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Neurophysiology > Cellular & Molecular Neuroscience > Flashcards

Cellular & Molecular Neuroscience Flashcards

1
Q

Neuroanatomy terminology review

nuclei Vs ganglia

A

nuclei (pleural) = CNS

ganglia (pleural) = PNS

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2
Q

reticular theory

A
  • connected through protoplasmic links
  • neurons linked together = “reticulum”
  • info can flow in any direction
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3
Q

5 Principles of “Contact theory”

A

1) neuron = elementary structural and signaling unit
2) law of dynamic polarization (dendrite –> terminal)
3) synapse
4) connection specificity
5) synaptic or neural plasticity

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4
Q

Electrophysiology - population recording

A
  • Utilizes macro-electrodes
  • Measures voltage
  • EEG (cortex) & EMG & ERP (specific sensory p/way)
  • Whole nerve (peripheral nerves)
  • Excellent temporal resolution, poor spatial resolution *
  • Clinical assessment
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5
Q

Electrophysiology - Single Cell Recording

A

-Utilizes micro-electrodes
-Measures ion current & voltage
-Resting membrane potential (RMP) & Graded potentials (IPSPs, EPSPs) & Action potentials (APs)
-Intracellular (in vivo/ in vitro) & Extracellular (in vivo)
& Patch clamp (in vitro)
-Experimental method

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6
Q

Neural Communication Properties

A
  • Electrical
  • Unique to “excitable” cells: neurons and muscle cells
  • Very fast (
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7
Q

Single-unit Electrophysiology : Extracellular unit recording

A

-in vivo

all-or-none action potentials (APs)

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8
Q

Single-unit Electrophysiology : Intracellular unit recording

A

-in vivo or vitro
resting membrane potential (RMP)
graded potentials (EPSPs, IPSPs)
APs

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9
Q

Single-unit Electrophysiology : Patch clamp

A

-in vitro

ionic current

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10
Q

Leak/leakage channels

A

-Open even in a resting state
• Selective for a single ion species
• Contribute to the RMP

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11
Q

Gated ion channels (active)

A

-Closed until opened by stimulus (voltage, ligand, sensory
stimuli)
• Can be selective for one or multiple ion species
• Necessary for graded and all-or-none action potentials
(APs) and neurosecretion
• Depolarizing & hyperpolarizing effects

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12
Q

Location of Leak channels

A

plasma membrane on cell body
dendrites
along the axon (nodes of ranvier)

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13
Q

Location of Ligand-gated channels

A

cell body & dendrites

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14
Q

Location of Voltage-gated channels

A
  • axon hillock
  • all along unmyelinated axons
  • nodes of Ranvier in myelinated axons
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15
Q

2 general classes of Synaptic Transmission

A

electrical and chemical.

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16
Q

Electrical synaptic transmission

A
  • intercellular region = gap junction
  • center pore = subunits called connexins = hexameric complex “connexon”
  • Transmission = bidirectional & very rapid
  • *Allows Synchronized electrical activity of a population
  • Minority of synapses*
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17
Q

Chemical synapses direct Vs non-direct

A
  • Directed: neurotransmitter release site and reception site are in close proximity
  • Non-directed: release site is at some distance from the site of reception
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18
Q

Gray type 1 Vs gray type 2

A 
Axodendritic synapses = Gray type I
-Larger synaptic cleft
-Often excitatory
Axosomatic synapses = Gray type II
-Smaller synaptic cleft
-Often inhibitory
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19
Q

Neuromuscular Junction (NMJ) -definition

A

chemical synapse that connects a motor neuron with the motor end-plates of multiple muscle fibers

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20
Q

NMJ

A
  • Activity = muscle fibers to contract.
  • Single motor neuron & all of the individual skeletal muscle fibers that it innervates = motor unit.
  • **All NMJs use acetylcholine (ACh).
  • r/c for ACh on sarcolemma = nicotinic r/c (nAChR)
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21
Q

Nicotinic ACh receptor

A
  • large protein consisting of 5 subunits (2α, 1β, 1γ, 1δ)
  • α subunits contain an ACh-binding region
  • Center pore = ion channel for Na+ ions
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22
Q

Electrical & then Chemical Synapses - compare

A 
Size of synaptic cleft & delay
-3.5 nm & 10-100 μsec
-20-40 nm & 1-5 msec

Functional attributes
-electrical = Synchronized firing of interconnected cells
-chemical = 
-Provides spatially & temporally focused transmission
-alterations in synaptic strength efficiency

Synaptic plasticity & amplification?
somewhat & no (all-or-none)
yes & yes
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23
Q

Properties of EPSPs/IPSPs

A
  • Depolarization = EPSP
  • Hyperpolarization = IPSP
  • Graded potentials (have varying amplitudes)
  • Travel passively & rapidly
  • Decremental (decrease in amplitude as they travel)
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24
Q

Features of an AP

A
  • Generated in axon hillock
  • Momentary reversals = negative to positive
  • all-or-none responses =magnitude =consistent
  • Voltage-gated channels mediate APs via membrane potential
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25
Q

Summation

A
  • majority of postsynaptic potentials (PSPs) = sub threshold
  • Spatial summation = PSPs from different synapses
  • Temporal summation = PSPs rapidly from same synapse
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26
Q

Stages of an action potential (AP)

A

1) Resting State: Na+ and K+ ion channels are closed = -70
2) Threshold: Na+ ion channels will open = AP

(3) Depolarization Phase:
Na+ ions = rush into the cell = alters membrane potential (less negative/more positive). ***K+ ion channels are still closed

(4) Repolarization Phase:
K+ ion channels begin to open while Na+ ion channels close. K+ ions rush out of the cell, which changes the membrane potential (making it more negative/less positive).

5) Undershoot: Na+ ion channels are closed and K+ ion channels are closing but slowly. = more (-) /less (+)
6) Refractory Period: In the wake of the AP, Na+ ion channels are deactivated and K+ ion channels are activated for a brief time. = harder to produce APs at this time.

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27
Q

Absolute Vs. Relative Refractory Period

A

**Absolute Refractory Period: Initiation of AP to immediately after the peak. ~1-2 ms.

**Relative Refractory Period: Following the absolute refractory period, Na+ channels begin to recover from inactivation. requires a stronger stimulation than normal.

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28
Q

AP Vs. postsynaptic potentials

A
  • APs are nondecremental
  • APs can travel in either direction
  • APs are conducted slower than post-synaptic potentials
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29
Q

Neurotransmitters (NTs)- defining criteria

A

1) Presynaptic Presence
2) Release -in response to presynaptic depolarization
- must be Ca2+ dependent
3) Postsynaptic R/c

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30
Q

Properties of NTs

A
  • contained in spherical vesicles in presynap
  • secreted via presynap –> synaptic cleft –> post synap
  • produce inhibitory effects, excitatory effects, or both
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31
Q

Categories of NTs (small)

A
  • slow. - ionotropic OR metabotropic r/c
    1) amino acids
    2) monoamines
    3) acetylcholine
    4) unconventional NTs
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32
Q

amino acids NTs

A
  1. Glutamate
  2. Aspartate
  3. Glycine
  4. Gamma-aminobutyric acid (GABA) inhib
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33
Q

Monoamine NTs

A

Slightly larger than AA NTs & more diffuse effects

  1. Dopamine
  2. Epinephrine
  3. Norepinephrine
  4. Serotonin (5-HTP, 5-HT)
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34
Q

Acetylcholine (Ach)

A
  • = add acetyl group to a choline molecule
  • Ach is the main NT at neuromuscular junctions (NMJs)
  • Also found at synapses in the ANS & CNS
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35
Q

Unconventional NTs

A

soluble-gases: nitric oxide & carbon monoxide

  • Produced in cytoplasm = diffuse cell membrane = (+) 2nd messenger cascades
  • Some = ~ few seconds!
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36
Q

Categories of NTs (large)

A 
Neuropeptides (NP) 
-Many act as NTs & hormones
5 loose categories:
 Pituitary peptides
 Hypothalamic peptides 
 Brain-gut peptides
 Opioid peptides
 Misc. peptides

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37
Q

Axonal Transport, Synthesis, & Packaging of Small-molecule NTs

A
  • synthesized = terminal button
  • Enzymes needed for synthesis = slow axonal transport
  • Packaged = small, clear core synaptic vesicles by Golgi in terminal button
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38
Q

Axonal Transport, Synthesis, & Packaging of Large-molecule/ Neuropeptides

A

-Synthesized = cell body on ribosomes
-Packaged into large, dense core synaptic vesicles by the Golgi in cell body
-Vesicles transported = fast axonal transport


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39
Q

Co-existence

A
  • neurons synthesize &release two or more different NTs
  • (not necessarily released simultaneously)
  • low frequency (+) = releases only small-molecule NTs
  • high frequency (+) = release of neuropeptides
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40
Q

Dale’s Rule (goes with co-existence)

A

A single neuron produces, packages, & releases the same chemical transmitter(s) at ALL of its synapses.

41
Q

Synaptic Vesicle Cycle

A

1) NTs = into synaptic vesicles @ PREsynaptic terminal
2) Vesicles–>‘active zones’ w/ voltage-gated Ca2+ channels
- synapsins = anchor vesicles
3) AP = depolarized = ion channels to open = more Ca2+ into the terminal
4) This Ca2+ influx = phosphorylation of synapsin proteins
5) Phosphorylation of synapsins = docking facing the synaptic cleft, fuse with it, and release their transmitters into the synaptic cleft (exocytosis)
6) Synaptic vesicles and/or membrane components are then rapidly retrieved (endocytosis)
- -Proposed mechanisms: “clathrin-mediated” endocytosis and/or “kiss-and-run”
7) Vesicles are recycled and re-filled with NT
- entire vesicle cycle lasts ~1 minute!>

42
Q

of vesicles released by a neuron?

A

directly related to the level of Ca2+ at terminal

  • low frequency (+) = releases only small-molecule NTs
  • high frequency (+) = release of neuropeptides
43
Q

importance of voltage-gated Ca2+ channels in neurotransmitter release:

A

-tetrodotoxin (blocks NA+ channels) still produced APs
-NT released is very sensitive to the exact amount of Ca2+
-Block voltage-dependent Ca2+ (via cadmium) = no NT
release or postsynaptic response
-Micro-injec of Ca2+ to presynaptic=NT release w/o AP

44
Q

postsynaptic basic r/c properties

A

-transmembrane protein with extracellular binding sites
-r/c are specific for NTs based on binding sites (ligand-
specific)

  • most NTs can bind to >1 receptor type
  • different brain regions
  • Often respond differently to the same NT
45
Q

postsynaptic Receptor subtypes

A
  • Ionotropic = ligand- or voltage-activated ion channels

- Metabotropic (aka G-protein coupled)

46
Q

Ionotropic Receptors

A
  • (+) via small molecule NTs
  • Binding = conformational change opening the ion channel
  • A postsynaptic potential will be immediately produced (an IPSP or an EPSP) Direct action leads to fast activation (~10 ms)
47
Q

Metabotropic Receptors

A
  • (+) both small NT or neuropeptides
  • (+) of a G-protein to the receptor –> intracellular r/n
  • longer lasting effects
48
Q

Autoreceptors

A
  • Metabotropic r/c located on the PREsynaptic:
  • Bind to their own neuron’s NT
  • homeostatic feedback system
49
Q

Agonist r/c binding

A
  • binds same receptor site & mimics the action of the endogenous ligand
  • Results in either full or partial response
50
Q

competitive antagonist r/c binding

A
  • binds to the same receptor site as the natural ligand (agonist)
  • Fully prevents activation by an agonist
51
Q

Non-competitive antagonist r/c binding

A

binds to a different binding site as the natural ligand

-Fully or partially prevents activation by an agonist

52
Q

Termination of Synaptic Messages

A
  1. Enzymatic degradation
  2. Reuptake
  3. Passive diffusion
53
Q

Molecular Signaling

A

mediates and modulates all brain functions

Signaling cell–> Signal –> R/c –> Target cell –> Response

54
Q

signal transduction pathway (STP)

A

-immediate and temporary changes in the physiological
state of the target cell
-or longer lasting and more permanent changes by
altering the transcription of genes, which affects the protein composition of the target cell

**allows for amplification of the signal as well as control of cell behavior

55
Q

Signal Amplification

A
  • Intracellular signal transduction is signal amplification
  • An individual signaling rxn can cause a greater response by generating a large number of molecular products
  • Similar amplification occurs in all signal transduction pathways
56
Q

Control of cell behavior

A

-Every signaling molecule’s concentration must return to baseline before the next stimulus arrives
-Keeping the intermediates activated is critical for sustained responses


57
Q

signalling molecule (3 classes)

A

1) Cell-impermeant molecules
2) Cell-permeant molecules
3) Cell-associated molecules

58
Q

1) Cell-impermeant molecules

A
  • extracellular receptors // short-lived

- includes: all NTs, other proteins, and peptide hormones

59
Q

2) Cell-permeant molecules

A
  • intracellular r/c in cytoplasm or nucleus
  • includes: steroid and thyroid hormones)
  • Tend to be insoluble and are often transported in the blood or other extracellular fluid by binding to specific carrier proteins
  • Unlike cell-impermeable molecules, these may persist in the bloodstream for hours or even days
60
Q

*Cell-associated molecules

A

bound to the extracellular surface of the plasma membrane of the signaling cell, bind to extracellular receptors
on target cells that they come into physical contact with (includes: integrins and neural cell adhesion molecules)

61
Q

Cell-impermeant molecule receptors

A

proteins that span the entire membrane
-Signal binding portion is extracellular & intracellular portion activates the signaling cascade

ex: ligand-gated ion channels, enzyme-linked receptors, and G-protein-coupled receptors

62
Q

Cell-permeant molecule receptors

A
  • intracellular proteins = cytoplasm or nucleus
  • Often bound to an inhibitory complex
  • Once activated, the complex is removed and a DNA-binding domain is exposed
  • Often activate signaling cascades that produce new mRNA and proteins within the target cell
63
Q

Two general classes of GTP-binding proteins:

A

Heterotrimeric & Monomeric

64
Q

Monomeric

A

G-proteins: made up of a single subunit

Often small GTPases involved in growth & development. not neurotransmitters

65
Q

Heterotrimeric

A

-Ligand binds to G-protein-coupled receptor
R/c = conformational change = G-protein activated = GDP bound to the G-protein complex is exchanged for GTP
-α subunit dissociates from β and γ subunits
-2nd messengers in the intracellular cascade
are activated by either the α subunit bound to
GTP or the βγ subunits

*Hydrolysis of GTP to GDP terminates the
signal

66
Q

Second Messengers =

A

cAMP, Ca2+, IP3, and nitric oxide (NO).

67
Q

Second Messenger Targets

A

2nd messengers can regulate neuronal function by modulating the phosphorylation state

  • Phosphorylation occurs via a wide variety of protein kinases
  • Dephosphorylation occurs via protein phosphatases
68
Q

basic brain connections are established

A
  • Formation of distinct brain regions
  • Neurogenesis: generation of neurons
  • Axogenesis: axon tract formation
  • Synaptogenesis: synapse formation
69
Q

Neuroplasticity- Critical periods

A

temporal windows = activity-mediated (environmentally-driven) influences on the brain are essential for development

70
Q

Neuroplasticity - Sensitive periods

A

temporal windows in which environmental activity influences brain circuitry however, to a lesser degree than during the critical period
** Majority of developmental = sensitive>critical periods *

71
Q

Evolutionary Perspective of Neuroplasticity

A

General principle: Once formed, neuronal circuits must be used. If not, they will often not survive or function normally.
**advantage = opportunities for experience

72
Q

Neuroplasticity: Early Studies

A
  • Sensory deprivation (Rats raised in total darkness)

- Environmental enrichment (rats in groups/complex cages)

73
Q

Competitive Nature of Experience and Neurodevelopment

A

Neural pathways that receive the most input form stronger connections and can potentially even ‘take over’ cortical regions
ex: Monocular deprivation

74
Q

Neurogenesis found where in humans?

A 
hippocampal neurons (via: dentate gyrus of hippocampus)
olfactory bulb (via: adult neural stem cells)
75
Q

Ischemia-induced Neural Injury Consequences

A
  • Limited or eliminated oxygen & glucose supply

* Prevention of removal of metabolic waste products

76
Q

Ischemia-induced Neural Injury Mechanisms:

A

1) Ionic imbalances
- no oxygen & glucose = no ATP = no [ion] gradients = depolarize = release NT = hinders re-uptake
2) Excitotoxicity (**main mechanism)
- prolonged exposure to excitatory NTs (e.g. glutamate)
- Deterioration cell structure & signaling capability

77
Q

The Role of Glutamate in Excitotoxicity

A

-Postsynaptic glutamate r/c (NMDA) over-(+) = excessive depolarization at postsynaptic = flood of Na+ and Ca2+
-overload of Ca2+ =
-Free radicals
􏰀-Mitochondrial dysfunction
􏰀-Disruption of the cell membrane
􏰀-Fragmentation of DNA
􏰀-Cell death via apoptosis, necrosis, or both

78
Q

Anterograde degeneration

A
  • degeneration = distal portion of the axon
  • rapid
  • Early regenerative changes do not guarantee that the neuron will survive- it must re-establish appropriate synaptic contacts or else it will die *
79
Q

Retrograde degeneration

A
  • degeneration = proximal segment
  • gradual
  • Early regenerative changes do not guarantee that the neuron will survive- it must re-establish appropriate synaptic contacts or else it will die *
80
Q

Conditions necessary for axonal regeneration:

A

1) gene expression

2) supportive environment:

81
Q

CNS & axonal regeneration

A

-unfavorable environment = Glia, astrocytes & other produce inhibitory signals
-protein called Nogo = block axon elongation by
interacting with the growth cone
-Macrophages do NOT promptly arrive

82
Q

PNS & axonal regeneration

A

favorable environment = Schwann cells & other non-neuronal cells produce cell adhesion molecules, extracellular matrix, neurotrophins = promote growth
-macrophages come rapidly

83
Q

Wallerian Degeneration & Repair

A
  • degeneration of the distal axon portion
  • cascade of cellular responses = clearing inhibitory debris & production of a supportive environment for axonal regrowth
84
Q

enhance the quality of life for CNS injuries

A

Blocking inhibitory molecules
Enhancing axon regeneration
Providing trophic (nutrition) support to surviving neurons

85
Q

Mechanisms of Neural Reorganization

A
  • Strengthening of existing connections

- new connections by collateral sprouting

86
Q

Treatment of Nervous System Damage

A
  1. Blocking neurodegeneration
  2. Promoting Regeneration
  3. Neurotransplantation
  4. Rehabilitative Training
87
Q

Blocking Neurodegeneration

A
  • apoptosis inhibitor protein
  • Estrogens = neuroprotective = limiting neuron death

** Also, may explain why several brain diseases are more prevalent in males (e.g. Parkinson’s disease)

88
Q

Promoting Regeneration

A

Segments of myelinated peripheral nerves were transplanted

89
Q

Neurotransplantation

A

1) fetal tissue (Fetal substantia nigra cells implanted = released dopamine)
2) stem cells (Cells migrated to damage, matured & regained some motor function BUT uncoordinated

90
Q

Rehabilitative Training

A

importance of experience in brain development and organization.

91
Q

Hebbian Dynamics/Plasticity

A

consistent and coordinated activation of one neuron by another neuron should strengthen their synaptic connection

92
Q

Short-term Facilitation (3 steps)

A

1) facilitation
2) augmentation (increase in efficacy)
3) potentiation (increase PSP)

93
Q

causes of Short-term Facilitation

A

-Transient increase in synaptic strength
􏰀-Necessary pattern of stimulation: high-frequency, APs arrive close together in time
􏰀-Ca2+ ion removal processes are overloaded
􏰀-Elevated concentration of Ca2+ ions in the presynaptic terminal
􏰀-Increased numbers of synaptic vesicles containing NT are released following an AP
􏰀-Increased amplitude of PSPs at the postsynaptic neuron

94
Q

Short-term Depression

A
  • Depletion of synaptic vesicles in the readily releasable
  • Inhibitory feedback from presynaptic autoreceptors
  • Ca2+ ion channel inactivation
95
Q

Long-term Potentiation (LTP)

A

=structural changes of the synapse=
1) Addition of AMPA receptors on the postsynaptic neuronal membrane
􏰁2) Recruitment of “silent” synapses
􏰁3) Increases in size and/or density of dendritic spines
􏰁4) Increased arborization of dendritic “trees”

96
Q

Long-term Potentiation Phases

A

Induction, Expression, and Maintenance

97
Q

NMDA receptors are activated when:

A
  1. Glutamate is bound to the receptor

2. The postsynaptic neuron is highly depolarized (removing the Mg2+ block)

98
Q

NT nitric oxide (NO)

A

coordinates recycling mechanism- (NO) therefore increases vesicle release

99
Q

LTP vs. LTD

A

LTP relies on the activities of protein kinases

LTD relies on protein phosphatases

Neurophysiology (3 decks)

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