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Transcript
Neurophysiology
Keri Muma
Bio 6
The Nervous System



The master controlling and communicating
system of the body
Cells communicate by electrical signals that
are rapid and cause immediate responses
Functions



Sensory input – monitoring stimuli occurring inside
and outside the body
Integration – interpretation of sensory input
Motor output – response to stimuli by activating
effector organs
Overall Organization
Neural Tissue

The two principal cell types of the nervous system
are:


Neuroglial – cells that surround and support neurons
Neurons – excitable cells that transmit electrical signals
Neuroglia
Anatomy of Neurons


Cell body – contains nucleus and organelles
Dendrites – branching extensions

Receptive to neurotransmitters from pre-synaptic neurons and
transmit graded potential towards cell body
Anatomy of Neurons


Axon hillock – where cell body tapers into the axon,
site where action potential originates
Axon – single process extending from the cell body,
transmits action potential away from cell body
Anatomy of Neurons

Myelin sheath – formed by
schwann cells wrapping around
the axon resulting in concentric
layers of plasma membrane

Nodes of Ranvier – gaps in the
myelin sheath
Anatomy of Neurons

Telodendrites – distant branches of the axon

Axon terminals – enlarged distal ends containing secretory
vesicles filled with neurotransmitters
Synapses

Synapses – junctions between neurons


Function as a control or decision point since they can be
excitatory or inhibitory
Occurs between axon terminals and a cell body, dendrite,
axon hillock, muscle or gland
Structure of Chemical Synapses



Presynaptic neuron – transmits impulse towards the
synapse, axon terminal with vesicles containing
neurotransmitters
Synaptic cleft – fluid filled space between pre and post
synaptic neuron
Postsynaptic neuron - transmits impulse away from
synapse, contains receptors for neurotransmitters
Types of Ion Channels found in Neurons




Ligand-gated channels – chemically gated, open when
neurotransmitters bind. Found on dendrites, cell bodies, and
axon hillocks
Mechanically gated channels – open in response to
physical forces
Voltage-gated channels – open or close in response to
changes in membrane potential. Found along axon
Leaky channels – always open, non-gated, found
everywhere
Neurophysiology

Electricity


When opposite charges are separated they contain
potential energy and when they come together energy
is released as electrical energy
In cells, the separation of charges by the plasma
membrane is referred to as the “membrane potential”
Membrane has no potential
Membrane has potential
Membrane
Remainder of
fluid electrically
neutral
Separated charges
responsible for
potential
Remainder of
fluid electrically
neutral
Principles of Electricity

Voltage – the measurement of potential energy created
by charge separation


In neurons voltage is measured in millivolts (1 mV = 1/1000 V)
The voltage depends on the quantity of charges and the
distance between the charges
Membrane Potentials

Resting Membrane Potential – potential difference
across the membrane in a resting neuron (-70mV)


Chemical gradient – higher concentration of Na+ in the
extracellular fluid and a higher concentration of K+ in the
intracellular fluid
Electrical gradient – the inside of the membrane is
negatively charged and the outside is slightly positive
EFC
IFC
Permeability
Na+
150
15
1
K+
5
150
50-75
65
0
Proteins (A- 0
)
Resting Membrane Potential

Factors contributing to the resting membrane
potential



Membrane is 50 – 75X more permeable to K+ so K+
ions leak out faster than Na+ leak in
Intracellular proteins - fixed anions inside the cell
Sodium-Potassium pump maintains the chemical and
electrical gradient – 3 Na+ out for every 2 K+ in
Membrane Potentials

Stimuli will trigger disruptions
in RMP
Can be stimulated by
neurotransmitters binding to
ligand gated channels,
mechanical stress, or
temperature change
Triggers a graded potential – a
localized change in membrane
potential
 Short lived and dissipates as it
travels
 Examples: receptor potentials,
post-synaptic potentials, motorend plate potentials


Changes in Membrane Potential


If the stimulus is excitatory it will cause depolarization of the
membrane
Depolarization – the membrane potential becomes less
negative

When neurons are stimulated Na+ channels open and Na+
rushes into the cell down its electrochemical gradient
Graded Potentials


Magnitude of the stimulus depends
on how many Na+ channels open
This determines the distance that the
graded potential will travel

Amount of Na+ channels
affected by the stimulus
depends on the:



Frequency of stimuli summation
Amplitude of stimuli - strength
Strong graded potentials can initiate
action potentials if the threshold
potential is reached at the trigger
zone
Graded Potentials
Membrane Potentials

Threshold potential = -55mV

The critical level the membrane potential must reach to open
voltage-gated Na+ channels on the axon to produce an action
potential
Membrane Potentials

Action Potential – brief reversal of the
membrane potential



Propagated away from the cell body down the entire
length of the axon without diminishing (all or none)
Wave of depolarization
followed by repolarization
Frequency of axon potentials
increases to reflect stronger
stimuli
Active area at peak
of action potential
Adjacent inactive area into
which depolarization is
spreading; will soon reach
threshold
Remainder of axon
still at resting potential
Local current flow that
depolarizes adjacent inactive
area from resting to threshold
Direction of propagation of action potential
Membrane Potentials

Repolarization - the
membrane returns to its
resting membrane
potential



Voltage gated Na+ channels
close
Voltage gated K+ channels
fully open and K+ efflux
restores the resting membrane
potential
Membrane potential becomes
more negative as K+ rushes
out
Previous active area
returned to resting
potential
Adjacent area that
was brought to
threshold by local
current flow; now
active at peak of
action potential
New adjacent inactive
area into which
depolarization is
spreading; will soon Remainder of axon
still at resting potential
reach threshold
Membrane Potentials

Hyperpolarization - the
inside of the membrane
becomes more negative
than the resting potential


Voltage gated K+ channels
are sluggish to close
K+ permeability lasts longer
and membrane potential dips
below resting potential
(between -80 mV and -90mV)
Membrane Potential

Restoring the Resting Membrane Potential:


Repolarization restores the electrical gradient
Na/K pump restores resting ionic concentrations
Voltage gated Na+ Channels
Voltage Gated Na+
Channels
Voltage gated K+ Channels
Refractory Periods

Refractory Periods – amount of time required for a
neuron to generate another action potential
Refractory Period

Absolute Refractory Period - when another AP
cannot be generated

From the opening of the Na+ activation gates until the
resetting of the activation gates


Ensures that each action
potential is separate
Enforces one-way transmission
of nerve impulses
Previous active New active area
area returned to at peak of action
resting potential potential
New adjacent inactive area
into which depolarization
is spreading; will soon reach
threshold
“Forward” current flow excites new inactive area
“Backward” current
flow does not re-excite
previously active area
because this area is
in its refractory period
Direction of propagation of action potential
Refractory Period

Relative Refractory Period


The interval following the absolute refractory period
Threshold is raised so only exceptionally strong stimuli
will trigger another action potential :



Sodium gates are reset
Potassium gates are still open
Hyperpolarization is occurring
Summary
Factors Influencing Conduction Velocity

Myelination of axon – increases impulse rate


Acts as insulator preventing charge leakage
Saltatory conduction – voltage gated channels are
concentrated at the nodes so electrical impulses jump from
node to node instead of having to travel down the entire
axon
Factors Influencing Conduction Velocity

Diameter of the axon – the larger the diameter the
quicker the impulse travels, less resistance to
current flow so adjacent membranes depolarize
quicker

Alcohol, sedatives, and anesthetics – slow or
block nerve impulses by reducing permeability to
Na+.
Insufficient blood flow – slows impulses, caused
by cold or pressure

Transmission Across the Synapse




Action potential reaches the axon terminal
Voltage-gated Ca2+ channels open and Ca2+ floods into the
terminal
Synaptic vesicles fuse with the plasma membrane and release
neurotransmitters into the synaptic cleft
Neurotransmitters diffuse across the synaptic cleft and bind to
receptors on chemical gated channels initiating a postsynaptic
potential
Neurotransmitter effects on Postsynaptic
Potentials


Binding of neurotransmitters cause a graded
potential (localized change in the membrane)
Depending on how the neurotransmitter
affects the membrane potential determines if
it will excite or inhibit the postsynaptic neuron
Postsynaptic Potentials

Excitatory postsynaptic potentials (EPSP) –
binding of neurotransmitter opens Na+ channels and
causes depolarization

Membrane potential becomes less negative and closer to
reaching threshold potential therefore closer to firing an
action potential
Postsynaptic Potentials

Inhibitory Postsynaptic Potentials (IPSP) – binding of
neurotransmitters cause hyperpolarization of the
membrane therefore moving away from threshold and
reducing the ability to initiate an action potential


Causes K+ or Cl- channels to open
K+ rushes out or Cl- rushes in, both causing the inside to
become more negative
Summation


A single EPSP cannot induce an
action potential but they can be
summed
The axon hillock keeps score of
all graded potentials received
Postsynaptic Potentials

Temporal summation –
a presynaptic neuron
increases the frequency
of impulses and more
neurotransmitters are
released in quick
succession
Postsynaptic Potentials

Spatial summation – postsynaptic neuron is
stimulated by multiple presynaptic neurons at the
same time

IPSPs and EPSPs can also be summed and cancel each
other out
Summary of Summation
Summary of Summation
Modulator Neurons


The effectiveness of the presynaptic input can be
affected by another neuron (see neuron B in picture below)
Allows for the selective inhibiting/enhancing of a
specific presynaptic neuron without affecting the input
from other neurons or effecting all targets
Modulator Neurons


Presynaptic inhibition – the amount of
neurotransmitter released from neuron “A” is
decreased
Presynaptic facilitation – the amount of
neurotransmitter released from neuron “A” is
enhanced
Presynaptic Inhibition vs. Postsynaptic Inhibition
Effects of Neurotransmitters

Neurotransmitter receptors mediate changes
in membrane potential according to:



The amount of neurotransmitter released
The amount of time the neurotransmitter is bound
to receptors
Neurotransmitters will affect the membrane
potential as long as they are bound so they must
be deactivated
Deactivation of Neurotransmitters

Three ways neurotransmitters are inactivated:



By enzymes
Through reuptake by presynaptic axon terminals or
astrocytes
They diffuse away from synapse
Termination of Neurotransmitter Effects

Acetylcholine



Degraded by the enzyme acetylecholinesterase
found in the synaptic cleft
Ach
Acetate + Choline
Choline is actively transported back into the
presynaptic terminal and recycled
 Choline + acetyl CoA
Ach
Choline
acetyltransferase
Termination of
Neurotransmitter Effects

Norepinephrine,
dopamine, serotonin



Taken back up by
presynaptic terminal
Repackaged or broken
down by monoamine
oxidase (MAO)
Catechol-Omethytransferase is used
by liver and kidney cells
to break down NE & E in
the circulation
Classification of Neurotransmitters by
Chemical Structure





Acetylcholine (ACh)
Biogenic amines – catecholamines, serotonin
Amino acids – glutamate, glycine, GABA
Peptides – endorphins, substance P
Messengers: ATP and dissolved gases NO
Classification by Function



Excitatory neurotransmitters (e.g., glutamate)
Inhibitory neurotransmitters (e.g., GABA and
glycine)
Some neurotransmitters have both excitatory and
inhibitory effects


Determined by the receptor type of the postsynaptic
neuron
Example: acetylcholine
 Excitatory at neuromuscular junctions with skeletal
muscle (nicotinic receptor)
 Inhibitory in cardiac muscle (muscarinic receptor)
Neurotransmitter Receptor Mechanisms

Direct: neurotransmitters that open ion channels


Promote rapid responses “fast synapses”
Examples: ACh and amino acids
Neurotransmitter Receptor Mechanisms

Indirect: neurotransmitters that act through second
messengers


Promote long-lasting effects, “slow synapses”
Examples: biogenic amines, peptides, and dissolved
gases
Fast vs. Slow Responses in Postsynaptic Cells
Types of Circuits in Neuronal Pools

Divergent – one incoming fiber stimulates ever
increasing number of fibers, often amplifying
circuits
Figure 11.25a, b
Types of Circuits in Neuronal Pools

Convergent –
opposite of
divergent circuits,
resulting in either
strong stimulation
or inhibition
Figure 11.25c, d
Types of Circuits in Neuronal Pools

Reverberating – chain of neurons containing
collateral synapses with previous neurons in
the chain
Figure 11.25e
Types of Circuits in Neuronal Pools

Parallel after-discharge – incoming neurons
stimulate several neurons in parallel arrays
Figure 11.25f