Unformatted text preview: 2/16/2010 BIOL 260: Human Physiology Human
Spring 2010 Spring W, Feb. 17, 2010 Feb. www.smccd.edu/accounts/staplesn/biol260
1. Pre-Lab Writeups: Be sure to prepare before each Monday Lab W riteups Be before each Monday or Wednesday labs (for WHOLE week!)!! or Wednesday
– (What? Why? How? are we doing in the lab??) 2. THIS Week: Open lab/review session today!!!
• (Nerves Report #2 Due week of 2/22) • Expt. 4 Lab Data is POSTED under “Additional Materials”. Expt. 3. Review sessions next week in Review (after/before?) labs …… ……
• Midterm 1 study guide will be updated by this Midterm weekend!! weekend!! • Work-out ALL short essays!! Know your terms!! 1. Compare and contrast 4 characteristics of graded potentials and action Compare graded and potentials. (re: initiation and conduction) potentials 2. Describe and diagram the sequence of events leading from neuron Describe stimulation, to Action Potential production, conduction, and release of Action conduction, neurotransmitter at axon termini. neurotransmitter 3. Explain what causes (what is happening to ion channels?) the Relative Explain and Absolute Refractory Periods following an AP. Refractory 4. Describe and diagram 2 ways to increase speed of neural conductance, Describe increase and diagram the movement of ions during saltatory conduction…… saltatory REVIEW TODAY: Students should be able to…...
1. Describe and diagram the process by which neurotransmitters are Describe neurotransmitters are released ffrom axon termini and act on a target cell. released rom act 2. Ch. 11: Describe several processes controlled by the efferent division of Describe the peripheral NS. (autonomic & somatic) the (autonomic 1 2/16/2010 3. Electrical Signals: 3. Chemical Factors Chemical
Effect of extracellular potassium (-kalemia) Effect extracellular concentration of the excitability of neurons
Less potassium leakage Less out, but slow repolarization. out, HyperK HypoK More potassium leakage out. Fig. 8-19 8.5) Cell to Cell Conduction: Cell The Synapse The
1. Electrical synapses: gap junctions
a) Very fast conduction Very fast b) Example: cardiac muscle 2. Chemical Synapses: 3 components – components
a) Pre synaptic terminal
1) Synthesis of Neurotransmitters 2) Ca2+ releases Neurotransmitters Few to 150K Few per target cell! per b) Synaptic cleft c) Postsynaptic cell: Neurotransmitter receptors Neurotransmitter in membrane in 2 2/16/2010 A. The Synapse: Structure
Figure 8-20: A chemical synapse http://www.mind.ilstu.edu/flash/ synapse_1.swf http://outreach.mcb.harvard.edu /animations/synaptic.swf B. Synapse Mechanism
VG, Ca2+ Channels “Kiss and Run” pathway? Figure 8-21: Events at the synapse 3 2/16/2010 C. Acetylcholine synthesis Figure 8-22: Synthesis and recycling of acetylcholine at the synapse D. Neurocrines D. Neurocrines
1. 2. 3. Neurotransmitters Neuromodulators Neurohormones / antagonist ß blockers 4 2/16/2010 Neurocrines Caffeine = antagonist Table 8-4-2: Major Neurocrines E. Multiple Receptors Modify E. Signal Signal
1. Amplification – depolarization (EPSP); );
• trap K+ inside (less out), or open Na+ Channels. 2. Inhibition – hyperpolarization (IPSP); );
• open Cll- influx channels, extra K+ efflux, less open C efflux, Na+ influx. Na 3. Duration
a) Fast – channel opening. (direct channel activation) Fast channel (direct b) Slow – require protein synthesis; use Slow require secondary messengers. (indirect channel activation) (indirect 5 2/16/2010 Multiple Receptors modify signal
nACh, Glu AMPA Glu mACh, Adr Adr Figure 8-23: Fast & slow responses in postsynaptic cells F. Inactivation of Neurotransmitters F. (Termination of Signal) (Termination
1. 2. 3. Recycled Enzyme degradation Diffuse away
Figure 8-24: Inactivation 24: of neurotransmitters 6 2/16/2010 8.6) Integration of Signals 8.6)
1. Information transfer at each exchange
a) Signal can be lost b) Signal can be enhanced 2. Divergence – one cell to many 3. Convergence – many cells to one many A. Divergent Integration A. Divergent
Result: multiple Result: multiple responses & effector effector organs from one signal
Collateral Collateral axons axons Figure 8-25a: Convergence and divergence 25a: 7 2/16/2010 B. Convergent Integration B. Convergent Purkinje dendrites Result: multiple inputs Result: multiple control same response. control • summed to determine summed outcome outcome Figure 8-25b: Convergence and divergence Integration of Signals Figure 8-26: Locations of synapses on a postsynaptic neuron 8 2/16/2010 C. Convergent Integration: C. Additive Summation Additive
1. Multiple excitatory graded potentials (GPs) Multiple 2. Temporal summation – subthreshold potentials 2. potentials delivered close together in time summate at TZ AP. 3. Spatial summation – graded potentials originate at different graded sites on the soma/dendrites summate at TZ AP summate 4. Additive strength at trigger zone Fig. 8-29 Convergent Integration: Convergent Additive Summation Additive Figure 8-28a: Spatial summation 9 2/16/2010 D. Convergent Integration: D. Inhibitory Summation Inhibitory
• Inhibitory GPs Inhibitory cancel strength of excitatory GP of • Signal at trigger Signal too weak – no no AP produced AP
Figure 8-28b: Spatial summation 8.7) Synaptic Modulation 8.7) Synaptic
1. Presynaptic terminal
a) Inhibitory neuron(s) – less NT released Inhibitory neuron(s b) Excitatory neuron(s) – more NT released Excitatory neuron(s Only affects selective targets of axon termini 2. Postsynaptic membrane and receptors
a) b) c) Receptor numbers Degradation rates Permeability Equally affects all targets of axon termini 10 2/16/2010 A. Pre-/Post-Synaptic Inhibition
At bouton/terminus of At bouton/terminus final efferent neuron final Figure 8-31: 31: Presynaptic & postsynaptic inhibition inhibition At Cell Body/integration ctr of final efferent neuron At ctr B. Long-Term Potentiation Term Potentiation
• Sustained changes
– In synapses • May be key to learning & memory May processing. processing.
– Glu (Glutamate) = main excitatory CNS NT – Glutamate receptors: (CNS)
• NMDA receptor channel – (= glutamate agonist)
1)Ca++/Na+ entry blocked by gate and Mg++ ion 2)Needs GLU + depol’n to open (AMPA receptor = glu agonist) Needs depol glu 3)Depol’n ejects Mg++ ion, and Ca++/Na+ enter 4)Paracrine enhance NT release (presynaptic!!) and !!) upregulates GLU Receptors (postsynaptic!)…….. upregulates Strengthens pathway for the long term!! 11 2/16/2010 Long-Term Potentiation Term Potentiation
Figure 8-32: 32: Long-term Long term potentiation potentiation ~ Positive feedback cycle: • Glu Ca++ paracrine Ca++ ↑Glu…. 8.8) Nervous Tissue 8.8) Development Development
• 100 billion neurons find their 100 target target • Growth cones
– Follow growth factors, Follow structural proteins (PM, ECM) structural – Neurotrophic factors – sustain new synapse – "Use it or loose it" Figure 8-33 Figure 8-34 12 2/16/2010 Chapter 11
Efferent Division: Autonomic Efferent and Somatic Motor Control and Ch. 11 Overview:
1. Efferent peripheral nervous division, and Efferent what it controls what 2. Pathways, receptors, and neurotransmitters 3. Antagonistic controls: sympathetic and Antagonistic parasympathetic (AUTONOMIC EPNS) parasympathetic 4. Control of cardiac, smooth muscle and Control glands in homeostasis glands 5. CNS control of skeletal muscles through CNS neuromuscular junctions (SOMATIC EPNS) neuromuscular 13 2/16/2010 11.1) Autonomic Division: 11.1) Homeostatic balancing Homeostatic
• Controls: Visceral Organs…. Controls: Visceral
– Smooth & cardiac muscle Smooth – Glands & adipose • Antagonistic branches:
• "Rest & digest"
– Restore body – Sympathetic
• "Fight or flight"
– Energetic action Autonomic Division: Autonomic Homeostatic balancing Homeostatic
Figure 11-1: Homeostasis and the autonomic division 14 ...
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This document was uploaded on 03/18/2010.
- Spring '09