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Chapter 3 Resting

Depolarization
DEFINITION
A regenerative electrochemical signal.
DEFINITION
Both excitable and non-excitable cell
membranes have an electrical potential
Faithfully transmit information along the
reversal of An electrical potential across their cytoplasmic membranes.
membrane (axon) of excitable cells
Tetrodotoxin (TTX) membrane difference that exists between Resting potential are membrane potential of
(nerves).
from the puffer fish. potential. Main Stages the inner and outer surfaces excitable cells that are at rest.
Allow for rapid communication between of the plasma membrane.
selective antagonist for rapid opening of
voltage gated Na distant parts of a neuron. Due to the differential
Na selective
channels distribution of ions. FACTORS
channels
both channel blocker. The permeability of the membrane
to differentions.
Repolarization
Difference in ionic concentrations
Tetraethylammonium (TEA) return of
K channel blocker. membrane
ACTION
may be effective either potential to RMP. MEMBRANE
POTENTIAL Ion pumps maintain the concentration
on outer face of K closure POTENTIAL difference by actively moving ions against
channel or inner face. (inactivation) of the gradient using metabolic resources.
Na+ selective Two Ion channels allow the passage of ions in
channels. independent the direction of the concentration gradient.
channels

INCREASING CONDUCTION VELOCITY OHM'S LAW V is Voltage (Volts, V)


Driving force or “pressure” on
CONDUCTION VELOCITY Increasing axon diameter electrons to move.

axial resistance decreases in proportion to square of axon diameter.


capacitance increases in direct proportion to diameter Neural the voltage difference across the
plasma membrane is equal to the R is Resistance (Ohms, Ω)

membrane capacitance, Cm limits the


conduction velocity.
increases rate of passive spread.

myelination of axons
Signalling product of membrane current (I)
and membrane resistance (R).
Opposition to flow that the
electrons encounter.
lipid bilayer = great insulator properties
and very thin = high capacitance. increases the functional thickness of the axonal membrane. I is Current (Amperes, A)
VELOCITY decreases capacitance of the membrane. Number of electrons that are
increases the conduction velocity of action potential.
moving for a given driving force
(V) and resistance to flow (R).
FAMOUS FINAL EXAM QUESTION
TIME CONSTANT

Ionic Gradients as Batteries Any construct that can separate HODGKIN-HUXLEY MODEL NEURON AS AN ELECTRICAL CIRCUIT
Concentration of ions differ between inside the MEMBRANE AS electric charge.
neuron and outside the neuron. CAPACITORS Ion separations across membranes
LENGTH CONSTANT Permeate the membrane (FACTORS) : Difference in
create an ionic potential. Batteries
✢ Selective for passage of certain ions
ion concentration
✢ Vary in their permeability
✢ Always open to some degree "leaky"
Membrane capacitance (Cm)
proportional to the cells surface Cell membrane Capacitor
Ion Channels as Resistors
Leak channels (resting channels) area and membrane resistance.
Rm (membrane resistance) ✢ Fixed resistors how fast the cell membrane
✢ Linear conductance relationship, gL Ionic channels Resistors
Ra (axial resistance) potential responds to the flow of
Voltage-gated channels ion channel currents.
✢ Variable resistors Factors : membrane area (A) and
✢ Non-linear conductance relationship, gn (t,V) membrane spacing (d).
1. Selectivity 2. Activation ✢ Voltage-activated (A,top):
✢ Increase length constant Change in MP change in CC (favor open state)
Increases what is able to cross control of gating
✢ Depolarization current moves Activated by depolarization (common) /
quickly
resistance(Rm)
✢ Non-selective: anions,cations,small hyperpolarization
✢ Current flow not sufficient to organic molecule ✢ Stretch-sensitve (A,bottom):
discharge capacitance along entire
✢ Charge-selective: permeable to only Change in membrane tension alters CC
length of axon. Stretch-activated and inactivated channels are
anions/cations
common
Myelination ✢ Ion-specific: depends on specific ions Properties
✢ Ligand-gated (B):
"to form myelin sheath" (eg: K+,Cl-,Na+)
Specific binding site change in channel
✢ Depends upon: pore size and charge
structure that alter its open state
✢ Exposed bare membrane(~2um) in pore
✢ Leak (non-gated):
✢ Increases capacitance
consitutively open ion channels (pores)
✢ Depolarization currents lows
Node of Ranvier * MP; membrane potential / CC; channel conformation *
✢ High density of Na+ channels 'short length where the axonal

SIGN
✢ Intense depolarization membrane is exposed'
Ion channels ✢ +ve charge flowing into the cell is
3. Gating

URAL

ALLI
defined as -ve(inward)current
open(conductive)/closed
✢ -ve charges leaving the cell would also
state(non-conductive)
NG of the channel be -ve current
NE ✢ if steady-state response is measured,
linear current-voltage relation is obtained

Examples ✢ Voltage>+ve than RP=depolarization


Demyelination "Membrane protein ✢ Voltage>-ve than RP=hyperpolarization
"Loss of the myelin sheath complexes that span
that insulates axons" (or traverse)the membrane"

Types Gated channels


✢ Charcot-Marie Tooth Disease exist in 3 states
✢ Multiple sclerosis Recording
✢ Alexander’s Disease "patch clamp technique" ✢ Resting state: Channel is closed but can
Result ✢ Voltage-activated:Open when MP changes be activated
✢ Transverse myelitis
✢“clamp” MP at different voltages &
✢ Chronic inflammatory
& exceeds threshold ✢ Active state: Channel is open
establish effects on channel activity
demyelinating neuropathy Only present in excitable cells ✢ Refractory state: Channel is inactivated
✢ Current randomly switches
✢ Ligand-gated: Open non-covalent binding between two levels due to channel ✢ Opening of channel is stimulus-driven
✢ Impaired or lost conduction
of an intracellular ligand (cAMP)/extracellular (open/closed)
✢ Neuronal death
ligand (neurotransmitters) ✢Channel being in open/closed state
✢ Symptoms vary widely and
for a greater proportion of time(but
✢ Stress-activated:Physical force pulls open
depend on the collection of still opening and closing at random)
neurons affected channel
Exocytosis stimulated by release of intracellular
The process of information transfer at a
calcium
synapse Synaptic Proteins alter conformation - activated
Neuron to target cell
Transmission Vesicle membrane incorporated into presynaptic
membrane
Depends on nature of transmission:
Neurotransmitter released
Electrical synapse and Chemical synapse
Vesicle membrane recovered by endocytosis

Found in neuroblasts (during


Electrical
development), mammalian brainstem,
synapse Mechanism of exocytosis
and retina
Types of transmitter

Pre-and postsynaptic cell membranes


Disadvantages
are in close to each other, separated
Loss of signal strength 50 different neurotransmitters have
by gap junctions.
No amplification of synaptic

ur
been identified

e a
Instant transfer, no delay seen with

l
signal Classified chemically and functionally

N
chemical synapses
Cannot transmit inhibitory Acetylcholine being the first identified
Important for mental attention, arousal
information
from sleep, and ion & water
Harder to regulate
homeostasis

Si Serotonin (5-HT) is derived from amino

g n a lli n
Chemical acid tryptophan

g
synapse Serotonin is few in number but important
in regulating mood, behavior and sleep

Converts an electrical signal to a


Neuromuscular junction
chemical signal & back to an electrical
Presynaptic 1. Vesicle clustering /restraint
signal
Transmitter: Acetylcholine 2. Targeting (scaffolding proteins at the
Presynaptic neuron releases
enclosed in vesicles active zone recruit synaptic vesicles)
transmitter via vesicles & diffuses
3. Docking (Vesicles fuse by interaction
through synpatic cleft to bind to Neurotransmitter criteria
Postsynaptic between protein of vesicle and cell
postsynaptic receptors
Receptor: Nicotinic acetylcholine membrane)
Delay is due to release of transmitter,
receptor 4. Exocytosis
diffusion across synaptic cleft, binding
5. Endocytosis (NSF and SNAPs mediate
to receptors, and opening of ligand-
Presynaptically synthesized and disassembly of the SNARE complex,
gated channels
Advantages stored Life cycle of synaptic leading to vesicle recycling)
Can amplify & transform Released from presynaptic terminal vesicles 6. Vesicle maturation (Acidification,
signals upon stimulation neurotransmitter uptake, Insertion of
Prolongs the effects of the Induce a postsynaptic response vesicle membrane protein, Vesicle
signal Mimic with agonists, block with clustering)
Easier to regulate antagonists

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