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neuroscience > Neural Communication, Synaptic Transmission, and Neuroplasticity > Flashcards

Neural Communication, Synaptic Transmission, and Neuroplasticity Flashcards

1
Q

Describe propagation of information through neurons

A
  • Electrically: through the neurons
  • Chemically: between the neurons using synapse
  • using membrane ion channels
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2
Q

Describe membrane ion channels

A
  • they span the cell membrane
  • they let ions pass through selectively, Na+, K+, Cl-, etc.
  • there are 4 major types: modality-gated, ligand-gated, voltage-gated, and leak channels
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3
Q

What do modality-gated ion channels respond to

A
  • touch
  • pressure
  • chemical changes
  • temperature changes
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4
Q

What do voltage-gated ion channels respond to

A
  • mostly open in response to voltage or electrical changes
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5
Q

Describe resting membrane potential

A
  • neuron is at rest and is not conveying information
  • not unique to neurons
  • at resting state, K+ more on the inside, Na+ more on the outside
  • K+ ion channels open at resting state, Na+ channels closed
  • K+ diffuses outside, down the concentration gradient, until counteracted by equal & opposite electrical gradient, which establishes electrochemical equilibrium (-80mV)
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6
Q

What is resting potential predominantly determined by

A
  • potassium permeability (K+)
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7
Q

Difference in Na+ channel permeability and K+ channel permeability and there effects on resting membrane potential

A
  • Na+ channels are also permeable but Na+ permeability is 5% of K+, so resting membrane potential is less than -80mV and sits around -70mV
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8
Q

What are the two ways that neurons use potential differences to generate & convey information

A
  • local/graded potentials (any value)
  • action potentials (finite value)
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9
Q

Describe the types of local/graded potentials

A
  • Synaptic potentials: between nerve endings
  • Receptor potentials: at receptor endings
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10
Q

Define action potentials

A
  • they are transient changes in potential difference in local areas of the axon membrane that are propagated rapidly down the axon to convey information
  • all or nothing response
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11
Q

Define local/graded potentials

A
  • they are potential differences that are created in specific areas in the membrane of nerve cell bodies or dendrites that are ultimately summated at the initial segment to generate action potentials
  • are graded depending on the strength of the incoming stimulus
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12
Q

How does changes in local potential differences create an action potential through the axon

A
  • resting potential is about -70mV to -80mV
  • if a small region of the plasma membrane is stimulated either electrically, chemically, or mechanically, the Na+ channels become more permeable and allow the Na+ ions to diffuse inside the cell which results in minute reversal of the voltage potential (graded potential and depolarizes the cell)
  • the cell can also be hyper polarized if Cl- ion channels become open & Cl- ions diffuse inside the plasma membrane resulting in an even higher negative potential
  • the different regions of neurons cell bodies/dendrites constantly receive depolarizing (less negative state) or hyperpolarizing (more negative state) stimuli from several connections it makes to neighboring neurons resulting in a summation of potentials at the initial segment & if the summation results in a large enough depolarization then the neuron will fire an action potential down the axon
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13
Q

Describe triggering of an action potential

A
  • it starts at the initial segment: the area with dense Na+ ion channels
  • the threshold stimulus is between -70mV to -55mV
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14
Q

Describe propagation of action potential

A

1) Resting potential: voltage-gated Na+ & K+ channels closed
2) Threshold potential: voltage-gated Na+ channels open & Na+ enters the axon, beginning to depolarize the axon
3) Depolarization: more Na+ channels open, Na+ rushes in depolarizing the membrane, Na+ channels close about 1 ms after opening
4) Depolarization: many K+ channels open, K+ exits the cells, taking positive charges out of the axon
5) Hyperpolarization: K+ channels remain open, K+ continues to leave the axon, restoring the polarized membrane potential
6) Restoration of Na+ & K+ ion levels by Na+-K+ pump plus K+ leak channels

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15
Q

What part of action potential propagation requires energy

A
  • Only the very end requires energy in order to restore the Na+ & K+ ion levels after an action potential has passed
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16
Q

What drives the action potential process

A
  • sodium ion channels opening & coming inside
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17
Q

What are the features of an action potential

A
  • Propagated by voltage-gated Na+ channels
  • Refractory period: absolute phase (no chance of restimulating) and relative phase (might be stimulated again but difficult
  • Refactory period needed to prevent back flow of stimulus
  • Active restoration of ions across membrane by Na+-K+ pumps following refractory period, needs energy from ATP
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18
Q

Describe the different summations of local potentials trigger action potentials

A
  • Single weak stimulus: results in only local depolarization
  • Spatial summation: multiple weak stimuli in different areas results in significant depolarization
  • Temporal summation: multiple weak stimuli in rapid succession in the same area results in significant depolarization
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19
Q

Sequence of potential changes that causes flow of information

A

1) Deformation of receptor membrane
2) Generation of receptor potential
3) Generation of action potential
4) Propagation of action potential
5) Depolarization of presynaptic membrane
6) Release of neurotransmitter
7) Stimulation of receptors on postsynaptic membrane
8) Opening of ion channels
9) Generation of synaptic potential

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20
Q

What is the effect of myelination

A
  • faster conduction of action potential
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21
Q

What do myelin internodes do

A
  • the exchange of ions does not happen all throughout the length of the axon due to myelin internodes but only happens at the nodes of Ranvier
22
Q

What are the nodes of Ranvier

A
  • they are the small areas of exposed axon membrane not covered in a myelin sheath
23
Q

Describe what myelination does

A
  • Helps action potential travel faster using saltatory conduction (jumping from one node to the next)
  • Actual ion exchange/depolarization of membrane happens only at the nodes: potential difference is ‘sensed’ by the next Node of Ranvier to trigger the action potential there
  • Helps action potential travel a longer distance: insulates axons, minimizes current loss, maintains potential difference/current strength by minimizing resistance & maximizing capacitance
24
Q

Sequence of events at a synapse to transmit information

A

1) action potential reaches presynaptic terminal
2) calcium enters presynaptic terminal
3) vesicles move toward release site
4) presynaptic terminal releases neurotransmitter
5) neurotransmitter binds to postsynaptic membrane receptor
6) membrane channel changes shape & ions enter postsynaptic cell

25
Q

Types of synapses

A
  • Axodendritic: axon terminal to dendritic synapse
  • Axosomatic
  • Axoaxonic: between axon of a presynaptic neuron & axon of postsynaptic neuron
26
Q

Types of graded/local potentials (post/synaptic potentials)

A
  • EPSP (excitatory post synaptic potential):when neurotransmitter binding to receptor causes local depolarization
  • IPSP (inhibitory post synaptic potential): when neurotransmitter binding to receptor causes local hyper polarization, summation of EPSP & IPSP can determine when action potential is generated
27
Q

Describe presynaptic facilitation

A
  • axon terminal 1 slightly depolarizes axon terminal 2
  • Ca2+ influx
  • the action potential of 2 causes more Ca2+
  • more than normal amounts of vesicles released
  • intensifies pain sensations when patient concentrates
28
Q

Describe presynaptic inhibition

A
  • axon terminal 1 slightly hyperpolarizies axon terminal 2
  • action potential of 2 causes less Ca2+ influx
  • less vesicles released
  • when therapist asks patient to focus on a task to block thoughts of pain
29
Q

2 classes of neuromessengers

A
  • Neurotransmitters: action occurs at synapse, excitatory or inhibitory postsynaptic potential, milliseconds to minutes
  • Neuromodulators: action occurs at extrasynaptic sites (not a synapse), change gene expression, open ion channels, alter metabolism, & other processes, minute to days, bind G-protein-coupled receptors, & slow prolonged action
30
Q

Describe acetylcholine (ACh)

A
  • in the cholinergic category
  • usually excitatory action on postsynaptic membrane
  • major excitatory neurotransmitter in PNS, also found in CNS
  • can be fast acting (on nicotinic receptors) or slow acting/longer lasting (on muscarinic receptors)
  • can act on Nicotinic receptors (ligand-gated): associated with learning, memory, impairment of receptor is hallmark of Alzheimer’s or Myasthenia graves, drugs to treat these increase levels of Ach
  • Can act on Muscarinic receptors (GPCR): regulate cardiac muscle, smooth muscle of gut, glands
31
Q

Describe Glutamate (Glu)

A
  • in the amino acid category
  • excitatory action on postsynaptic membrane
  • principle excitatory neurotransmitter of CNS, open sodium channels
  • fast point-point depolarization
  • NMDA-receptor: associated with learning/memory
  • excessive glutamate can cause excitotoxicity
  • overactivity of NMDA receptors: epileptic seizures, chronic pain, Parkinson’s
32
Q

Describe GABA (y-Aminobutyric acid)

A
  • in the amino acid category
  • inhibitory action on postsynaptic membrane
  • inhibitory in CNS, opens chloride channels
  • GABAa and GABAb receptors
  • Diazepam, barbiturate mimic GABA, used to treat anxiety, seizures
  • Baclofen (GABA agonist): reduces excessive muscle tone, hyper polarizes motor neurons (reduces Ach release from the), used as a common anti-spastic medication
33
Q

2 classes of receptors

A
  • Synaptic receptors: ligand-gated ion channels (fast response) and G-protein-coupled ion channels (slower response)
    -Extrasynaptic receptors
34
Q

What do Ligand-gated ion channels act as

A
  • they act as both receptors of neurotransmitters and as ion channels
35
Q

Describe G-protein-coupled ion channels

A
  • have messenger proteins called ‘G-proteins’ attached to the receptor, which gets activated upon neurotransmitter binding
  • slower opening of ion channels using G-protein subunit
36
Q

Describe extrasynaptic receptors

A
  • neuromodulators usually bind to these receptors
  • also use G-proteins, but here it activates a second messenger system
  • have a slower, more profound, longer-lasting and more global effect
  • can also amplify incoming signals
  • receptor binds sequentially to 3 G-proteins
  • the different subunits of G-protein signal to multiple effector molecule
  • signal amplified
37
Q

In what ways do second messengers act

A
  • prolonged opening of ion channels
  • activation of genes to alter neurotransmitter production
  • release internal stores of Ca2+ to regulate metabolic processes
38
Q

Effects of Acetylcholine (Ach) based on binding site

A
  • Skeletal muscle membrane: initiates skeletal muscle contraction, Myasthenia graves destroys Ach receptors, Botulinum toxin is an antagonist
  • Autonomic NS: slows HR, constricts pupil, increases digestive secretions & smooth muscle contraction, Atropine is an antagonist
  • Brain: arousal pleasure, feeling of reward, cognitive function, tobacco smoking and Alzheimer’s disease effect this, nicotine is an agonists
39
Q

Describe Glycine

A
  • inhibitory, opens chloride channels
  • in brainstem & spinal cord
  • low levels of glycine: seizures, unwanted skeletal contractions
40
Q

Effects of GABA based on binding site

A
  • CNS: inhibition. sedation, anti anxiety, anti seizure, & sleep inducing, low GABA results in seizures, unwanted skeletal muscle contraction, & anxiety, Alcohol, Benzodiazepines (including Valium), Barbiturates, Epilepsy drugs, & Baclofen are all agonists
41
Q

Effects of Glutamate based on binding site

A
  • Brain: excitation, learning, & memory, excess Glutamate results in epileptic seizures, excitotoxicity, chronic pain, Parkinson’s disease, & schizophrenia, Phencyclidine is an antagonist
42
Q

Effects of Glycine based on binding site

A
  • Spinal cord: inhibition, low GABA results in unwanted skeletal muscle contractions, Strychnine is an antagonist and results in convulsions, spasms, & respiratory paralysis
43
Q

Describe Dopamine

A
  • motor activity, cognition, behavior, motivation driven by wanting reward
  • cocaine & amphetamines block dopamine re-uptake and increases dopamine release (feeling of euphoria/energy)
  • Parkinson’s: low dopamine supplemented by L-Dopa (crosses BBB)
44
Q

Describe Norepinephrine (noradrenaline)

A
  • increases attention and vigilance
  • fight or flight response of the sympathetic nervous system
  • excessive levels cause panic disorders and PTSD
  • Cymbalta (duloxetine) SNRI (selective norepinephrine re-uptake inhibitor) blocks re-uptake of norepinephrine (anti-depressant)
45
Q

Describe serotonin

A
  • arousal, alertness, and cognition
  • Low levels associated with depression and suicidal behavior
  • Prozac (fluoxetine) SSRI (selective serotonin re-uptake inhibitor) blocks re-uptake and enhances serotonin activity in synapses
46
Q

Describe neuroplasticity

A
  • the property that the nervous system is ‘plastic’ or modifiable
  • ability of the brain to reorganize its structure, function, and connections in response to internal or external stimuli
  • can occur during development in response to environmental inputs, physiological basis of learning and memory, occur in response to disease/injury, and in response to physical rehab
  • requires activity
47
Q

Cellular mechanisms of neuroplasticity

A
  • changes in gene expression
  • synthesis of proteins for neurotransmitters or receptors
  • functional changes in synaptic strength (short term)
  • structural changes in synaptic connections (long term)
48
Q

Observable changes of neuroplasticity

A
  • learning/memory long term effects
  • response to injury, recovery/restoration or maladaptation
  • short term, simple types, habituation
49
Q

Describe habituation in physical therapy

A
  • decrease in response to repeated stimulus
  • due to pre-synaptic changes and decrease in neurotransmitter release
  • reduce tactile defensiveness by rubbing/brushing in autistic kids
  • habituation exercise to reduce dizziness/nausea to visually challenging environments
50
Q

steps in the nervous system to neuroplasticity

A

1) enhanced connection between neurons (LTP)
2) structural changes between neurons to maintain environment
3) enhanced neural motor network
4) enhanced neural representation of movements

51
Q

Describe long-term potentiation (LTP) and long-term depression (LTD)

A
  • best known cellular physiological substrate for experience dependent plasticity, learning, and memory
  • occurs in the hippocampus
  • also occurs in motor, somatosensory, visual, auditory cortices, and cerebellum, contributing to learning
  • LTP converts weak/silent synapses into strong/active synapses & LTD does the opposite
  • LTP needs correlated presynaptic & post-synaptic firing of neurons: based on the concept of Hebbian plasticity
  • lack of synchronous firing or absence of synaptic activity causes LTD
52
Q

When does best/optimal recovery of cortical injury happen

A
  • it happens when cortical remapping looks almost like the original (ie. areas adjacent/closest to injury take up lost function)

neuroscience (10 decks)

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