Biopsychology Week 3
Biopsychology Week 3
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This 6 page Reader was uploaded by Monica Stert on Friday April 18, 2014. The Reader belongs to a course at University of California Santa Barbara taught by a professor in Fall. Since its upload, it has received 104 views.
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Date Created: 04/18/14
Week 3 Notes 415 I Neurophysiology A Cell membrane 1 Lipid bilayer two layers of linked fatty molecules within which specialized proteins float one important use of protein is an ion channel 2 Ion atom or molecule that has acquired electric charge 3 Ion channel pore in cell membrane 4 Selectively permeable allows some substances to pass through respond to voltage changes B Resting membrane potential of a neuron 1 Inside of neuron more negatively charged 70mV ltresting potential than the outside Outside Inside Sodium 440 50 Potassium 20 400 Calcium 10 00001 Chloride 560 40150 Protein Few many 2 Four factors establish resting potential a Concentration gradient molecules collected in high concentration will move to an area of lower concentration b Electrostatic pressure like charges repel each other opposite charges attract each other c Permeability of membrane voltagegated channels 1 Sodium channels mostly closed open at 50mV 2 Potassium mostly open open at 90mV 3 Chloride channels are open open at 70mV d Active ion transport sodiumpotassium pump transporter that pumps 3 sodium out of neuron for every 2 potassium into the neuron via mitochondria 3 At rest a Sodium wants to enter neuron 1 Passive concentration gradient 2 Electrostatic pressure because sodium is positive and attracted to internal negative neuron 3 Most sodium ions are closed what comes in is pumped out by sodium potassium pump b Potassium wants to leave neuron 1 Passive concentration gradient it s inside 2 Electrostatic pressure keeps them in 3 Channels are leaky so less resistance c Chlorine wants to remain in equilibrium 1 As it moves out passive concentration gradient moves it inside 2 Electrostatic pressure forces it out no resistance to crossing membrane 4 Polarizing membrane of neuron a Some neurotransmitters diffuse across synapse dendrite and changes electric potential of postsynaptic neuron called postsynaptic potential PSP 12 kinds of PSP a Excitatory PSP EPSP make inside of cell more positive relative to the outside gt depolarization b Inhibitory PSP IPSP inside of cell more negative relative to outside gt hyperpolarization positive charge greater outside or negative charge less inside b PSPs are graded their size depends upon the intensity of the stimulus that elicited them 1 Amount of neurotransmitters released 2 Number of receptors activated 3 Degrade as they travel along dendrite or cell body c Spatial summation integration of PSPs arriving at different parts of the neuron 1 Scenario 4 presynaptic neurons synapsing on a postsynaptic neuron a EPSP EPSP strengthened stimulus b IPSP IPSP strengthened stimulus c EPSP IPSP none d Temporal summation PSPs arrive at different time 1 Scenario 2 presynaptic neurons a EPSP bigger EPSP fires rapidly b IPSP bigger IPSP fires rapidly e Review size type and effect of PSPs depend on 1 Frequency of firing and neurotransmitter release 2 Number and identity of presynaptic neurons simultaneously firing 3 Neurotransmitterreceptor combination 4 Number of a particular type of receptor 5 Distance of receptors from axon hillock C Starting site of action potential 1 Axon hillock initial a High in votage gated sodium channels b Highly sensitive to ionic flux c Action potential is generated 2 Ionic basis of AP action potential a Action potential rapid reversal of electric potential in membrane 70mV gt 50mV 1 Not graded all or none Has to reach threshold 2 Propagated down the entire neuron 3 Generated when depolarization reaches threshold of excitation 5 to 20 mV depolarization at axon hillock 4 Depolarization is change in voltage that opens voltagegated sodium channels sodium comes rushing in depolarizing membrane to 50 mV b Influx of sodium activates additional potassium gates to open allowing sodium to flow out 1 Out flux of potassium does not alter affect of sodium on the membrane potential rising phase 2 When membrane becomes depleted 50 mV sodium channels close have thresholds for openings as well as closings 3 potassium leaves neuron gt repolarization 4 potassium channels slow to close drops membrane potential below the resting membrane potential gt undershoot hyperpolarized 5 Now less likely o fire another action potential creates refractory period where axon is less likely to fire another action potential 6 Absolute refractory period impossible to fire AP 7 Relative refractory period possible to fire AP but requires greater than normal stimulation 8 Keeps AP moving in 1 direction because there s only one way for it to go 9 Rate or neural firing related to intensity of the simulation 3 Propagation ofAP a Travels axon without degrading b Continuous triggering of next sodium channel c Do not degrade because of amount of sodium channels d Conclusion 1 Myelin rapid and saltatory keeps ions inside wire 2 Saltatory conduction a Sodium channels open b Myelin prevents potassium leakage c Depolarization spreads very rapidly d AP is triggered at nodes of ranvier 3 Myelin disorder multiple sclerosis MS a Loss of myelin motor function loss of conductance degeneration of myelin weakness paralysis spasms impaired coordination 417 ll Neurotransmission A Synthesis transport and storage 1 Neurotransmitters chemical gas hormone a Large peptide and hormones synthesized in cell body and then transported down axon b Small amino acids monoamines acetylcholine and gases synthesized at terminals c Terminal storage is vesicles d Release when vesicles dump chemicals in synapes 2 Steps a AP travels down axon b Depolarization of terminal membrane activated voltage gated calcium channels exocytosis c Calcium docs at vesicles to activation zone d Membrane fuses with cell membrane and neurotransmitters are released 1 Small neurotransmitters get released for every action potential 2 Large are only released when there are high rates of action potentials and calcium levels rise substantially take AP buildup e Receptors ligand molecule of correct shape not just any neurotransmitter 1 lonotropic receptor if neurotransmitters connect it directly opens up the channel 2 Metabotropic receptor when it connects neurotransmitters creates chemical cascade that releases G proteins these activate neighboring ion channels 3 Autoreceptors on presynaptic neuron metabotropic tell axon how much of neurotransmitter has been released regulate calcium channel and exocytosis function requires precision f Other ways to end neurotransmission 1 Reuptake trasporters take neurotransmitters back into presynaptic membrane to repackage or degrade 2 Enzymatic degradation enzymes in fluid degrade neurotransmitters after release 3 Diffusion neurotransmitters move out of synaptic cleft g Basic steps 1 Neurotransmitters synthesized 2 Stored in vesicles 3 Leaked neurotransmitters from vesicles are destroyed 4 Vesicles fuse with presynaptic membrane 5 Bond with auto receptors 6Bind to post synaptic receptors 7 Neurotransmitters are deactivated 3 Neurotransmitters a Neuropeptides large molecules 1 Over 100 different types 2 Endorphines pain and pleasure runners high opiate for brain 3 Slower signal than the small molecule neurotransmitter 4 Broken down by degradative enzyme in synaptic cleft b Amino acids small 1 Building blocks of protein 2 Glutamate glycine aspartate from food excitatory more likely to create AP 3 GABA glutamate in neurons and astrocytes inhibitory 4 Found in majority of fast acting directed synapses 5 Use reuptake mechanisms c Soluble gases small 1 Nitric oxide and carbon monoxide 2 Made in cell body and diffuse across membrane no exocytosis or channels 3 Believed to help retrograde signals post communication to pre 4 Very short lived inside and outside enzymes break them down d Acetycholine ACh small 1 Class of its own 2 Made from acetyl and choline 3 Found at neuromuscular junctions 4 Degraded by acetylcholinesterase 5 Cholinergic pathways cholinergic cells in the basal forebrain project throughout the cortex and to the hippocampus and amygdala systems crucial for learning and memory e Monoamines small 1 Single amino acid 2 Dopamine neorepeniphrine epinephrine 3 Diffuse effects more than amino acids 4 Highly branched axons 5 Dopaminergic pathway mesostriatal DA system motor control parkinson s can t produce this dopamine none in basal ganglia mesolimbocoritcal DA system verbal learning cognition 6 Norepinephrine noradrenergic implicated in modd arousal and sexual behavior 7 Serotonin made from tryptophan like milk and turkey serotonergic implicated in control of sleep states mood anxiety and some cognitive func ons 4 Drug effects agonists and antagonists a The endrogenous within self ligand naturally occurring molecule like neurotransmitters that bind and active receptors b Agonists facilitate neurotransmission resemble endogenous ligand and receptor 1 Effects facilitation a Drug increases synthesis of neurotransmitters b Increase neurotransmitters release at axon terminal more exocytosis c Block reuptake keeping neurotransmitters out in gap facilitates neurotransmission d Examples i Morphine binds to endorphine receptors mimics actions can give same euphoric feeling heroine cocaine serotonin norepenephrinedopamine reuptake inhibitor leaves more neurotransmitters out c Antagonish binds the receptor but fails to open it blocks agonists 1 Effects prevents a Drug blocks synthesis of neurotransmitters b Activates autoreceptors and inhibit neurotransmitter release autoreceptor typically prevents exocytosis c Examples i Naloxone binds to receptors and blocks endorphines used to combat overdosing morhpines ii Antihistamines block synthesis of histamine blocking neurotransmission
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