Neurons: Structure and communication

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Transcription:

Neurons: Structure and communication http://faculty.washington.edu/chudler/gall1.html

Common Components of a Neuron Dendrites Input, receives neurotransmitters Soma Processing, decision Axon Transmits signal Terminal Buttons Output, release neurotransmitters to target Myelin Sheath Insulates axon Synapse Junction between neuron and target

Neuronal connections

Overview of Neural Signaling 2 types of communication: Electrical Synaptic and action potentials Chemical Neurotransmitters

Electrical neuronal communication Cell is not firing: resting potential (-70mV) Cell fires: action potential (+40) All-or-none signal Must exceed threshold in axon hillock Refractory period

Synaptic Potential Function: Turns a chemical signal (neurotransmitter) into an electrical signal Location: Primarily in the dendrites How: Neurotransmitters bind to receptors opening ion pores Pumps move ions in and out of neuron if unequal concentrations (of +/- charge to get back to -70) Electrical signal due to movement of ions (positively charged molecules in and out of neuron

Synaptic Potential Neurotransmitters bind to receptors on the surface of the neuron s dendrite and this causes different ions to move across the membrane: Na+ (moves in creates depolarization) K+ (moves out creates hyperpolarization) Cl- (moves in creates hyperpolarization)

Signal Processing Function: Decision to send an action potential or not based on strength of synaptic potential Location: Axon soma (axonal hillock) Synaptic potential will create an action potential when charge reaches -50mV 2 ways can occur: Temporal summation: enough signals arrive in short time that it leads to a decrease in the synaptic potential (move faster than the pump) Spatial summation: enough signals arrive from different neurons that the sum exceeds the threshold

Action Potential Function: Output signal to terminal button Location: Axon How it works: All-or-nothing signal; exactly same each time The synaptic potential is regulated by chemicals, the action potential is regulated by voltage Voltage-gated channel process: Na+ opens at -50mV and moves into cell Moves voltage toward +30mV K+ opens at -40mV and moves out of cell (reducing voltage) Na+ closes but K+ stays open Brings voltage from +30mV to -75mV Refractory period: moves Na+ back out and K+ back in until back to -70mV

Stimulus intensity http://faculty.washington.edu/chudler/son.html Cell s responses Stimulus Each spike or line represents an action potential This cell is specialized for a right diagonal line. Intensity: # of action potentials in period of time

Chemical neuronal communication Many types of neurotransmitters Produce excitatory or inhibitory effect

Neurotransmitters Acetylcholine (ACh) Dopamine (DA) Norepinephrine (NE) Serotonin (5-HT) GABA Otto Loewi s experiment 1921 Fluid from heart 1 allowed to flow to heart 2 Whatever change in heart 1 occurred for heart 2

Neurotransmitter release Function: Convert electrical signal (action potential) into chemical signal (to cross synapse) Location: How: Terminal button Neurotransmitters (NTs) stored in bubble-like vesicles inside terminal button Action potential allows NTs to be released into synapse NT connects to specific receptor NTs then removed (reuptake, breakdown, or absorbed/recycled) And, then the story repeats itself (back to synaptic potentials!)

Chemical signaling NT and receptor fit like lock and key Action depends on the lock Allows: Two neurons to send different signals to the same target e.g. heart muscle under NE vs. ACh Two synapses can be very close and not interfere with each other (no cross-talk) Different neurotransmitters are used in different locations for different purposes

Common Drug Actions 2 categories of drugs Agonist increases the effect of a neurotransmitter Antagonist decreases the effect of a neurotransmitter Ways drugs can be Agonists: Mimic the NTs; artificially activate the receptors Increase the production of NTs Inhibit the breakdown of NTs Inhibit or block NTs reuptake from synapse Increase the release of NTs Ways drugs can be Antagonists Block access to the receptor Inhibit production of the neurotransmitter Breakdown or inactive neurotransmitter (speed metabolism) Cause neurotransmitter leakage from vesicles

Communication in the Nervous System Electrical Signals within neurons: Discrete on/off signal Fast over long distances Caused by movement of ions in or out of the neuron 2 types: synaptic potentials action potentials Chemical Signals between neurons: Slower but only used for short distance (synapse) Chemicals provide selectivity that electricity does not have due to lock and key binding

HOW to study the brain Most complex object in the world Clinical observation - Case studies Observable behavior linked with physical brain damage or abnormality Phineas Gage http://www.deakin.edu.au/hbs/gagepage/ Albert Einstein http://faculty.washington.edu/chudler/ein.html H.M. December 2-4, 2009: live webcam of brain sectioning http://thebrainobservatory.ucsd.edu/hm_live.php http://thebrainobservatory.ucsd.edu/hmblog/

Methods of Investigation http://faculty.washington.edu/chudler/image.html Lesions Activating the brain Direct stimulation Imaging technology CT PET MRI fmri Electrical activity EEG: electroencephalography ERP: event-related potential http://www.pbs.org/wnet/brain/sc anning/eeg.html