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
2
Q
Anatomy of a Neuron
A
- A typical neuron is composed of:
- dendritic region
- a cell body
- axon hillock
- an axon
- axon terminals
3
Q
Parts of the Neuron: cell body
A
- houses nucleus and organelles
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
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
6
Q
Kinesins
A
- carry nutrients, enzymes, organelles away from cell body
7
Q
Dyneins
A
- carries recycled vesicles, chemical messengers back towards cell body
8
Q
Microtubule
A
- railway that the kinesins and dynein’s use
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
10
Q
movement of ions depends on
A
- permeability
- electrical gradient
- concentration gradient
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)
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+
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
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
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
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
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)
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)
19
Q
Action potential characteristics
A
- All or none principle
- refractory periods
- self propagating
- uni-directional movement
20
Q
what are the two types of propogation
A
- contiguous conduction
- conduction in unmyelinated fibers
- AP spreads along every portion of membrane - saltatory conduction
- rapid conduction in myelinated fibers
- impulse jumps over sections of the fiber covered with insulating myelin
- 50x faster
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)
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
23
Q
what is a synapse
A
- junction between two neurons
- this is the primary way that neurons interact with eachother
24
Q
Convergence and Divergence
A
- Convergence: many neurons input into one
- Divergence: one neuron synapses with many
25
Q
presynaptic neuron
A
- conducts action potential towards synapse
26
Q
synaptic knob
A
- contains synaptic vesicles
27
Q
synaptic vesicles
A
- stores neurotransmitter (carry signals across
28
Q
Postsynaptic neuron
A
- neuron whose action potentials are propagated away from the synapse
29
Q
synaptic cleft
A
- space between the presynaptic and postsynaptic neurons
30
Q
what occurs at a synapse
A
- 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
31
Q
How are NT released?
A
- calcium binds to synaptotagmin
- stimulates SNARE proteins (ensnare vesicles)
- causes NT release
32
Q
Post Syaptic membrane
A
- activates ionotropic receptors (actual ion channels)
- otherwise activates metabotropic receptors (2nd messenger activation of the channel)
33
Q
How long is the synaptic delay?
A
0.2-0.5 msec
34
Q
What are the two types of synapses
A
- Excitatory synapses - effect Na+ or ion gates
- Inhibitory synapses - effect K+ or Cl- gates
35
Q
What does the size of post-synaptic potential depend on?
A
- calcium levels (fatigue)
- NT levels
- Desensitization/hypersensitization
- presynaptic inhibition or facilitation
35
Q
What is spatial summation
A
- summation of many EPSPs occur at different locations on the dendrites at the same time
- the impulses can combine to reach threshold
36
Q
What is temporal summation
A
- summation of many EPSPs occur at the same location over a short period of time
37
Q
How do EPSP and IPSPs interact
A
- some neurons have up to 200,000 terminals
- the means that it can have inhibitory and excitatory transmission cancelling each other out
38
Q
Presynaptic facilitation/inhibition
A
- Neuron A releases neurotransmitter that can either increase or decrease the release from neuron B
- Ex. Opiates
39
Q
Common types of neurotransmitters
A
- 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)
40
Q
what are neuropeptides?
A
- large molecules consisting of 2-40 AA
- substance P (pain)
- enkephalins/endorphins
- dynorphins
- hypothalamic releasing and inhibiting hormones
- angiotensin II
- cholecystokinin
41
Q
Acetylcholine (Ach)
A
- cholinergic receptors
- parasympathetic system/muscle
- muscarinic vs nicotinic receptors (agonists)
- broken down by acetylcholinesterase and recycles
- sarin inhibits this enzyme
42
Q
Catecholamines
A
- 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
43
Q
Seratonin
A
- 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
Q
What is the impact of drugs around the synapse
A
- 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
45
Q
Categories of drug interactions
A
- Agonists: mimic NT when they bind
- Antagonists: bind but do not activate, so they block site
46
Q
What are two examples of drugs that alter synaptic transmission
A
- cocaine: blocks reuptake of NT dopamine at presynaptic terminals
- Strychnine: competes with inhibitory NT glycine at postsynaptic receptor site
47
Q
What are two examples of bacterial toxins that alter synaptic transmittion
A
- 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
48
Q
Batrachotoxin
A
- 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
49
Q
Black Mamba Snake Toxin - Dendrotoxin K
A
- 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
50
Q
Increasing Extracellular K+
A
- 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
51
Q
Curare
A
- 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)
52
Q
Tetrodotoxin (TTX) - Poison from Puffer Fish
A
- also in newts, octopus, sea stars
- ingestion, inhalation, injection
- inhibits voltage sensitive Na+ gates
- no depolarization possible
- loss of sensation, paralysis of voluntary muscles
53
Q
Box Jellyfish Toxin
A
- 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
54
Q
General Anaesthetic - Sevoflurane
A
- 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)
55
Q
Lidocaine - Local anaesthetic
A
- Aka xylocaine
- blocks voltage-sensitive Na+ channels in sensory neurons (no AP)
- also block in cardiac motor neurons
56
Q
DDT - in insects
A
- acts to open Na+ gates
- over-firing
- spasms and death
- overuse in humans
- stimulates estrogens
- cancer causing
- neural degradation
57
Q
what are afferent neurons
A
- ascending
- dendrites in periphery
- terminal end in CNS
58
Q
what are efferent neurons
A
- descending
- dendrites in CNS
- terminal ends in periphery
- only autonomic nerves have synapses outside the CNS
59
Q
what are interneurons
A
- all in CNS
- make up 99% of all neurons
- very small
60
Q
Glial cells
A
- 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
61
Q
what are microglia
A
- immune cells
- protect CNS from pathogens
62
Q
Neuroglia - Astrocytes
A
- holds neurons in place
- general maintenance of space
- helps form blood-brain barrier
63
Q
Myelin
A
- increases conduction velocity
- secreted by schwann cells in PNS
- secreted by oligodendrocytes in CNS
64
Q
Ependymal Cells
A
- 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
65
Q
Brain Waves
A
- Alpha: lower frequency, relaxed state
- Beta: higher frequency, alert and concentrating
- Theta: light sleep
- Delta: deep sleep
66
Q
Brain during sleep
A
- alternates between non REM and REM sleep
- stage 1 through 4, back to 1 and then REM sleep
67
Q
Sleep patterns
A
- 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.
68
Q
What are the speech association areas
A
- Broca’s area (speech)
- Wernicke’s area (speech comprehension)
- Dyslexia is the poor connection between visual and language ares
69
Q
Limbic system
A
- 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
70
Q
Transfer from STM to LTM
A
- relates to past events and memories
- emotional response related to memory
- repetition
- sleep
- exercise and diet
71
Q
Habituation and sesnsitiation
A
- 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)
72
Q
Spinal cord
A
- neuronal link between brain and PNS
- integrating center for spinal reflexes
- sensory input via the dorsal root
- motor output via the ventral root
73
Q
Matter in the spinal cord
A
- Gray matter: Unmyelinated nerve cell bodies
- White matter: Myelinated axons that contain very few cell bodies
74
Q
Spinal reflexes
A
- faster when brain is not involved
- often monosynaptic
- brain receives impulse as an afterthought
75
Q
Skeletal muscle reflexes
A
- proprioceptors
- golgi tendon organ and muscle spindle
- located in muscle, joints, and ligaments
- Alpha motor neurons carry input to muscle
76
Q
Stretch reflex
A
- stretch of receptor sends AP’s up sensory neuron
- this increases the firing or motor neuron to have a reflex contraction
77
Q
A
78
Q
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