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myelin sheath
- only on axons
- make up white matter
- dev during late fetal period thru 1st yr
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PNS myelin sheath cells
schwann cells
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CNS myelin sheath cells
oligodendrocytes
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multipolar neurons
several dendrites - one axon
most neurons in CNS
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bipolar neuron
1 dendrite - one axon
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unipolar neuron
1 process (axon)
sensory root of spinal nerves
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functional classifications of neurons
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neurons are excitable
inherent ability to generate and conduct electrical impulses
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membrane potential
exists when a barrier prevents movement of opposite charges toward each other
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polarized
all cells have slightly different charges
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voltage
a form of potential energy measured in volts (or millivolts-mV)
a difference in charge between two points
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current
movement of charged particles
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resistance
possessed by the membrane as it restricts the movement of charges
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ions
- cant diffuse across cell membranes
- must pass through channels
- channels are located at particular sites on membrane
- ion channels are selective
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Passive channels
- leakage, non-gated
- always open
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resiting neuron
high concentration of K inside and high concentration of Na outside cell
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Gated (active) channels
- *may be open (activated)
- * closed but able to open
- * closed but unable to open (inactivated)
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chemically gated
open when the appropriate chemical (neurotransmitter) binds
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voltage gated
open in response and close in response to changes in membrane potential
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maintenance of resting potential
- around -70 mV
- varies from -40mV to 90mV
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maintenance of RP
- passage of ions through leakage channels
- * permeability of membrane for K leaking out 75X greater than Na leaking in
- * activity of Na-K pump
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Na-K pump
- membrane proteins that actively transport ions
- (3) Na exported
- (2) K imported
- stabilizes the resting potential
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neurons use changes in their membrane potential as communication signals
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change
produced by changes in membrane permiability to any ion
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signals
graded potentials (incoming over short distances)
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action potentials
- long distance signals of axons
- same as nerve impulses
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depolarization
reduction in membrane potential (becomes less negative)
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hyperpolarization
membrane potential increases (becomes more negative)
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graded potentials
- short lived, localized changes in membrane potential;
- triggered by stimuli in neurons' environment that cause gated channels to open
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current in graded potentials
- dissipates quickly
- die out w/ increasing distance from site of origin
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action potential
- nerve impulse
- incolves 3 consecutive but overlapping changes in membrane potential
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1) resting (non-conducting) state:
voltage gated channels closed;only leakage channels open
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Each Na channel has 2 gates
activation gate: closed at rest, open w/ depolarization
inactivation gate: blocks channel once opened
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2) depolarizing phase
*huge increase in permiability to Na (about 1000x more permeable to resting)
*axon membrane depolarized, Na rushes in, more depolarization
*becomes self-generating when it reaches a critical level threshold (-55mV to -50mV)
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positive feedback
more Na enters, greater depolarization, opens more Na channels
overshoots to +30mV
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3) repolarizing phase
- decreased Na permeability (inactivation gates closing)
- increased K permeability (k channels open; it leaves cell)
*decrease of Na going in; Increase of K going out= repolarization= internal negativity restored
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4) hyperpolarization
K permeability continues fro a bit (more than needed to restore resting state; excess K efflux = afterhyperpolarization)
- * Na channels are resting
- * electrical condition back to resting; but not ion distribution
- * ion distribution restores quickly by Na-K pumps after repolarization
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propagation
transmission of action potential; begins at one end and is conducted to axon terminal (domino effect)
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threshold
usually depolarization of 15 to 20 mV from resting required to generate an ap
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absolute refractory period
neuron cannot respond to another stimulus (from opening of Na channels to their resetting)
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relative refractory period
follows absolute; exceptionaly strong stimulus could reopen Na channels
(most Na channels reset; some K channels still open; repolarization occuring)
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conduction velocity
- axon diameter
- degree of myelinzation
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continuous conduction
depolarization the entire length of the axon
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saltatory conduction
concentration of Na channels @ nodes
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group A
- large diameter heavily myelinated
- 150 m/sec
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group b
- lightly myelinated intermmediate diameter
- 15 m/sec
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synapses-
functions between neurons sites of information transfer
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presynaptic neuron
conducts impulses towards synapse sender
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post synaptic neuron
- conducts impulses away from synapse
- reciever
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electrical synapse
- uncommon
- connected by protein channels to adjacent neurons
- ions flow directly from one to another
- rapid synchronized communication
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chemical synapse
release and reception of neurotransmitters; 2 parts
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chemical synapse parts
axon terminal- lots of synaptic vessicles that contain neurotransmitters
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receptor region
receptors that bind to neurotransmitters
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information transfer at chemical synapse
- 1. calcium channels open at presynaptic axon terminal
- 2. neurotransmitter released
- 3. neurotransmitter binds to synaptic receptors
- 4. ion channels open in post synaptic membrane
- 5. neurotransmitter effects are terminated
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3 ways NT effects are terminated
- degrade NT enzymatically in cleft
- reuptake NT and store or degrade
- diffusion away from synapse
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post synaptic potential and synaptic integration
- neurotransmitters bind to receptors and open ion channels
- * mediate graded potentials
- * either excitatory or inhibitory
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timing
fast timing of bursts of NT release by one or more presynaptic neurons
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spatial
large number of neuron terminals from one neurons simultaneously stimulate a postsynaptic neuron
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ACH
best known, action varies with type of receptor
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biogenic amines
norepinephrine, dopamine, seratonin, histamine
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amino acids
GABA, glutamate, glycine
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peptides
endorphines, substance P, somatostatin
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dissolved gasses
nitric oxide, carbon monoxide
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botulinus toxin
inhibits ACH release, paralyzing voluntary muscle
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curare
prevents ACh binding to receptors, paralyzes muscle, arrow poision
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nerve gas and malathion
prevent ach breakdown by ache, prolonged muscle spasm
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barbituates
decreased rate of ACH release, acts as CNS depressant
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