri -proportional to r^2 (volume of cylinder) Increasing axon diameter increases length constant - increases conduction speed Limits number of neurons that can fit into nervous system (take up too much space) Large volumes of cytoplasm make them expensive to produce and maintain |
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Circuit properties of the membrane In series vs. in parallel |
Ions moving through VG channels cause a current across the membrane which spread through the cytoplasm Some leaks out of the axon completing the circuit Membrane = capacitor (Cm), two conducting layers (ICF and ECF) and an insulating layer of phospholipids Resistors ECF (Re or Ro) Membrane (Rm) Cytoplasm (Ri) Voltage drop (potential) is divided among the components vs. potential across a region is the same |
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Predict how changes in myelination will affect membrane resistance and capacitance |
Myelin acts as insulation - decreases current loss through leak channels Increases membrane resistance (Rm) --> increases lambda Decreases membrane capacitance - increases thickness of insulating layer Increases conduction speed without greatly increasing space required Current spreads electrotonically through internodes while new AP occur at nodes of Ranvier VG ion-channels only present at nodes of Ranvier |
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Explain why membrane capacitance affects the generation of new currents but not signal conduction along the axon |
Capacitance - amount of charge needed to create a potential difference between two surfaces of a capacitor Capacitors cause a delay in Vm change when putting charge in and also causes it to discharge more slowly Cm = SA/diameter Charge that first enters gets stuck on the capacitor first - slows down generation of new current Once the capacitor is full, charge flows freely down the membrane resistor and no longer affects current flow |
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Calculate the time constant for a change in membrane potential given the membrane resistance and membrane capacitance Effect of axon diameter and myelin |
Time taken for membrane potential to increase to 63% of its maximal value t = RmCm When charge travels across the membrane, it will first go through the capacitor. If capacitor charges faster, Vm will change faster When T is low - capacitor becomes fully charged faster, membrane depolarizes faster, electrotonic current spread is faster, current decays faster Higher T = faster signal conduction - current decays slower Axon diameter increases K+ channels, decreasing Rm but it also increases Cm thus T is not changed Decreases capacitance but increases Rm more - increases T |
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Define the parts of synapse |
1. Presynaptic cell 2. Synaptic cleft - space between presynaptic and postsynpatic cell 3. Postsynaptic cell |
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Explain how Ca2+ regulates neurotransmitter release |
Action potential depolarization opens VG Ca2+ channels. Intracellular [Ca2+] is very low, resting Vm also negative so strongly favours Ca2+ influx Ca2+ in active zone causes vesicles in the readily releasable pool (RRP) to fuse with the plasma membrane - exocytosis Ca2+ near reserve pool (RP) causes vesicles to move to the active zone and bind to docking proteins - NT ready for release following subsequent APs Ca2+ ATPase pumps Ca2+ out of the cytoplasm, intracellular buffers bind to Ca2+ internally |
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Determine how neurotransmitters causes distinct changes in postsynaptic cells. |
End-plate potentials: each receptor bound with 2 ACh causes a depolarization of 0.5uv; stronger stimulus = stronger EPP Always in unitary values - amount of NT released from a vesicle is always the same NT diffuses across synaptic cleft and binds to receptors in the postysynaptic cell Inhibitory - cause hyperpolarization, makes postsynaptic cell less likely to generate AP Excitatory - cause depolarization, more likely to generate AP Magnitude of response depends on [NT] in cleft and number of receptors in postsynaptic membrane |
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Distinguish between the major types of receptors |
Ionotropic NT receptors - ligand-gated ion channels; relatively fast (nicotinic) Metabotropic NT receptors - activation initiates signal transduction pathway - Opens ion channels - Modifies other proteins via second messengers that can produce slow, long-term changes (muscarinic) |
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Explain how neurotransmitter concentration is regulated in the synaptic cleft. |
1. Passive diffusion 2. Active uptake by surrounding cells (presynaptic neuron, astrocytes) 3. Degradation by enzymes in synaptic cleft - acetylcholinesterase |
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Myasthenia gravis - treatment SSRIs mechanism of action Cocaine Which DA receptor is involved in reward system Which DA receptor is lost in Parkinson's |
Autoimmune condition where acetylcholine receptors are attacked by antibodies - muscle weakness; treated by acetylcholinesterase inhibitors Inhibits reuptake of serotonin in the presynaptic cell - increases [serotonin] High efficacy in severely depressed, low in moderate Alkaloid that blocks reuptake of 5HT, NE, Da (triple reuptake inhibitor TRI) Hydrophilic and lipophilic - crosses BBB Blocks dopamine transporter (DAT) to increase DA Habitual use leads to down regulation of dopamine receptors - depressive mood D5 in limbic system D3 and D4 in the midbrain |
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Describe the mechanisms by which a receptor can be inactivated How is ligand signalling inactivated? |
1. Receptor down regulation - continued stimulation by the ligand causes the cell to break down existing receptors so as to maintain homeostasis
2. Receptor sequestration - receptor is moved into a vesicle during times of high [ligand] and is brought back to the membrane during times of low [ligand] 3. Receptor inactivation - ligand within the cell binds and inactivates the receptor 4. Inhibitory protein production - ligand-binding causes the receptor to produce a protein that inhibits the original receptor 5. Signal protein inactivation - protein-coupled receptor is inactivated by a ligand within the cell Enzymes in the liver and kidney break down hormones in blood - decreased extracellular [hormone] causes shift in equilibrium causing bound hormone to dissociate from their receptors |
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Describe the long-term effects of agonists and antagonists on receptor concentration Effect of adenosine as a neurotransmitter. Effect of caffeine, what happens after long-term use |
Agonists: receptors down-regulate as there is more ligand than usual; when agonists stop being used, effects opposite to those of the normal receptor are felt Antagonists: receptors up-regulate in response to decreased amount of ligand; when stop being used, hypersensitivity occurs Decreases CNS activity Blocks adenosine receptors in the CNS - gets up-regulated; people are more tired without coffee (more sensitive to adenosine) |
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Predict the relative number of receptors based on a saturation curve Why is nicotine considered a time-averaged antagonist |
More receptors = stronger response Higher curve means more receptors per cell After initial agonist action on nicotinic receptors, it causes desensitization and inactivation of neuronal nicotinic receptors Causes up-regulation of the receptors, smokers have more nicotinic receptors than non-smokers |
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Predict the receptor sensitivity based on a saturation curve |
Dissociation constant (Kd) = [ligand] at which half the receptors are bound to ligand Affinity constant Ka = 1/Kd Response increases when Ka increases (Kd decreases) Steeper saturation curve = higher affinity/sensitivity |
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Describe the four types of cell signalling |
1. Direct cell signalling - chemical messenger goes through a gap junction to another cell 2. Autocrine and paracrine signalling - chemical messenger goes a short distance past a synapse to another cell (auto = back to self) 3. Endocrine signalling - chemical messenger goes through bloodstream to another receptor 4. Neural signalling - signal is first sent electrically then chemically to a receptor |
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Mechanisms for termination of ligand-receptor signalling |
Concentration dependent
1. Ligand removed by distant tissues into the bloodstream - extracellular [ligand] low so ligand dissociates 2. Ligand taken up by adjacent cells - same mechanism Degradation 3. Ligand degraded by extracellular enzymes 4. Ligand-receptor complex removed by endocytosis of cell and then degraded Inactivation 5. Receptor inactivation throguh phosphorylation 6. Inactivation of signal transuction pathway through inactivating intracellular signalling proteins |
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Describe the components of transducers (4) How are signals amplified within a cell? |
1. Receiver
2. Transducer 3. Amplifier 4. Responser Transduction pathways usually have multiple steps where many substances are converted into active forms The greater the number of steps, the greater the amplification |
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Transduction pathway for intracellular receptors What are the binding domains of intracellular receptors Examples of intracellular hormone ligands |
1. Hydrophobic ligands pass through the cell membrane
2. Ligand binds to the intracellular ligand-binding domain causing a conformational change 3. Receptor-ligand complex diffuses through the nuclear membrane 4. DNA-binding domain of receptor binds to response element DNA sequences 5. Transactivation domain interacts with other transcriptional factors 6. Rate of transcription of target genes into mRNA changes 7. Transcriptional cascades may be activated as the proteins transcribed may also act as transcriptional factors or effect other pathways Ligand-binding, DNA-binding, transactivation Estrogen (ER-alpha), T, cortisol (steroid derivatives) |
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Transduction pathway for ligand-gated ion channels |
Ligand binds to binding-domain of receptor causing a conformational change
Conformational change allows ion into the cell changing the membrane potential/pH Change in cell environment leads to activation of other effects |
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Receptor enzyme binding domains Transduction pathway for receptor enzymes |
Extracellular ligand-binding, transmembrane, intracellular catalytic 1. Ligand binds to extracellular domain causing a conformational change in the receptor (some are dimerized) - activated form 2. Activated receptors phosphorylate or dephosphorylate proteins via the intracellular catalytic domain often leading to long phosphorylation cascades |
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Receptor tyrosine kinase (most common receptor-enzyme) transduction pathway up until Ras protein Ras protein phosphorylation cascade with MAP kinases Describe VEGFs, when are they produced, what is their effect |
1. Ligand (chemical messengers; growth factors, insulin) binds to the receptor causing dimerization and autophosphorylation 2. Phosphorylated receptors interact with protein kinase 3. Protein kinases signal to Ras protein switching it between the active (GTP) and inactive (GDP) forms GAP - active --> inactive GNRP - inactive --> active 1. Activated Ras signals to MAPKKK and phosphorylates it 2. MAPKKK phosphorylates MAPKK 3. MAPKK phosphorylates MAPK 4. MAPK (active) phosphorylates a variety of other target proteins Vascular endothelial growth factor receptors - tyrosine kinases in the cell membrane of endothelial cells lining blood vessels Produced by cells not receiving enough oxygen Induce cell proliferation and growth of new blood vessels (angiogenesis) |
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Transduction pathway of G-protein coupled receptors (GPCRs) Effects of the BY subunit of G proteins |
1. Ligand binds to GPCR and induces a conformational change 2. Change in shape stimulates alpha subunit of G protein to release GDP and bind GTP, releasing the beta-gamma subunit complex 3. Activates alpha-subunit or by complex interact with an amplifier enzyme activating it 4. Amplifier enzyme activates a second messenger which affects other cellular pathways Stimulates ion channels to open, sometimes activates enzymes |
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G protein second messengers with amplifier enzyme (4) |
Ca2+ - none Activated G-proteins open or close Ca2+ channels - bind to calmodulin (in every eukaryotic cell); 4 Ca2+ bound activates calmodulin - regulates many other cellular proteins cGMP - guanylate cyclase Activates protein kinases (usually G) - phosphorylates proteins and opens/closes ion channels cAMP - adenylate cyclase Activates protein kinases (usually A) - phosphorylates proteins and opens/closes ion channels Phosphatidylionsitol (IP3)/diacylglycerol (DAG) - phospholipase C Activates protein kinase C, stimulates Ca2+ release from intracellular stores - phosphorylates proteins, alters enzyme activity |
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G-protein regulation of cAMP cAMP activation of protein kinase A |
Gs - stimulatory G proteins activate adenylate cyclase Gi - inhibitory G proteins inhibit adenylate cyclase 1. cAMP binds regulatory subunit of PKA - dissociates from catalytic subunit - PKA now active 2. Activated catalytic subunit phosphorylates proteins - causes response 3. Phosphorylated proteins are rapidly dephosphorylated by serine/threonine phosphatases - terminates response 4. Gi protein then inhibits adenylate cyclase inhibiting the signal transduction pathway |
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What are taste receptors Signal transduction of sweet molecules |
Modified epithelial cells that release NT onto afferent neurons - each receptor expresses many taste proteins 1. Sweet substance induces a conformational change that activates a G-protein (gustducin) 2. Activated gustducin activates adenylate cyclase - catalyzes conversion of ATP to cAMP 3. cAMP activates protein kinase that phosphorylates and closes a K+ channel 4. Intracellular [K+] increases - cell depolarizes resulting in an opening of VG Ca2+ channels 5. Ca2+ causes neurotransmitter release |
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G-protein regulation of phosphatidylinositol (IP3) Signal transduction of bitter molecules How do G-proteins increase blood pressure |
1. Phospholipase C (PLC) is activated by the activated alpha-subunit of a G protien and breaks down phosphatidylinositol biphosphate (PIP2) into diacyl glycerol (DAG) and IP3 2. DAG activates PKC which initiates a phosphorylation cascade 3. IP3 releases Ca2+ into the cell from the endoplasmic reticulum 1. Bitter substance binds to G protein (transducin) activating PLC 2. PLC catalyzes conversion of PIP2 into IP3 3. IP3 causes release of Ca2+ from intracellular stores (ER) 4. Ca2+ causes NT release Angiotensin (hormone by liver) binds to receptors in smooth muscles activating a G-protein - activates PLC IP3 releases Ca2+ from ER - stimulates muscle contraction (Ca2+ itself causes contraction, not NT release)- vasoconstriction |
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Examples of signal transduction pathways interacting with one another |
Ca2+ bound calmodulin interacts with adenylate cyclase producing cAMP Ca2+ bound calmodulin interacts with cAMP phosphodiesterase breaking down cAMP cAMP activates PKA which can phosphorylate Ca2+ channels and pumps - increasing or decreasing activity |
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Definition of learning and memory - how are they possible Synaptic facilitation Synaptic depression Post-tetanic potentiation (PTP) |
Learning: acquiring new information Memory: retention and retrieval of learned information NS alters synaptic connections and properties of neurons Increased APs -> increased NT release Increased APs -> decreased NT release After many high frequency APs, single stimulus increases NT release |
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Gill-withdraw reflex in Aplysia habituation neural circuit Gill-withdrawal sensitization neural circuit and mechanism |
Gill withdrawal declines with repeated touching due to inactivation of VG Ca2+ channels in the motor neurons AP still fires but no Ca2+ = no NT release Sensory neuron synapses on interneuron and motor neuron; interneuron synapses on motor Sensory neuron of tail --> facilitating interneuron --> sensory neuron and interneuron of original circuit Electric shock on tail results in gill withdrawal stronger and longer - increase in Ca2+ influx and NT release 1. Facilitating neuron releases serotonin which binds to a GPRC 2. a-subunit activates adenylate cyclase forming cAMP which activates PKA 3. PKA inactivates VG K+ channels by phosphorylating it - depolarizing the cell |
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Roles of the hippocampus Patient H.M. procedure and symptoms |
Converts short-term memory to long-term memory Involved in spatial memory and navigation as well as episodic memory Removal of amygdala and most of hippocampus to treat epilepsy Lost the ability to create long-term episodic memory; still could form procedural memories and retained some episodic memories from before surgery |
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Long-term potentiation Mechanism in hippocampal neurons |
Repetitive stimulation of a presynaptic neuron leading to an increased response in a postsynaptic neuron Glutamate release from the presynaptic neuron is dependent on frequency of APs - low AP low glutamate 1. When low amount of glutamate is released - only AMPA receptors open on the postsynaptic cell causing influx of sodium 2. When high amount of glutamate is released - AMPA receptors open; influx of sodium - Mg is expelled out of NMDA receptors causing them to open - Ca2+ influx - Ca2+ activates phosphorylation of the AMPA receptor increasing sensitivity to glutamate - Ca2+ activates PKC causing a paracrine signal to the presynaptic cell, increasing glutamate release The more frequently a neuron fires, the stronger the response via positive feedback mechanisms |
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Compare and contrast the basic organization of the nervous system in different animal taxa |
Evolutionary trend: cephalization - brain and ganglia development Cndiarians: diffuse nerve net No brain, neurons carry info in all directions, impulses radiate out in many directions from a stimulus Can still perform complex behaviors Cephalopods: large brains with large ganglia functioning independently of brain in each arm |
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How is the vertebrate CNS protected How do signals reach the brain from the blood and from the blood to the brain |
CNS is encased in cartilage or bone Meninges: layer of connective tissue surrounding CNS (pia mater, arachnoid, dura mater) Cerebral spinal fluid (CSF): fill space within meninges - absorbs shock BBB - isolates brain from potential toxins in blood - capillaries lined by endothelial cells; tight junctions limits cellular transport - Thick basal membrane and end-food processes of astrocytes - Pericytes regulate blood flow 1. No pinocytosis, small lipid soluble molecules can dissolve through - specialized carrier proteins can uptake glucose and amino acids 2. BBB more permeable around pineal gland, pituitary gland and hypothalamus - hormones released from CNS can travel throughout body |
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Spinal cord reflex arc |
Spinal cord acts as an integrating centre for information - sensory neuron < interneuron < motor neuron - response At the same time sensory neuron < brain so that sensory information can be processed after the initial fast response |
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Why is neuroregeneration not common in the CNS Role of glial cells in recovery from injury |
Neural networks all stem from the CNS, any miswiring could cause severe problems in the rest of the body PNS: stimulate regrowth by releasing neurotrophic factors CNS: inhibits regrowth by forming a physical barrier (glial scar) and releasing chemicals |
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Divisions of the peripheral nervous system Four major types of neurons in PNS Evolution of PNS neuroanatomy |
Efferent --> autonomic --> SNS, PSNS, enteric Efferent --> motor Afferent Somatic sensory, somatic motor, visceral sensory, visceral motor Over time, the dorsal horn has become more responsible for sensory signals and the ventral horn more responsible for motor signals |
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Somatic pathway characteristics (4)
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1. Cell bodies in the PNS
2. Synaptic cleft between the motor neuron and muscle is narrow 3. Releases ACh 4. Always excitatory on the muscle |
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Role of enteric nervous system What features of the PSNS and SNS allow them to maintain homeostasis |
Affects digesting by innervating the GI tract, pancreas, and gall bladder Dual innervation - most organs are innervated by both Antagonistic action - effects are opposite of each other |
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Autonomic pathway synapse location How are signals amplified Differences in SNS and PSNS pathways |
1. Contain two neurons in series that synapse within the autonomic ganglia 2. Preganglionic neurons can synapse with intrinsic neurons One preganglionic neuron may synapse with many postganglionic neurons (SNS - 10+), (PSNS - 3-) 1. SNS releases NE, PSNS releases ACh 2. SNS short pre, long post, PSNS long pre, short post Only preganglionic neurons are myelinated in both |
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Subdivision of the hindbrain with functions What does the brain stem include |
1. Medulla oblongota - autonomic functions and essential reflexes; pathways between spinal cord and brain 2. Pons - relay station between medulla, cerebellum and forebrain; alertness, sleep/dreaming, regulates breathing Damage causes locked-in syndrome 3. Cerebellum - contains half of the neurons in the brain, sensorimotor integration, maintaining equilibrium and refining motor action Continuous with the spinal cord, medulla, pons and midbrain |
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Midbrain divisions How is this different in fish and amphibians when compared to mammals |
Tectum 1. Superior colliculi - reflex optical responses 2. Inferior colliculi - auditory signals Tegmentum - fine motor control Primary centre for coordinating and initiating behavioral responses; size and function; reduced in mammals |
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Forebrain, midbrain and hindbrain developmental names |
Prosencephalon Mesencephalon Rhombencephalon |
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Divisions of the forebrain Cerebrum divisions and functions What allows the mammalian cortex to process so much information |
1. Cerebrum (telencephalon) 2. Diencephalon 1. Corpus callosum - connects two hemispheres together 2. Cerebral cortex (outer) - Voluntary movements - Interpretation and integration of sensory info - Concentration, reason, speech, abstract thinking Layered arrangement (6 layers) where shape and density of neurons differs between the layers |
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Function of diencephalon divisions How is intelligence correlated with increased folding Limbic system functions - includes which parts |
Epithalamus: establishes circadian rhythms Thalamus: integrates and filters sensory info (not smell) and relays it to the appropriate cortical regions Hypothalamus: maintains homeostasis by interacting with autonomic nervous system - regulates secretion of pituitary hormones Gyrus - folds, sucli - grooves Smoother brains in less intelligent animals Influences emotions, motivation, and memory Hypothalamus, amygdala, olfactory bulbs, hippocampus |
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Allometric terms (3) with example for each Function of association areas |
1. Positive allometry - legs grow quickly relative to torso 2. Negative allometry - head grows slowly relative to torso 3. Isometry - salamander, fish Receive information from adjacent areas and further process and integrate the information - bigger in animals with complex behaviours |
