E109 Lecture 3: Nervous System I (Fall 2024) PDF

Lectures 2 + 3 Finish hormonal control (end of lecture 2) Learn how ion concentration gradients and membrane permeability impact membrane potential Observe that changes in membrane permeability (Na+ & K+) cause the formation of action potentials Understand that action pot...

Lectures 2 + 3 Finish hormonal control (end of lecture 2) Learn how ion concentration gradients and membrane permeability impact membrane potential Observe that changes in membrane permeability (Na+ & K+) cause the formation of action potentials Understand that action potentials are triggered by local current flow (a graded potential) Learn that the strength of graded potentials depends on resistance to current flow Observe that myelination increase the speed of AP Hormone Regulation Sensor & Integrator Trophic hormones: endocrine regulation of hormonal release Often involves the hypothalamus-anterior pituitary axis Hypothalamus-anterior pituitary axis HYPOTHALAMUS 1 1 Neurons synthesizing trophic hormones release them into capillaries of the portal system. Capillary bed 2 Artery 2 Portal vessels carry the trophic hormones directly to the anterior pituitary. 3 Endocrine cells release POSTERIOR PITUITARY 3 their hormones into the second set of capillaries Capillary bed for distribution to the rest of the body. ANTERIOR PITUITARY Veins TO TARGET ORGANS Figure 7-16 Hypothalamus-anterior pituitary axis HYPOTHALAMUS Growth Hormone ACTH TSH LH FSH liver Prolactin IGF Cortisol Thyroxine I Sex hormone secretion Gamete production Metabolic actions Breast growth Stress response Metabolic rate Milk production Growth non'm Endocrine Pathologies Hypersecretion: excess hormone secretion Loss of feed back regulation 14 It touch hormone excess hormone production Hyposecretion: deficient hormone secretion Loss/deficiency of hormone production Target cell pathologies Loss/down-regulation of target cell receptor signal not relieved not Transduction of signal in target cells enough hormone Review: homeostasis and communication in the body beable toexplain each indetail Negative feedback control loops allow us to regulate physiological function Local communication regulate the state of nearby cells Nervous system provides rapid but short lasting shifts in physiology, whereas the endocrine system produce slower but longer lasting affects The membrane permeability of peptide hormones and steroid hormones alters the nature and speed of their actions Endocrine responses can involve complicated cascades that can be regulated at various steps E109 Lecture 3: Nervous System I Paul de Koninck Organization of the Nervous System bearrunning u fear signalissent to afferentneurons afferentneurons sendsignalto centralnervous system youcannotchangethestrength ofan actionpotent but youcan changespeed Figure 8-1 Cells of the Nervous System Glial Cells Neurons dendrites Input signal Caffrey c neurons nucleus astrocytes cleansthehouse cell body Integration i deceives 59.9.1 signal enough in axon axon hillock ina m 1191119 besent oligodendrocytes incentralnervoussystem myelin sheath axon insulatingtheaxon Preventschargeloss Schwann cells inpns Output signal post-synaptic neuron stem cells Chemical Disequilibrium 160 140 KEY Na+ Ion concentration (mmol/L) 120 I K+ 100 Cl- 80 HCO3 - Proteins 60 40 20 Intracellular fluid Interstitial fluid Plasma howmanytransporters arethere aretheyopen there4open morepermeability Permeability: how readily a given substance (ion) moves across a membrane. Membrane Potential: Nernst Equation Cell Membrane Cytoplasm Extracellular fluid K+ K+ Na+ K+ K+ K+ K+ Na+ K+ Na+ K+ K+ K+ Na+ Na+ Na+ K+ K+ + K+ K+ K K+K+ Na+ Na+ Na+ K+ Na+ Na+ K+ K+ Na+ Na+ Ek+ = 61 log (1/29) = -90 mV Charge permeability 1membrane potential Resting Membrane Potential: charge inside vs outside (-) Cell Membrane Dynamic changes in membrane permeability Cytoplasm Extracellular fluid to Na and K lead to action potentials + + Na+ Na+ K+ K+ K+ K+ K+ Na+ K+ Na+ K+ Na+ Na+ K+ K+ Na+ - 70 mV ENa +60 0 -70 Vm -90 EK changepermiabilityofthe membraneto potassiumleak channelsalwayson which change membranepotential is the to  7 Resting Membrane Potential: charge inside vs outside (-) Cell Membrane At rest, we have some K+ permeability, but Cytoplasm Extracellular fluid nearly none for Na+. So, we sit at -70 mV. Na+ Na+ K+ K+ K+ K+ K+ Na+ K+ Na+ K+ Na+ Na+ K+ K+ Na+ - 70 mV ENa +60 0 -70 Vm -90 EK Phases of the action potential 1 Resting basic shape of 2 Rising (rapid depolarization) action potential 3 Overshoot (peak) 30 4 Falling (repolarization) 10 Membrane potential (mV) 3 5 Recovery (undershoot) 0 4 2 -30 Threshold -70 1 5 0 1 2 3 4 Time (ms) Resting Phase: driven by permeability of K+ inactivation Gothingcangointo unless its charged a toldtoopen 30 0 -70 Rising Phase (depolarization): high permeability for Na+ mm in theopenconfiguratio 30 causing permeability to rise 0 -70 Falling Phase (repolarization): high permeability for K+ 0 potassium gate is open while sodium 30 ff8 0 is inactivated causing permeability -70 to drop Recovery Phase (undershoot): back to resting permeability Potassium gates are slow to close undershoo leading to 0 30 0 -70 Phases of the action potential 1 Resting: K+ permeability determines Vm 2 Rising: Voltage gated Na+ channels cause depolarization É 3 Overshoot: Na+ inactivation gates close, K+ channels open 4 Falling: K+ flows out of the cell (repolarization) 5 Recovery: K+ channels close and slowly restore Vm 30 3 10 Membrane potential (mV) 0 4 2 -30 Threshold -70 1 5 0 1 2 3 4 Time (ms) Changes in Permeability AP initiation through positive feedback ACTION POTENTIAL Rising phase Peak Falling phase Na+ enters timecontrols how cell. channels longthese are open To stop cycle, Na+ channel slower Na+ channel activation gates + Feedback cycle inactivation gate open rapidly. closes (see Fig. 8.10). More depolarization triggers Depolarization Slow K+ K+ leaves channels open. Repolarization cell. Action Potential Propagation Action Potential Propagation Refractory Periods Both Na+ Both channels channels Na+ channels close and Na+ channels reset to original position closed open channels K+ channels open while K+ channels remain open closed Na+ Na+ and K+ channels K+ K+ K+ Absolute refractory period Relative refractory period Membrane potential (mV) Action potential Ion permeability Na+ K+ High High Excitability sincethesodiumchannels Increasing are inactivated they 18 9 I Zero to flability Time (msec) what the chance is that  e p n you Propagation Rates/Graded potentials The rate of action potential propagation depends on the resistance of the axon to current loss Increased resistance to current loss across the membrane Amplitude of graded maintains signal strength over potential (mV) longer distance Distance Distance Stimulus point of origin Propagation Rates Speed of action potential in neuron influenced by Diameter of axon Larger axons are faster Resistance of axon membrane to ion leakage out of the cell Myelinated axons are faster Schwann cells Saltatory Conduction Myelin Degeneration Myelin degeneration can result in significant loss of function Diseases: Multiple Sclerosis, Meylitis, Leukodystrophy Review Ion concentration gradients and membrane permeability determine membrane potential in cells Dynamic changes in membrane permeability (Na+ & K+) cause the development of an action potential Action potentials are triggered by local current flow (a graded potential) The strength of graded potentials depends on resistance to current flow Myelination increase the speed of AP propagation