Lecture 7 - Neurons and the Nervous System Flashcards
Central Nervous System
- brain
- spinal cord
Peripheral Nervous system
- nerves and neurons outside of the brain and spinal cord that connect to limbs and organs
SOMATIC
- innervative skin, joints, muscles
- voluntary
AUTONOMIC - innervative organs, blood vessels and glands (visceral functions) - involuntary - two divisions 1, sympathetic - fight or flight 2, parasympathetic - rest and digest
Two Cell Types in Nervous System
Neurons
- generate and transmit electrical signals (action potentials)
Glia
- 90% of the cells in your brain
- do not conduct action potentials
- support neurons physically, immunologically and metabolically
- importance in modulating proper neural function becoming increasingly recognized
Types of Glia
- astrocytes
- oligodendrocytes
- schwann cells
- microglia
astrocytes
- most numerous glia
- fill spaces between neurons
- regulate chemical content of extracellular space (remove excess ions, recycle neurotransmitters)
oligodendtocytes
- provide wrapping of insulating fatty layers around axons - myelin
- central nervous system
schwann cells
- provide myelin for the peripheral nervous system
microglia
- mediate immune and inflammatory response
Neuron and its structure
100 billion in the nervous system
3 parts:
- dentrites
- highly branched “tree”
- receives input to neuron
- short, spiny stubby - soma
- cell body of the neuron
- contains nucleus and other organelles - axon
- few branches (collaterals)
- sends output from neuron
- long, smooth
information flows from dendtrites through cell body to axon
Axon
- typically only one from the soma of neuron
- a few collaterals branch out
-where the action potential occurs
- serves as a “telegraph wire” to send info over long distances
- can be less than 1 mm or up to a meter
- nerve= bundle of axons
axon hillock - beginning near soma, integrates information and initiates action potential
axo terminals - end, forms synapse
Synapse
Where the axon of one neuron meets the dendrite of another
- presynaptic side = axon
- postsynaptic side = dendrite
synaptic cleft
- space in between axon and dendrite
~25 nm wide
electrical signal of the AP is converted to a chemical signal
- neurotransmitters
- bind to receptors on postsynaptic dendrite
a given neuron in the brain can have 1,000 synapses
How a signal is transmitted…
- information received in dendrites (neurotransmitters bind to receptors)
- integrated in axon hillock (ions flow from dendrites to hillock, aggregated, if enough, will induce AP)
- transmitted down long axon in form of action potential
- converted to chemical signal at axon terminal int he form of neurotransmitter release
- neurotransmitter can cross synapse to bind to receptors on another dendrite and start cycle over
How does an action potential work?
- based upon movements of ions
arise due to propagation of electrical charge down axon
electrical charge is created by charged ions
Membrane of axon
- divides charge to create a resting membrane potential
- allows selective flow of ions to generate the action potential
- reliable conduction of action potential down axon
Monitoring Voltage of inside of the cell
- movement of ions across the membrane results in a change in voltage
- value is expressed in terms of the inside of the neuron relative to the outside solution
- measured by voltmeter
Distribution of K+ ions
high concentration inside
Distribution of Na+ ions
high outside
Sodium Potassium Pump
- uses ATP to pump ions against their concentration gradients
- create a large driving force for ion flow
- pumps Na+ outside of cell (keeps extracellular Na+ high)
- pumps K+ in (keeps intracellular K+ high)
Potassium and Na+/K+ pump
potassium wants to rush out
+ charge leaving
inside of cells becomes more negatively charged
negative voltage inside
Sodium and the Na+/K+ pump
sodium wants to rush in
+ entering
inside of cell becomes more positively charged
positive voltage inside
Importance of distribution of charges
- equilibrium potential
2. membrane potential
equilibrium potential
- takes one ion into account
- the voltage of the cell that would result from that one ion moving freely across the membrane achieving equilibrium
- specific potential for each ion - each ion has its own equlibrium potential (might be different fo Na+ and K+)
membrane potential
- the actual value of the voltage inside the cell compared to the outside of the cell
- take into account all ions
- also dependent on permeability (which ions can cross the membrane at that point in time)
- voltage across neural membrane at any moment
- inside relative to outside
Nernst Equation
used to calculate the equilibrium potential
E = 61.6 log (outside/inside)
- increasing outside conc of a positive ion will make the eq more positive
- increasing the inside conc of a positive ion will make the eq potential more negative
Equilibrium potential is specific to…
- each ion
- what the voltage of the cell would go to if a channel for that ion and that ion only was opened
two factors in membrane potential
1.Equilibrium potential of each ion
- how permeable the membrane is to each ion compared to the others
- if an ion cannot flow across the membrane, it cannot be creating a charge difference (voltage)
- the more permeable the membrane is to an ion, the close the membrane potential will be close to that ion’s equilibrium potential
*resting membrane potential = the membrane potential when no gated channels have been signaled to open
Resting membrane potential
Vm = resting membrane potential
- at rest, cell membrane is impermeable to most ions
- except POTASSIUM LEAK CHANNELS
- always allow K+ to flow across membarne more readily than other ions
- therefore, at rest, membrane potential of the cells is close to the equilibrium potential for K+
Expected resting membrane potential
- at rest, the membrane potential of the cell is close to the equilibrium potential for K+
- constant (weak) flow of K+ out of cell makes inside negative
Vm = -65mv
Significance of ion gradients
- they are used to create electrical signals in the neuron
ion channels:
- selective for specific ions
- gated: open/close in response to particular stimuli
Two kinds:
- voltage gated
- ligand gated
Voltage gated ion channels
- open in response to a change in voltage across plasma membrane in axon
- in AXON
ligand gated ion channels
- open in response to a specific molecule (such as a neurotransmitter) binding
- in DENDRITES
How movements of ions change voltage in cells
Depolarization
- change in the cell’s membrane potential, making it more POSITIVE
Hyperpolarization
- change in the cell’s membrane potential, making it more negative
action potential
“robust and fast electrical signal that neurons use to convey information”
- change in membrane voltage that propagates down the axon
- generated by actions of voltage-gated Na+ and K+ channels in the plasma membrane of the axon
properties of the action potential
- resting potential
- rising phase
- falling phase
- undershoot
Resting potential
- Greater permeability to Potassium K+
- leak channels always open
- Vm = -65mv
- voltage gated sodium channels and voltage gated - potessium chanels both closed
threshold
- depolarization above threshold (-50mv) initiates rising phase
- threshold = membrane potential at which voltage gated sodium channels open
- initial depolarization due to signals from dendrites
- initiated at Axon hillock
Rising phase
- once the threshold is reahed, voltage-gated sodium channels open briefly (voltage gated potassium channels still closed)
- sodium influx
- rapid depolarization
- membrane potential gets close to the na+ equilibrium potential of +56mv
- rises to ~40mv
falling phase
- voltage gated Na+ channels close
- voltage gated K+ channels open
- K+ ions rush out of the cell
- hyperpolarization
undershoot
- membrane very permeable to potassium since K+ channels are open
- therefore membrane potential gets close to the K+ equilibrium potential of -80mv
- extra hyperpolarization until v-gated K+ channels close
refractory period
- na+ channels close based on time (after ~1-2ms of being open) regardless of the voltage around them
- once Na+ channels close they cannot open again for ~1-2 ms (inactivation)
- that reagion of the axon CANNOT fire another action potential during this time
propagation of action potential
- action potential is initiated when depolarizing signal (from dendrites) brings Na+ channels at axon hillock past threshold
- sodium influx in axon hillock leads some Na+ ions to diffuse to adjoining area
- depolarizes that adjoining area past threshold, opening those Na+ channels
- action propagates down length of axon
- refractory period prevents the signal from propagating backwards
Tetrodotoxin
How does it effect action potential?
(TTX)
- selective sodium channel blocker
- potent toxin
- causes muscle paralysis, including breathing
Importance of Myelin
- provides insulation - increases conduction velocity
- like wrapping a leaky hose in duct tape
- regularly spaced gaps in myelin sheath
- nodes of ranvier
- voltage gated ion channels are clustered here
- action potential at node recharges the depolarizing current
- saltatory conduction
Multiple Sclerosis
- demylenating disease
- autoimmune disease where body produces antibodies to myelin
- muscle weakness
- can also experience symptoms such as vision problems, speech problems, pain, fatigue, dizziness, changes in mood
Action potential and neurotransmitters
- action potential signals the release mof neurotransmitters into synaptic celft
- axon terminal contains vesicles filled with neurotransmitters
- when action potential arrives at the axon terminal, depolarization triggers the opening of voltage gated calcium channels (Ca++ flows into axon terminal)
- increased Ca++ triggers vesicles to fuse with presynaptic membrane and release neurotransmitter
neurotransmitters
- small molecules stored in synaptic vesicles
- released from presynaptic neuron into the synaptic cleft
- bind to specialized receptors on the postsynaptic neuron
- many drugs mimic the actions of neurotransmitters while others block the receptors that bind them, preventing their action
ex:
- serotonin
- dopamine
- glutamine
- GABA
- aetylcholine
excitatory receptor
- depolarization
- potitive ion in
- or negative ion out
- move membrane potential towards threshold
- make the postsynaptic cell more likely to fire an action potential
inhibitory receptor
- hyperpolarization
- negative ion in
- or positive ion out
- move membrane potential away from threshold
- male postsynaptic cell less likely to fire an action potential
Summation of information
- neuron integrates and sums all of the information from dendrites
- summation takes place in the axon hillock
- summation must depolarize to reach threshold (-50mv)
- one output for all this input = action potential
How action potentials differ/do not differ
alter
- frequency
- pattern
DO NOT differ in:
- size
- duration
“all-or-none” to cross threshold value
Neurotransmitters and their receptors
- released into synaptic cleft
- bind to receptors of postsynaptic cell
- on dendrite
- ligand-gated ion channels
- open in response to neurotransmitters binding
- allow influx of specific ions that cause depolarization of hyperpolarization
NOT an action potential, NOT voltage gated
can be
- excitatory
- inhibitory
Depolarization spread to axon hillock
- NO voltage gated ion channels in dendrite
- no action potential in dendrite
- depolarizations from the neurotransmitter receptors travel to the axon hillock
- inputs from many synapses on the neuron’s many dendrite branches sum together
- hillock integrates and sums the information from many inputs
- if sum of depolarization is enough to cross threshols, will induce action potential in axon
Summary of Neuron Information Flow
- Dendrites
- ligand gated ion channels
- neurotransmitter binds
- depolarization or hyperpolarization
- no action potential - Axon Hillock
- voltage changes from dendrites are summed
- if depolarization reaches threshold (-40mv) action potential is initiated - Axon
- Voltage gatd ion channels
- Action potential
- Rising Phase: Na+ in
- Falling phase: K+ out - Synapse
- voltage gated Ca++ chanels
- Ca++ in causes neurotransmitter release into synaptic cleft
Membrane Potential of Potassium
-75 mv
Membrane potential of Sodium
+56 mv
What would happen if you depolarized the middle of an axon?
What would happen if you depolarized each end?
- AP would go in both directions (no refractory period)
- would cancel each other out
Saltatory Conduction
Process of jumping from node to node while propagating a signal
Node of Ranvier
- regularly spaced gaps in myelin sheath
- voltage-gated ion channels clustered there
- action potential re-charges the depolarizing current