Neurophysiology Flashcards

1
Q

what does neural communication refer to?

A
  • nerve and muscle are excitable tissues
  • they can undergo rapid changes in membrane potentials, which is critical to the function of the neurons and muscles
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2
Q

Anatomy of a Neuron

A
  • A typical neuron is composed of:
  • dendritic region
  • a cell body
  • axon hillock
  • an axon
  • axon terminals
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3
Q

Parts of the Neuron: cell body

A
  • houses nucleus and organelles
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4
Q

Parts of the Neuron: Dendrites

A
  • increases surface area for receiving signals
  • sends signal towards cell body
  • this is the neurons input zone
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5
Q

Parts of the Neuron: Axon

A
  • Nerve “fiber”
  • conducts impulses (AP’s) away from the cell body
  • the axon hillock is where the axon meets cell body and is the neurons trigger zone
  • Axon terminals are the sight of synapse with other neurons or effector organs so they release chemical messengers
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6
Q

Kinesins

A
  • carry nutrients, enzymes, organelles away from cell body
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7
Q

Dyneins

A
  • carries recycled vesicles, chemical messengers back towards cell body
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8
Q

Microtubule

A
  • railway that the kinesins and dynein’s use
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9
Q

Membrane potential

A
  • the plasma membrane of all living cells has a membrane potential (polarized electrically)
  • separation of opposite charges across plasma membrane
  • occurs due to differences in concentration and permeability of key ions
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10
Q

movement of ions depends on

A
  • permeability
  • electrical gradient
  • concentration gradient
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11
Q

Nernst Equation

A
  • describes equilibrium potential for an ion
  • Eion = (61/z)log (Co/Ci)
  • Co – outside concentration
  • CI - inside concentration
  • Z – valence of the ion (Na / K are +1)
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12
Q

E Na

A
  • If only Na+ were allowed to move, equilibrium would be reached at +60mV
  • both electrical and concentration gradients encourage the inward movement of Na+
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13
Q

E K

A
  • if only K+ were allowed to move, equilibrium would be reaches at -89mV
  • this is due to opposing electrical and concentration gradients
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14
Q

Resting membrane potential for Neurons

A
  • both Na+ and K+ gates are closed
  • The potential is maintained by 4 things
    1. impermeable membrane
    2. Na+/K+ ATPase pump
    3. Increased permeability to K+ (it leaks out)
    4. anions inside of the membrane
  • resting membrane potential is around -70mV
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15
Q

what are the different membrane states of a neuron

A
  • polarization: state when the membrane potential is a value other than 0mV
  • depolarization: membrane becomes less polarized than at rest
  • repolarization: membrane returns to resting potential after a depolarization
  • hyperpolarization: membrane becomes more polarized than at rest
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16
Q

Graded Potentials

A
  • serve as short-distance signals
  • initiated by mechanical, chemical, and electrical stimulus
  • usually initiated in dendrites
  • they are local and die away quickly
  • can be added together together to become larger in amplitude (summate)
  • amplitude of a graded potential depends on the stimulus strength (vary in size)
  • can be excitatory or inhibitory
  • no refractory period
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17
Q

Action Potentials

A
  • brief, rapid, large (100mV) changes in membrane potential
  • They don not decrease in strength as they travel from their site of initiation
  • Na+ gates require time to reset
  • ion changes produce the 4 phases of action potential
  • when GP’s reach threshold (-55mV)
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18
Q

Stages of Action Potential

A
  • reaching threshold triggers Na+ gates to open - depolarization (+30mV)
  • Na+ gates close as K+ gates open with causes K+ to rush out - repolarization
  • K+ gates are too slow to close - hyperpolarization (-80mV)
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19
Q

Action potential characteristics

A
  • All or none principle
  • refractory periods
  • self propagating
  • uni-directional movement
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20
Q

what are the two types of propogation

A
  1. contiguous conduction
    - conduction in unmyelinated fibers
    - AP spreads along every portion of membrane
  2. saltatory conduction
    - rapid conduction in myelinated fibers
    - impulse jumps over sections of the fiber covered with insulating myelin
    - 50x faster
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21
Q

Regeneration of Nerve Fibers

A
  • Depends on the location
  • Schwann cells of PNS guide the regeneration of cut axons
  • fibers in CNS myelinated by oligodendrocytes do not have regenerative ability (inhibit regeneration)
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22
Q

What is Myelin

A
  • fatty insulator (primarily composed of lipids)
  • formed by oligodendrocytes in CNS
  • formed by Schwann cells in PNS
  • leaves exposed nodes of Ranvier
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23
Q

what is a synapse

A
  • junction between two neurons
  • this is the primary way that neurons interact with eachother
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24
Q

Convergence and Divergence

A
  • Convergence: many neurons input into one
  • Divergence: one neuron synapses with many
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25
presynaptic neuron
- conducts action potential towards synapse
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synaptic knob
- contains synaptic vesicles
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synaptic vesicles
- stores neurotransmitter (carry signals across
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Postsynaptic neuron
- neuron whose action potentials are propagated away from the synapse
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synaptic cleft
- space between the presynaptic and postsynaptic neurons
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what occurs at a synapse
- AP arrives at terminal end - voltage gated Ca2+ open - Ca2+ moves into knob - triggers release of neurotransmitter (NT) - NT migrates across synapse - NT binds to receptor site to open ion gates and trigger graded potential
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How are NT released?
- calcium binds to synaptotagmin - stimulates SNARE proteins (ensnare vesicles) - causes NT release
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Post Syaptic membrane
- activates ionotropic receptors (actual ion channels) - otherwise activates metabotropic receptors (2nd messenger activation of the channel)
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How long is the synaptic delay?
0.2-0.5 msec
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What are the two types of synapses
1. Excitatory synapses - effect Na+ or ion gates 2. Inhibitory synapses - effect K+ or Cl- gates
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What does the size of post-synaptic potential depend on?
- calcium levels (fatigue) - NT levels - Desensitization/hypersensitization - presynaptic inhibition or facilitation
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What is spatial summation
- summation of many EPSPs occur at different locations on the dendrites at the same time - the impulses can combine to reach threshold
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What is temporal summation
- summation of many EPSPs occur at the same location over a short period of time
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How do EPSP and IPSPs interact
- some neurons have up to 200,000 terminals - the means that it can have inhibitory and excitatory transmission cancelling each other out
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Presynaptic facilitation/inhibition
- Neuron A releases neurotransmitter that can either increase or decrease the release from neuron B - Ex. Opiates
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Common types of neurotransmitters
- NT vary from synapse to synapse - same NT is always released at a particular synapse and quickly removed from synaptic cleft * Acetylcholine *dopamine/serotonin * Norepinephrine/epinephrine * Histamine * Glutamate * Gamma-aminobutyric acid (GABA)
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what are neuropeptides?
- large molecules consisting of 2-40 AA - substance P (pain) - enkephalins/endorphins - dynorphins - hypothalamic releasing and inhibiting hormones - angiotensin II - cholecystokinin
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Acetylcholine (Ach)
- cholinergic receptors - parasympathetic system/muscle - muscarinic vs nicotinic receptors (agonists) - broken down by acetylcholinesterase and recycles - sarin inhibits this enzyme
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Catecholamines
- epinephrine/norepinephrine * affect consciousness, mood, attention *BP, HR - Adrenergic/noradrenergic receptors *broken down by monoamine oxidase or MAO *MAO inhibitors increase epi levels in synapse
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Seratonin
- from tryptophan - modulates slow onset - excitatory on muscle control - inhibitory on sensory mediation - mood, anxiety, wakefulness - block reuptake with paxil (antidepressant) as well as LSD
44
What is the impact of drugs around the synapse
- altering the synthesis, axon transport, storage or release of a NT - modifying neurotransmitter interaction with the postsynaptic receptor - influencing neurotransmitter reuptake or destruction - replacing a deficient NT with a substitute transmitter
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Categories of drug interactions
- Agonists: mimic NT when they bind - Antagonists: bind but do not activate, so they block site
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What are two examples of drugs that alter synaptic transmission
- cocaine: blocks reuptake of NT dopamine at presynaptic terminals - Strychnine: competes with inhibitory NT glycine at postsynaptic receptor site
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What are two examples of bacterial toxins that alter synaptic transmittion
- tetanus toxin: prevents release of inhibitory NT GABA, affecting skeletal muscles * destroys SNARE proteins - Botulism: interferes with SNARE proteins for excitatory NT which causes muscle paralysis
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Batrachotoxin
- poison dart frogs - causes the nerves to reach threshold easier (more likely to get AP) - can lower threshold by 30-50mV - can fire at resting membrane potential in some cases - neurons cannot depolarize - causes: initial muscle spasms (including the diaphragm), eventual depletion of Ach stores which then block the stimulation of muscles
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Black Mamba Snake Toxin - Dendrotoxin K
- inhibits K+ gates - prevents AP repolarization, meaning AP is prolonged and neuron releases more NT - causes: muscle spasms and tremors, then convulsions, eventually die of respiratory failure or cardiac arrest
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Increasing Extracellular K+
- KCl injection * concentration gradient of K+ across the cell membrane is reduced * less K+ flows out of the cell through the "leak" channels * Intracellular concentration rises * membrane potential closer to threshold - In the brain it is likely to produce seizures - astrocytes usually absorb excess potassium from extracellular space via potassium channels in their membranes
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Curare
- south and central america - is the paralyzing poison used on arrows - competes with Ach at nicotinic Ach receptors * inhibits action of Ach at neuromuscular junction * causes muscle weakness/paralysis * eventual death by asphyxiation (paralysis of diaphragm)
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Tetrodotoxin (TTX) - Poison from Puffer Fish
- also in newts, octopus, sea stars - ingestion, inhalation, injection - inhibits voltage sensitive Na+ gates * no depolarization possible * loss of sensation, paralysis of voluntary muscles
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Box Jellyfish Toxin
- Sea wasp - enough toxin to kill 60 people - cells become porous * Allows potassium leakage * Hyperkalemia * lose K+ gradient for neural cells * cardiovascular collapse and death within 2-5 mins
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General Anaesthetic - Sevoflurane
- affects K+ leak channels that help maintain the resting membrane potential - this will hyperpolarize the membrane making it harder to reach threshold - inhalation anaesthetics prefered to tager neurons in the brainstem that control consciousness and respiration)
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Lidocaine - Local anaesthetic
- Aka xylocaine - blocks voltage-sensitive Na+ channels in sensory neurons (no AP) - also block in cardiac motor neurons
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DDT - in insects
- acts to open Na+ gates * over-firing * spasms and death - overuse in humans * stimulates estrogens * cancer causing * neural degradation
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what are afferent neurons
- ascending - dendrites in periphery - terminal end in CNS
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what are efferent neurons
- descending - dendrites in CNS - terminal ends in periphery - only autonomic nerves have synapses outside the CNS
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what are interneurons
- all in CNS - make up 99% of all neurons - very small
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Glial cells
- make up 90% of CNS cells and 1/2 of the volume - these are support cells that help with physical and metabolic functions for CNS - there are astrocytes, microglia, ependymal cells and oligodendrocytes
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what are microglia
- immune cells - protect CNS from pathogens
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Neuroglia - Astrocytes
- holds neurons in place - general maintenance of space - helps form blood-brain barrier
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Myelin
- increases conduction velocity - secreted by schwann cells in PNS - secreted by oligodendrocytes in CNS
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Ependymal Cells
- ciliated epithelial membrane lining ventricles - secrete cerebrospinal fluid * shock absorption * nutrients - CSF made in choroid plexus - flows through ventricles into arachnoid space before being absorbed into arachnoid villi
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Brain Waves
- Alpha: lower frequency, relaxed state - Beta: higher frequency, alert and concentrating - Theta: light sleep - Delta: deep sleep
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Brain during sleep
- alternates between non REM and REM sleep - stage 1 through 4, back to 1 and then REM sleep
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Sleep patterns
- Non REM sleep (4 stages): rest and repair, theta and delta waves - REM sleep is a dream state, where problem solving and reverse learning occur.
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What are the speech association areas
- Broca's area (speech) - Wernicke's area (speech comprehension) - Dyslexia is the poor connection between visual and language ares
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Limbic system
- emotion, learning, and memory - hippocampus (learning and memory) - inputs to hypothalamus - short term memory has limited capacity, temporary neural trace but fast retrival - long term has a huge capacity with permanent neural trace but a slower retrieval
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Transfer from STM to LTM
- relates to past events and memories - emotional response related to memory - repetition - sleep - exercise and diet
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Habituation and sesnsitiation
- Habituation: decreased response to repeated in different stimuli causes decreased calcium at synapse - Sensitization: increased response to mild stimuli, causes more calcium to be released at syapse (emotional response included)
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Spinal cord
- neuronal link between brain and PNS - integrating center for spinal reflexes - sensory input via the dorsal root - motor output via the ventral root
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Matter in the spinal cord
- Gray matter: Unmyelinated nerve cell bodies - White matter: Myelinated axons that contain very few cell bodies
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Spinal reflexes
- faster when brain is not involved - often monosynaptic - brain receives impulse as an afterthought
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Skeletal muscle reflexes
- proprioceptors * golgi tendon organ and muscle spindle * located in muscle, joints, and ligaments - Alpha motor neurons carry input to muscle
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Stretch reflex
- stretch of receptor sends AP's up sensory neuron - this increases the firing or motor neuron to have a reflex contraction
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