Transcript a14b NeuroPhysII

Membrane Potentials That Act as Signals
 Two types of signals
potentials
• Graded
Graded potentials
o Incoming short-distance signals
o Short-lived, localized changes in membrane
potential
o Depolarizations or hyperpolarizations
o Graded potential spreads as local currents change
the membrane potential of adjacent regions
• Action potentials
o Long-distance signals of axons
Graded Potential: Depolarization
Depolarizing stimulus
Inside
positive
Inside
negative
Depolarization
Resting
potential

Stimulus causes gated ion channels to open
•
E.g., receptor potentials, generator
potentials, postsynaptic potentials

Magnitude varies directly (graded) with
stimulus strength

Decrease in magnitude with distance as
ions flow and diffuse through leakage
channels
Time (ms)
(a) Depolarization: The membrane potential
moves toward 0 mV, the inside becoming
less negative (more positive). Increases the
probability of producing a nerve impulse.
Figure 11.9a
Graded Potential: Hyperpolarization
Hyperpolarizing stimulus
Resting
potential
Hyperpolarization
Time (ms)
(b) Hyperpolarization: The membrane
potential increases, the inside becoming
more negative. Decreases the probability of
producing a nerve impulse.
Figure 11.9b
Membrane potential (mV)
Active area
(site of initial
depolarization)
–70
Resting potential
Distance (a few mm)
(c) Decay of membrane potential with distance: Because current
is lost through the “leaky” plasma membrane, the voltage declines
with distance from the stimulus (the voltage is decremental ).
Consequently, graded potentials are short-distance signals.
Figure 11.10c
Membrane Potentials That Act as Signals
 Two types of signals
• Graded potentials
o Incoming short-distance signals
o Short-lived, localized changes in membrane potential
o Depolarizations or hyperpolarizations
o Graded potential spreads as local currents change the membrane
potential of adjacent regions
• Action potentials
o Long-distance signals of axons
Action Potential (AP)
 Brief reversal of membrane potential with a
total amplitude of ~100 mV
 Occurs in muscle cells and axons of neurons
 Does not decrease in magnitude over distance
 Principal means of long-distance neural
communication
Anatomy of an Action Potential
•Na+ channel slow inactivation gates close
• All gated
and
channels are closed
Na+
•Slow voltage-sensitive K+ gates open
Na+
K+
influx causes more
depolarization
1 Resting state
Membrane potential (mV)
•Membrane permeability to Na+ declines to
resting levels
Depolarizing local currents open
voltage-gated Na+ channels
•K+ exits the cell and internal negativity is
restored
3 Repolarization
2 Depolarization
33
22
Action
potential
Na+
permeability
Action
potential
K+ permeability
Threshold
1
1
44
Time (ms)
1
Relative membrane permeability
• Only leakage channels for
Na+ and K+ are open
•Some K+ channels remain open,
allowing excessive K+ efflux
•This causes afterhyperpolarization of the membrane
(undershoot)
4 Hyperpolarization
Channel gating (online
animation)
Figure 11.11 (1 of 5)
Voltage Change at Point in Neuron as Action Potential Passes By
Voltage
at 0 ms
Recording
electrode
(a) Time = 0 ms. Action potential has not yet
reached the recording electrode.
Resting potential
Peak of action potential
Hyperpolarization
Figure 11.12a
Voltage Change at Point in Neuron as Action Potential Passes By
Voltage
at 2 ms
(b) Time = 2 ms. Action
potential peak is at the
recording electrode.
Figure 11.12b
Voltage Change at Point in Neuron as Action Potential Passes By
Voltage
at 4 ms
Action
potential
online
Figure 11.12c
(c) Time = 4 ms. Action potential peak is past
the recording electrode. Membrane at the
recording electrode is still hyperpolarized.
Threshold Stimulus
 Subthreshold stimulus—weak local depolarization that does not reach
threshold
 Threshold stimulus—strong enough to push the membrane potential
toward and beyond threshold (Membrane is depolarized by 15 to 20 mV)
 AP is an all-or-none phenomenon—action potentials either happen
completely, or not at all
 All action potentials are alike and are independent of stimulus intensity
Action
potentials
Threshold
Stimulus
Time (ms)
Figure 11.13
Refractory Periods
Absolute refractory
period
Depolarization
(Na+ enters)
Relative refractory
period
ARP
Time from the opening of the Na+ channels until the
resetting of the channels
Ensures that each AP is an all-or-none event
Enforces one-way transmission of nerve impulses
RRP
•Most Na+ channels have returned to their resting state
•Some K+ channels are still open
•Repolarization is occurring
Threshold for AP generation is elevated
Exceptionally strong stimulus may generate an AP
Repolarization(K+ leaves)
After-hyperpolarization
Stimulus
Time (ms)
Figure 11.14
AP Velocity a Function of Axon Diameter and Myelination
Stimulus
Size of voltage
(a) In a bare plasma membrane (without voltage-gated
channels), as on a dendrite, voltage decays because
current leaks across the membrane.
Voltage-gated
Stimulus
ion channel
(b) In an unmyelinated axon, voltage-gated Na+ and K+
channels regenerate the action potential at each point
along the axon, so voltage does not decay. Conduction
is slow because movements of ions and of the gates
of channel proteins take time and must occur before
voltage regeneration occurs.
Stimulus
Myelin
sheath
(c) In a myelinated axon, myelin keeps current in axons
(voltage doesn’t decay much). APs are generated only
in the nodes of Ranvier and appear to jump rapidly
from node to node, about 30 times faster than a bare axon.
Continuous
conduction
Saltatory
conduction
Node of Ranvier
1 mm
Myelin sheath
Figure 11.15
Multiple Sclerosis (MS)
 Nature
• An autoimmune disease that mainly affects young adults
• Symptoms: visual disturbances, weakness, loss of muscular control,
speech disturbances, and urinary incontinence
• Myelin sheaths in the CNS become nonfunctional scleroses
• Shunting and short-circuiting of nerve impulses occurs
• Impulse conduction slows and eventually ceases
 Treatment
• Some immune system–modifying drugs, including interferons and
Copazone:
o Hold symptoms at bay
o Reduce complications
o Reduce disability
Nervous Tissue and Function
 Function of the Nervous System
 Organization (Structural and Functional)
 Supporting Cells of the Nervous System
 Anatomy of a Neuron
 Classification of Neurons by Function
 Graded and Action Potentials
 Myleination and MS
 Reflexes
 Synapses
 EPSPs and IPSPs
 Neurotransmitters
The Reflex Arc
Types of Reflexes and Regulation
 Autonomic reflexes
• Smooth muscle regulation
• Heart and blood pressure regulation
• Regulation of glands
• Digestive system regulation
 Somatic reflexes
• Activation of skeletal muscles
Nervous Tissue and Function
 Function of the Nervous System
 Organization (Structural and Functional)
 Supporting Cells of the Nervous System
 Anatomy of a Neuron
 Classification of Neurons by Function
 Graded and Action Potentials
 Myleination and MS
 Reflexes
 Synapses
 EPSPs and IPSPs
 Neurotransmitters
Two Kinds of Synapses
 Chemical Synapses
• Specialized for the release and reception of neurotransmitters
• Typically composed of two parts
o Axon terminal of the presynaptic neuron, which contains synaptic vesicles
o Receptor region on the postsynaptic neuron
 Electrical Synapses
• Less common than chemical synapses
• Neurons are electrically coupled (joined by gap junctions)
• Communication is very rapid, and may be unidirectional or bidirectional
• Are important in:
o Embryonic nervous tissue
o Some brain regions
How Neurons Communicate at Synapses
Events at the Synapse (online animation)
Narrated synapse (online)
 Irritability – ability to respond to stimuli
 Conductivity – ability to transmit an
impulse`
SodiumPotassium pump (online animation)
Chemical synapses
transmit signals from
one neuron to another
using neurotransmitters.
Presynaptic
neuron
Presynaptic
neuron
Postsynaptic
neuron
1 Action potential
arrives at axon terminal.
Mitochondrion
Ca2+
Ca2+
Axon
terminal
Ca2+
Ca2+
Synaptic
cleft
Synaptic
vesicles
Postsynaptic
neuron
Figure 11.17, step 1
Chemical synapses
transmit signals from
one neuron to another
using neurotransmitters.
Presynaptic
neuron
Presynaptic
neuron
Postsynaptic
neuron
1 Action potential
arrives at axon terminal.
2 Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Mitochondrion
Ca2+
Ca2+
Axon
terminal
Ca2+
Ca2+
Synaptic
cleft
Synaptic
vesicles
Postsynaptic
neuron
Figure 11.17, step 2
Chemical synapses
transmit signals from
one neuron to another
using neurotransmitters.
Presynaptic
neuron
Presynaptic
neuron
Postsynaptic
neuron
1 Action potential
arrives at axon terminal.
2 Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Mitochondrion
Ca2+
Ca2+
3 Ca2+ entry causes
neurotransmittercontaining synaptic
vesicles to release their
contents by exocytosis.
Axon
terminal
Ca2+
Ca2+
Synaptic
cleft
Synaptic
vesicles
Postsynaptic
neuron
Figure 11.17, step 3
Chemical synapses
transmit signals from
one neuron to another
using neurotransmitters.
Presynaptic
neuron
Presynaptic
neuron
Postsynaptic
neuron
1 Action potential
arrives at axon terminal.
2 Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Mitochondrion
Ca2+
Ca2+
3 Ca2+ entry causes
neurotransmittercontaining synaptic
vesicles to release their
contents by exocytosis.
4 Neurotransmitter
diffuses across the synaptic
cleft and binds to specific
receptors on the
postsynaptic membrane.
Axon
terminal
Ca2+
Ca2+
Synaptic
cleft
Synaptic
vesicles
Postsynaptic
neuron
Figure 11.17, step 4
Ion movement
Graded potential
5 Binding of neurotransmitter
opens ion channels, resulting in
graded potentials.
Figure 11.17, step 5
Enzymatic
degradation
Reuptake
Diffusion away
from synapse
6 Neurotransmitter effects are terminated
by reuptake through transport proteins,
enzymatic degradation, or diffusion away
from the synapse.
Figure 11.17, step 6
Chemical synapses
transmit signals from
one neuron to another
using neurotransmitters.
Presynaptic
neuron
Presynaptic
neuron
Postsynaptic
neuron
1 Action potential
arrives at axon terminal.
2 Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Mitochondrion
Ca2+
Ca2+
Ca2+
3 Ca2+ entry causes
neurotransmittercontaining synaptic
vesicles to release their
contents by exocytosis.
Axon
terminal
Ca2+
Synaptic
cleft
Synaptic
vesicles
4 Neurotransmitter
diffuses across the synaptic
cleft and binds to specific
receptors on the
postsynaptic membrane.
Postsynaptic
neuron
Ion movement
Enzymatic
degradation
Graded potential
Reuptake
Diffusion away
from synapse
5 Binding of neurotransmitter
opens ion channels, resulting in
graded potentials.
Events at the Synapse (online animation)
Narrated synapse (online)
6 Neurotransmitter effects are
terminated by reuptake through
transport proteins, enzymatic
degradation, or diffusion away
from the synapse.
SodiumPotassium pump (online animation)
Figure 11.17
Nervous Tissue and Function
 Function of the Nervous System
 Organization (Structural and Functional)
 Supporting Cells of the Nervous System
 Anatomy of a Neuron
 Classification of Neurons by Function
 Graded and Action Potentials
 Myleination and MS
 Reflexes
 Synapses
 EPSPs and IPSPs
 Neurotransmitters
Excitatory Synapses and EPSPs
Neurotransmitter binds to and opens chemically gated channels that allow simultaneous flow of Na + and
K+ in opposite directions

Na+ influx is greater that K+ efflux, causing a net depolarization

Excitatory postsynaptic potential (EPSP) helps trigger AP at axon hillock if EPSP is of threshold strength
and opens the voltage-gated channels
Membrane potential (mV)

Threshold
An EPSP is a local
depolarization of the
postsynaptic membrane
that brings the neuron
closer to AP threshold.
Neurotransmitter binding
opens chemically gated
ion channels, allowing
the simultaneous passage of Na+ and K+.
Stimulus
Time (ms)
Figure 11.18a
Inhibitory Synapses and Inhibitory Postsynaptic Potential (IPSPs)
Neurotransmitter binds to and opens channels for K+ or Cl–

Causes a hyperpolarization (the inner surface of membrane becomes more negative)

Reduces the postsynaptic neuron’s ability to produce an action potential
Membrane potential (mV)

Threshold
An IPSP is a local
hyperpolarization of the
postsynaptic membrane
and drives the neuron
away from AP threshold.
Neurotransmitter binding
opens K+ or Cl– channels.
Stimulus
Time (ms)
Figure 11.18b
Nervous Tissue and Function
 Function of the Nervous System
 Organization (Structural and Functional)
 Supporting Cells of the Nervous System
 Anatomy of a Neuron
 Classification of Neurons by Function
 Graded and Action Potentials
 Myleination and MS
 Reflexes
 Synapses
 EPSPs and IPSPs
 Neurotransmitters
Chemical Classes of Neurotransmitters
 Acetylcholine (Ach) (Mostly excitory in CNS, PNS if prolonged prod. tetanus (with nerve
gases), receoptors destroyed in myasthenia gravis)
•
Released at neuromuscular junctions and some ANS neurons
•
Synthesized by enzyme choline acetyltransferase
•
Degraded by the enzyme acetylcholinesterase (AChE)
 Biogenic amines
o
Catecholamines
 Dopamine (“Feeling good” CNS neurotransmitter, uptake blocked by cocaine, excitory or inhibitory), norepinephrine
(NE), and epinephrine
o
Indolamines
 Serotonin (Roles in sleep, appetite, nausea, mood; blocked by seritonin-specific reuptake inhibitors (SSRIs) like
Prozac and LSD, enhanced by ecstasy (3,4-Methylenedioxymethamphetamine)), histamine
•
Broadly distributed in the brain; play roles in emotional behaviors and the biological clock
 Amino acids include:
o
GABA—Gamma ()-aminobutyric acid (inhibitory brain NT augmented by alcohol, benzodiazepine-valium)
o
Glutamate (excitory in CNS, causes stroke when overreleased, overstimulation of neurons) , Glycine, Aspartate
 Peptides (neuropeptides) include:
o
Substance P, endorphins, somatostatin, cholecystokinin
 Purines such as ATP
 Gases and lipids
•
NO, CO, Endocannabinoids