neurophysiology Flashcards
2 types of electrical signals b/t neurons
action potentials - travel long distances
graded potentials local membrane changes
Segments of a neuron
- Cell body = receptive segment–> binds neurotransmitters to create graded potentials
- Axon Hillock = initial segment - summation of graded potentials and initiation of action potential
- axon = conductive segment - propagation of action potential
- axon terminal = transmissive segment - AP causes release of neurotransmitters
Types of Ion Channels
- Leakage = always open -> more K+ ones than Na+ ones
- Ligand gated = open and close in response to stimulus (results in neuron excitability)
- voltage gated = respond to change in membrane potential
- mechanically gated = respond to mechanical vibration or pressure
RMP
- what is the #
- where’s + vs -
- the rmp is -70mV
- exists bc extracellular fluid is rich with Na+ and Cl- and inside is rich with K+, organic phosphate and AAs
- inward flow of Na+ can’t keep up with outward flow of K+
- Na+/K+ pump removes Na+ as fast in leaks in
Graded potentials
- small deviations from -70mV
- vary in amplitude depending on strength of stimulus
- lovalized
- occur most often in dendrites and cell body
2 types of graded potentials
- EPSP
- opens Na+ and K+ chem-gated channels
- Na+ influx > K+ efflux
- depolarization - IPSP
- Neurotransmitter binding causes hyperpolarization
- opens K and/or Cl chem-gated channels
- K efflux and/or Cl influx
Generation of APs
voltage gated na and k channels open in sequence
all or none principle
if stimulus reaches threshold the ap is always the same –> a stronger stimulus won’t cause a larger impulse
Depolarizing phase
- chem or mech stimulus causes graded potential to reach at least -55mV
- voltage gated na channels open and na enters cell
- Resting membrane: inactivation gate of na channel is open and activation gate is closed
- when -55mV is reached, both open
- inactivation gate closes again really fast–> 20,000 Na get in
-positive feedback process
Repolarizing Phase
- When -55mV is reached, K channels open, but do it really slow
- K finally open once Na have already closed
- K outflow causes repolarization and often hyperpolarization to -90mV
- k channels close and rmp goes to -70mV
Refractory period
- period when neuron can’t generate another AP
- absolute refractory = even strong stimulus won’t do anything –> inactivated Na channels have to go back to resting state first
- relative refractory period = a suprathrshold stimulus will start and AP –> k channels are still open, but Na channels have closed
continuous vs saltatory conductions
continuous = step-by-step depolarization of each portion of the length of the axolemms
Saltatory = depolarization at nodes of ranvier where there’s high density of voltage gated channels –> current carried by ions flows through extracellular fluid from node to node
Factors that affect speed of propagation
- amount of myelination : more myelin = faster
- axon diameter: bigger diameter = faster
- temp: warmer = faster
NOT related to strength of stimulus
fiber types, biggest to smallest
A fibers = 5-20 microns and 130 m/s –> myelinated somatic sensory and motor
B fibers = 2-3 microns and 15 m/s –> myelinated visceral sensory and autonomic preganglionic
C fibers = 0.5 - 1.5 microns and 2 m/s –> unmyelinated sensory and autonomic motor
2 types of synapse
- electrical = fast, 2-way, ionic current goes to next cell through gap junction
- chemical= 1 way info transfer from presynaptic to postsynaptic neuron (axodendritic, axosomatic, and axoaxonic)
chemical synapse
- AP reaches end bulb and voltage gated ca channels open
- ca influx triggers release of neurotransmiters
- neurotransmiters cross synaptic cleft and bind to ligand gated receptors (more neurotransmitters= bigger change in postsynaptic cell)
- synaptic delay = 0.5 msec
neurotransmitters
- can be excitatory and inhibitory –> same one can be both depending on location
- acetylcholine, glutamate, aspartate, gamma aminobutyric acid (GABA), glycie, norepinephrine, epinephrine, dopamine
Small molecule neurotransmiters
Ach = released by many PNS neurons and some CNS –> exitatory on NMJ, but inhibitory on others –> inactivated by AchE
AAs = glutamate= released by almost all excitatory neurons in brain --> inactivated by glutamate specific transporters -GABA = inhibiting neurotransmitter for 1/3 of all brain synapses (valium enhances GABA activity)
Ionotropic and Metabotropic receptors
- Ionotropic = ligand gated (channel-linked)
- Metabotropic = 2nd messenger protein (G prot linked)
G-prot linked receptor
-neurotrans binds to it, activating G protein–> G prot controls production of 2nd messenger (cAMP/cGMP)–> 2nd messenger open/close channels, activate kinases, phosphorylate channel prots, or activate genes to induce prot. synth
- responses= indirect, complex, slow and prolonged
- involves transmembrane prot. complexes
- cause widespread metabolic change
channel linked receptor
- ligand gated channel
- action is immediate and brief
- Excitatory receptors = channels for small cations (influx contributes to depolarization)
- Inhibitory receptors allow influx that causes hyperpolarization
- e.g. ach and aa
Removal of neurotransmitter
- diffusion = move down conc. gradient
- enzyatic degradation = AchE
- Uptake by neurons or glia cells = neurotransmitter transporters (prozac= seratonin reuptake inhibitor)
Summation
- if several presynaptic end bulbs release neurotransmitters at same time, combined effect may generate a nerve impulse due to summation
- may be spatial or temporal
spatial summation
multiple axon terminals release neurotransmitters to one neuron
-effects are added
temporal summation
presynaptic neuron releases neurotransmitters in rapid succession, so the effects pile up on top of themselves
results of summation
Excitatory > inhibitory but < threshhold = facilitation
excitatory > inhibitory and threshhold = AP
inhibitory > excitatory = Inhhibition
Modifications of neurotransmitters
- Agonists = enhance the effects
- Antagonist = blocks its action
types of neural circuits
- diverging
- convergins
- reverberating
- parallel after-discharge
regeneration/ repair
- limited ability for repair –> PNS can repair damaged dendrites or axons, but CNS can’t repair stuff
- Plasticity is maintained, though –> new dentrites/ proteins and changes in synaptic contacts
Repair in PNS
- Damage causes chromatolysis = swelling of cell body (peaks 10-20 days aft injury)
- Wallerian degeneration of distal portion of neuron days 3-5
- retrograde degeneration of proximal portion to first neurofibril node
- Regeneration after chromatolysis = synthesis of RNA and proteins favoring rebuiding of axon (several months) –> schwann cell/neurolemma on each side of injury repairs tube and axonal buds grow down the tube
requirements for PNS repair
- no damage to cell body
- schwann cells remain active and form tube
- scar tissue doesn’t form too fast
Neurogenesis in CNS
- formation of new neurons from stem cells doesn’t happen
- no neurogenesis in CNS
- This is bc neuroglial cells inhibit it, no growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue
