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Fundamentals of Physiology > Exam 1 > Flashcards

Exam 1 Flashcards

Intro to the nervous system, Nerve electrophysiology, ANS, Muscle physiology, CV physiology, Electrical activity of the heart

1
Q

CNS is made up of:

A

Brain and spinal cord

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2
Q

PNS is made up of:

A

Cranial nerves and spinal nerves ( and their branches)

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3
Q

PNS is divided into:

A

Sensory (afferent) division and motor (efferent) division

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4
Q

Sensory division of PNS divisions

A

Somatic Sensory: Carries general sensory signals from muscles, bones, joints and the skin, as well as special sensory signals to the CNS

Visceral Sensory: Carries signals from organs to the CNS

AFFERENT!!!!!

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5
Q

Motor division of PNS is divided into:

A

Somatic motor division: Carries signals to skeletal muscles

Autonomic nervous system: Carries signals to smooth muscle, cardiac muscle and glands

EFFERENT!!!!!

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6
Q

Neuroglial cell types of the CNS

A

Astrocytes
Oligodendrocytes
Microglial cells
Ependymal cells

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7
Q

Astrocyte functions

A

Anchor neurons and blood vessels
Regulate the extracellular environment
Facilitate the formation of the BBB
Repair damaged tissue

CNS!!

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8
Q

Oligodendrocyte function

A

Myelinate certain axons in the CNS

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9
Q

Microglial cells function

A

Act as phagocytes in the CNS

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10
Q

Ependymal cell functions

A

Line cavities
Cilia circulate fluid around the brain and spinal cord
Some secrete CSF

CNS

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11
Q

Neuroglial cell types of the PNS

A

Schwann cells
Satellite cells

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12
Q

Schwann cell functions

A

Myelinate certain axons in the PNS

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13
Q

Satellite cell function

A

Surround and support cell bodies in the PNS

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14
Q

Dendrites

A

Receive signals and carry information to cell body
DO NOT GENERATE ACTION POTENTIALS

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15
Q

Cell body

A

AKA Soma
Contains nucleus, mitochondria and other organelles

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16
Q

Clusters of cell body in CNS are called…

A

Nuclei

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17
Q

Clusters of cell bodies in PNS are called…

A

Ganglia

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18
Q

Axon

A

Carries information away from cell body toward other cells (anterograde and retrograde axonal transport)

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19
Q

Clusters of axons in CNS are called…

A

Tracts

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20
Q

Clusters of axons in PNS are called…

A

Nerves

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21
Q

A membrane potential can trigger and action potential in what part of the nerve cell?

A

Axon hillock

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22
Q

Myelin sheath in CNS

A

Insulating layer around a nerve fiber
Oligodendroyctes in CNS can wrap around multiple axons
NO neurolemma

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23
Q

Nerves that are typically myelinated are…

A

Those found in muscle tissue, CNS and reflex arcs - need to have FAST conduction. Most motor nerves (efferent).

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24
Q

Nerves that are typically unmyelinated include…

A

Most sensory nerves (afferent)

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25
Q

Electrical synapses

A

Presynaptic and postsynaptic neuron
Axolemmas are nearly touching - bridged by gap junctions
Gap junctions create precisely aligned channel pores
Bidirectional
Instantaneous
Cardiac myocytes and some CNS (most are chemical though)

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26
Q

Chemical synapses

A

Presynaptic and postsynaptic neurons
MOST COMMON
Electrical signal –> chemical signal –> electrical signal
Synaptic vesicles containing neurotransmitters (40+)
Neurotransmitter receptors are linked to ion channels in postsynaptic tissue
Synaptic delay
UNIDIRECTIONAL
Signal can vary depending on neurotransmitter

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27
Q

Chemical synapse steps (4)

A
  1. An action potential in the presynaptic neuron triggers Ca2+ channels in the axon terminal to open
  2. Influx of Ca2+ causes synaptic vesicles to release neurotransmitters into the synaptic cleft
  3. Neurotransmitters bind to receptors on the postsynaptic neuron
  4. Ion channels open on postsynaptic tissue, leading to a local potential and possible an action potential
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28
Q

Presynaptic control is done by…

A

Regulatory neurons: facilitate of inhibit presynaptic activities by affecting the membrane of the cell body or sensitivity of axon terminals.

This is independent of what the dendrite is doing. Directly affects membrane potential of the cell body itself independent of what the dendrites are bringing in.

Can also directly affect how strong the AP is at the axon bouton and can change how much electrical signal/neurotransmitter is transmitted to the post-synaptic tissue.

The regulatory neuron directly affects the presynaptic neuron but ultimately is going to determine how strong of a signal the postsynaptic tissue receives.

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29
Q

Presynaptic inhibition is done via:

A

GABA
Inhibitory neuron releases GABA
GABA prevents voltage-gated calcium channels from opening in the presynaptic neuron which decreases the transmission of the signal
Less/no neurotransmitter is released and therefore the threshold is not reached in the postsynaptic neuron

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30
Q

Termination of neurotransmitter release (3)

A
  1. Diffusion and Absorption: Neurotransmitters diffuse away from the synaptic cleft and are returned to the presynaptic neuron
  2. Degradation: Neurotransmitters are degraded by enzymatic reactions in the synaptic cleft.
    Cholinesterase terminates signal at motor end plate
  3. Reuptake: Neurotransmitters are taken back into the presynaptic neuron
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31
Q

Ionotropic vs Metabotropic Receptors

A

Postsynaptic neurotransmitter receptors - same result but take a different path to get there.

Ionotropic receptor: Neurotransmitter binds to receptor site and the ionotropic receptor/ion channel opens

Metabotropic receptor: Neurotransmitter binds to the metabotropic receptor that is SEPARATE from the ion channel. the receptor is associated with an inactive G protein intracellularly that is activated when the neurotransmitter binds the metabotropic receptor. This causes in increase in second messengers which opens the ion channel.

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32
Q

How can sensory receptor be classified?

A

By the location of the stimuli they detect

and

by the type of stimuli that causes them to depolarize and generate a receptor potential

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33
Q

Sensory receptor types classified by the location of stimuli they detect (3)

A

Exteroreceptors: usually close to body’s surface; detect stimuli originating from OUTSIDE the body

Interoreceptors: usually found within body’s interior; detect stimuli originating from INTERNAL ORGANS

Proprioceptors: detect position and load

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34
Q

Sensory receptor types classified by the type of stimuli that causes them to depolarize and generate a receptor potential (5)

A

Mechanoreceptors: depolarize in response to anything that MECHANICALLY DEFORMS tissue where receptors are found - mechanically gated ion channels

Thermoreceptors: exteroceptors, most of which are slowly adapting receptors; depolarize in response to TEMPERATURE CHANGES. Separate receptors to detect hot and cold.

Chemoreceptors: can be either interoceptors or exteroceptors. Depolarize in response to binding to SPECIFIC CHEMICALS (in body fluids or in air); generate a receptor potential as sodium ion channels open. TASTE/SMELL

Photoreceptors: special sensory exteroceptors found ONLY in the eyes. Depolarize in response to LIGHT

Nociceptors: usually slowly adapting exteroceptors - some interoceptors. Depolarize in response to NOXIOUS STIMULI

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35
Q

Biogenic amine neurotransmitters include:

A

Catecholamines (norepinephrine, epinephrine, dopamine)
Serotonin
Histamine

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36
Q

Amino acid transmitters include:

A

Glutamate (excitatory)
GABA
Glycine

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37
Q

Neuropeptide neurotransmitters include:

A

Substance P (pain perception)
Opioids (pain control)
Neuropeptide Y

All excitatory and inhibitory, and all metabotropic

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38
Q

Major neurotransmitter of the body

A

Acetylcholine (excitatory)
Ionotropic and metabotropic

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39
Q

Membrane potentail occurs due to…

A

asymmetrical ion distribution across a selectively permeable membrane; non equilibrium and steady-state (flux)
Diffusion potential

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40
Q

Ions that affect membrane potential include:

A

Na+
Cl-
Ca2+
K+ (higher concentration inside the cell)

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41
Q

Vm stands for:

A

Membrane potential

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42
Q

Na+ units, plasma concentration and cell concentration

A

Units: mmol/L
Plasma conc: 142
Cell conc: 15

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43
Q

K+ units, plasma concentration and cellular concentration

A

Units: mmol/L
Plasma conc: 4.4
Cell conc: 140

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44
Q

Ca2+ units, plasma concentration, cellular concentration

A

Units: mmol/L
Plasma conc: 1.2
Cellular conc: 100 nM (VERY SMALL)

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45
Q

H+ units, plasma concentration and cellular concentration

A

Units: pH
Plasma conc: 7.4
Cell conc: 7.2

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46
Q

When talking about plasma and cellular ion concentration, we are talking about…

A

Unbound ions ONLY! Others are bound to albumin and those do not matter in terms of membrane potential.

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47
Q

Cl- units, plasma concentration and cellular concentration

A

Units: mmol/L
Plasma conc: 102
Cell conc: 10-20

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48
Q

HCO3- units, plasma concentration and cellular concentration

A

Units: mmol/L
Plasma conc: 24
Cell conc: 10-16

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49
Q

Protein units, plasma concentration and cellular concentration

A

Units: g/dL
Plasma conc: 7
Cell conc: 30-40

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50
Q

Glucose units, plasma concentration and cellular concentration

A

Units: mg/dL
Plasma conc: 100
Cell conc: –

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51
Q

Osmolality units, plasma and cellular concentration

A

Should be the same inside and outside the cell!
Units: mosmol/kg H2O
Plasma conc: 290 (300)
Cell conc: 290 (300)

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52
Q

T/F: Every cell is excitable

A

False: Distribution of ions is the same in every cell but not every cell is excitable. Excitable cells are excitable because certain ions are allowed through the cell membrane (either in or out).

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53
Q

Excitable cell types can QUICKLY AND SELECTIVELY alter…

A

membrane permeability for ions.

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54
Q

Permeability changes are due to…

A

coordinated opening and closing of ion channels.

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55
Q

Excitable cells use ___ and ___ as a means of signaling or initiating intracellular events.

A

Changes in Vm and transmembrane ion fluxes

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56
Q

Sensory cell examples and how they transduce sensory stimuli

A

Mechanoceptors, olfactory receptors and photoreceptors
By generating a Vm change called a receptor potential

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57
Q

Nerve cells signal to each other and to effector tissues by using…

A

Action potentials

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58
Q

How to myocytes and secretory cells facilitate contraction and secretion, respectively?

A

Use a change in Vm to increase intracellular Ca2+ concentrations

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59
Q

Classification of ion channels include (3):

A

Selectivity
Voltage dependence
Gating

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60
Q

Ion channel classification by selectivity

A

Basically ion channels (Na, K, Ca, Cl, etc)
Generally very selective, but not always!

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61
Q

Ion channel classification by voltage dependence

A

Present in electrically excitable tissue (nerve, muscle)
They open or close in response to Vm
Affects the probability of the channel being open or closed
Open/closed state is not black and white!!!!

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62
Q

Ion channel classification by gating

A

Channels do not open for the same length of time, even “similar” channels like Ca2+ channels.
Channels may have burst activity followed by quiescence.

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63
Q

T/F: Ion channels require metabolic energy

A

FALSE - no metabolic energy is required by ion channels

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64
Q

T/F: The ion channel determines direction of flow

A

FALSE: the electrochemical gradient determines the direction of flow

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65
Q

Ion channels are very selective to:

A

Ionic charge: anion vs cation
Cl- is really the only negatively-charged ion that can pass through anion selective channels
Bicarbonate is negatively charged but is too large to pass through these channels

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66
Q

Cation selective channels generally allow how many ion species to pass through?

A

Generally 1 but there are exceptions:
L-glutamate activation of N-methyl-D-aspartic acid (NMDA) receptor which allows both Na+ and Ca2+ to pass through

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67
Q

Example of a ligand preventing an ion from passing through its ion channel

A

Phencyclidine (PCP) binds to and blocksthe NMDA channel preventing Na+ and Ca2+ from passing through

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68
Q

Non-gated ion channels

A

Open most of the time
Control flow of ions during resting membrane potential
Leak channels!!!!!!!!! Na+ and K+. Will focus more on potassium leak channels in this course

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69
Q

Gated ion channels

A

All are allosteric proteins!! Exist in more than one conformation
They exist in open OR closed state, at least
At rest they are usually closed
They open in response to stimuli (voltage change, ligand, etc)
Voltage gated exist in 3 states (typically): Rest (closed), active (open), refractory (inactivated)

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70
Q

States of ion gated channels and voltage gated sodium channel example

A

Resting (closed): Activation gate is closed
Activated (open): Activation gate is open allowing ions through channel
Inactivated (refractory): Inactivation gate is closed

When activation gate is closed, sodium can not pass from the extra to intracellular space through the channel. When there is a change in membrane potential at the site of the pore, the activation gate open allowing Na+ to pass into the cell. When we reach a certain membrane potential, the inactivation gate will close no longer allowing Na+ to pass through the channel, but the channel/ion pore itself is not closed because the activation gate remains open - it is simply inactive.

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71
Q

“Certain cells, including neurons and myocytes, have a property called _______________… ________ above a certain _______ voltage triggers a spontaneous all-or-none response called and _________.

A

Electrical excitability
Threshold
Action potential

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72
Q

Action potentials

A

Transient, regenerative electrical impulse in which Vm rapidly rises about 100 mV (not TO 100 mV, but rises 100 mV total)
Can propagate long or short distances
Brain/CNS receives AP from peripheral sensory organs, generates efferent AP to effector organs (i.e. skeletal muscle)

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73
Q

Electrical currents in cells

A

In cells, current moves across the membrane and is mediated by movements of Na+, K+, Ca2+, Cl- and HCO3-.
Ion movements are mediated by ion channels, electrogenic ion transporters and pumps.

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74
Q

Ohm’s Law

A

Electrical currents across cell membranes

I = V/R OR V = IR
I = current, V = voltage, R = resistance

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75
Q

Ohm’s Law/Current for CV system

A

F = P/R OR F = (change)P/R
I = gV

F = flow and is equivalent to current
P = pressure
R = resistance
g = conductance
V = voltage

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76
Q

Ions

A

Electrically charged atoms
Cations (+)
Anions (-)

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77
Q

Influx of ions

A

Ionic flow INTO a (nerve) cell

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78
Q

Efflux of ions

A

Ionic flow OUT of a neuron

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79
Q

Electrical current

A

Movement of electrical charge (amps)
Depends on electrical potential and conductance (1/R)

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80
Q

The higher the voltage difference from one side of the membrane to the other, the ________ the current provided the _____ remains constant.

A

greater
resistance

The same goes for blood flow.

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81
Q

Electrical potential

A

Voltage (volts)
Difference in charge b/w the anode (+ pole) and the cathode (- pole)
More current flows when voltage is increased provided the resistance is held constant!!!

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82
Q

Electrical conductance

A

The ability of an electrical charge to move from one point to another (Siemens - unit of choice)

Inverse of resistance (Ohms)!!!

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83
Q

Direction of current flow is determined by:

A

Historically by the direction of NET cation flow

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84
Q

Inward current describes ______ flowing into the cell (neuron)

A

Cations

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85
Q

Outward current describes ______ flowing out of the cell (neuron)

A

Cations (and anions flowing INTO the cell)

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86
Q

Leakage current is the flow of ions through ______ _________.

A

Non-gated channels

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87
Q

Membrane potential definition

A

Vm
Electrical potential difference across a membrane at any given time

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88
Q

Resting membrane potential

A

Resting Vm
Vm of a membrane when not generating and action potential

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89
Q

Resting Vm of CNS neuron is typically:

A

-65 mV

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90
Q

Chloride flowing into a cell will produce an _______ current.

A

Outward current because current is described by the direct that cations are moving. If chloride anions are moving into the cell then cations will be moving out of the cell

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91
Q

Depolarization

A

reduction of (-) charge inside the cell
Ex: -65 to -50

Depolarization makes the cell less negative. The voltage difference b/w the inside and outside of the cell becomes less and moves closer to zero

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92
Q

Hyperpolarization

A

Increased (-) charge inside the cell
Ex: -65 to -70

Makes the cell more negative with respect to the outside of the cell. Vm moves further from zero in the negatives

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93
Q

Threshold potential

A

Vm at which sufficient voltage gated Na+ channels are open that can generate an AP

Relative permeability of Na+ exceeds K+

AP is generated beyond threshold

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94
Q

Ionic basis of membrane potential

A

Ions are symmetrically distributed across the cell membrane - this generates a membrane potential.

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95
Q

Membrane potential

A

Difference in electrical potential between intra and extracellular spaces

Vm (or Vrm) is typically -90 mV in RESTING skeletal muscle, alpha motor neurons, and -65 in CNS

Interior of the cell is more negative than exterior!!!

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96
Q

Which is more negative in terms of resting Vm: inside of outside of the cell

A

Inside!!

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97
Q

Resting Vm for skeletal muscle and alpha motor neurons

A

-90 mV

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98
Q

Resting Vm of CNS neurons

A

-65 mV

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99
Q

Nernst equation

A

The electromotive force (EMF) = Nernst potential

EMF (millivolts) = +/- 61 x log (concentration inside/concentration outside)

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100
Q

What happens when the membrane becomes permeable to a particular ion?

A

The ion is going to move in or out of the cell (according to electrochemical gradient) and change the membrane potential (Vm) toward its own equilibrium potential.

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101
Q

The Nernst equation calculates equilibrium potential based on ….

A

the ion’s intracellular and extracellular concentrations.
If ion concentrations change then the equilibrium potential changes.

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102
Q

If the membrane becomes permeable to a particular ion, the ion is going to move in or out of the cell and change…

A

the resting membrane potential (Vm) towards its own equilibrium potential

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103
Q

Potassium equilibrium potential is ________ relative to Vm.

A

NEGATIVE.
If K+ permeability increases (K+ channels open), then K+ flows out of the cell and makes Vm more negative.

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104
Q

Sodium equilibrium potential is ________ relative to Vm.

A

POSITIVE
If Na+ permeability increases, (Na+ channels open) and Na+ flows into the cell making Vm more positive.

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105
Q

Sodium equilibrium

A

ENa = +61 mV

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106
Q

Potassium equilibrium

A

EK = -90 mV
Potassium will flow out of the cell until Vm reaches -90, and the electrical gradients equilibrate.

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107
Q

Calcium equilibrium

A

ECa = +120 mV

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108
Q

Goldman equation

A

Looks at all ions at play (Nernst equation only looks at one ion at a time).
It allows you to figure out the instantaneous membrane potential at any given moment because it include ion concentration and permeability for each individual ion.

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109
Q

In quiescent tissue, the Goldman equation gives…

A

Resting membrane potential because P is always nearly zero

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110
Q

Determination of resting membrane potential

A

Electrochemical (net) driving force = Vm - Ex

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111
Q

When the Nernst potential for an ion is less than what the membrane potential is, the ion flows ______ of the cell when the membrane becomes permeable to the ion.

A

OUT OF THE CELL

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112
Q

When the Nernst potential for an ion is greater than the membrane potential, the ions flow _____ of the cell when the membrane becomes permeable to the ion.

A

INTO THE CELL

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113
Q

Inside/outside of the cell are negative or positive?

A

Inside = negative
Outside = positive

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114
Q

At rest the inside of a cell is always ______ (negative or positive) with respect to the ECF.

A

Negative

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115
Q

When a positively charged ion (cation) flows into a cell (influx), the membrane loses ___________.

A

Polarization

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116
Q

During depolarization, Vm becomes less _________.

A

NEGATIVE.
By convention an upward deflection on a voltage record.

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117
Q

During hyperpolarization, Vm becomes more ________.

A

NEGATIVE
Downward deflection on a voltage record.

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118
Q

During hyper polarization, cations leave (efflux) the cell and Vm becomes more _______ and the membrane becomes more __________.

A

NEGATIVE
POLARIZED

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119
Q

When positive charges flow into the cell, they generate an _______ current. By convention, these currents cause a _________ deflection.

A

Inward
Downward
Currents typically more in the opposite direction than Vm.

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120
Q

Positive charges leaving the cell cause an ________ current and an ________ deflection on a recording device

A

Outward
Upward
Currents typically move in the opposite direction than Vm.

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121
Q

Depolarization/repolarization/hyperpolarization is referring to…

A

membrane potential (Vm)

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122
Q

Current and membrane potential deflections are

A

opposite from one another.

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123
Q

Membrane potential changes definitions

A

All relative to resting potential:

Depolarization (Above threshold/resting potential)
Overshoot (Above 0 mV)
Repolarization (back down to resting potential)
Hyperpolarization (below resting potential)

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124
Q

What makes neurons excitable and gives them the ability of generate an action potential?

A

The density of voltage gated Na+ channels

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125
Q

Excitable cells exhibit two distinct types of electrical behaviors:

A
  1. Local graded potentials
  2. Far-traveling action potentials (all or nothing)
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126
Q

If the Na+ channel density is not sufficient, membrane is only capable of generating….

A

local currents that die out as you move further from the source.

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127
Q

Types of local (graded) potentials

A

Hyperpolarizing graded potentials (becoming more negative) caused by opening of K+ or Cl- channels
Depolarizing graded potentials (becoming less negative) caused by opening of Na+ channels

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128
Q

Graded/local action potentials will always remain below…

A

Threshold

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129
Q

Examples of graded potentials

A

Sensory receptor potentials - pushing harder on your skin will generate a larger graded potential

Dendritic postsynaptic potentials in CNS: depends on what is feeding into the cell at that time

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130
Q

Local currents/graded potential magnitude is proportional to…

A

the number of open channels. The amplitude is graded with input intensity and are minor membrane events.

They can summate in space and time – depending on the magnitude and direction, they can generate a greater change or cancel each other out.

Vm change is limited and ONLY spreads locally

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131
Q

The strength of the stimulus for a graded potential is encoded in the _______ of the graded potential.

A

amplitude

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132
Q

Graded potentials have limited reach due to ________ __________.

A

Electrotonic conduction (potential dies out further from source?)

133
Q

Graded potentials have limited reach due to ….

A

leak channels. The intensity of the stimulus decreases with distance (decremental conduction).

Leakage of charge (predominantly K+) across the plasma membrane reduces the local current at sites farther along the membrane from the site of initial depolarization.

134
Q

Decremental conduction is:

A

when the intensity of the stimulus decreases with distance.

135
Q

There is a membrane potential change where the is/isn’t myelin sheathing?

A

Where there is NOT myelin sheathing - nodes of Ranvier

136
Q

Why isn’t there a change in membrane potential where myelin sheathing is present?

A

There is no way for ions to access intra or extracellular space. The K+ leak channels are covered by myelin.

137
Q

Unmyelinated axon APs die out because…

A

K+ leak channels leak current out of the cell.

138
Q

The size principle of nerve fibers

A

Larger diameter fibers conduct at higher velocities
This is because of membrane resistance vs axonal cytoplasm resistance

Larger fibers have lower resistance vs small fibers

Larger fibers have lower cytoplasmic resistance relative to membrane resistance

139
Q

Graded potential signal is encoded in the …

A

Amplitude

140
Q

Action potential signal is encoded in the…

A

frequency

141
Q

Graded potentials occur in what type of cells?

A

Excitable and non-excitable

142
Q

Action potentials occur in what type of cells?

A

Excitable cells only!!!! Do not occur in non-excitable cells like graded potentials

143
Q

Are action potentials depolarizing and hyperpolarizing?

A

No - only depolarizing!

Graded potentials are depolarizing and hyperpolarizing

144
Q

Graded potentials have ______ amplitudes.

A

Varying.

Action potentials are always the same amplitude - all or nothing!

145
Q

Graded potentials vs action potentials for signal conduction

A

Graded = electrotonic conduction

AP = regenerative signal propagation

146
Q

What does it mean when we say the signal is encoded in the amplitude of graded potentials?

A

The hyperpolarization/deplolarization amplitude size determines the effect

147
Q

Frequency is measured in…

A

hertz

148
Q

What is the principal mechanism of nerve impulse propagation and transmission?

A

Action potentials

149
Q

Action potentials are explosive membrane events that are a set _________ no matter how often it’s depolarized.

A

amplitude

150
Q

Action potentials are always ________ meaning that they are due to the opening of ____ ______.

A

Depolarizing
Na+ channels

151
Q

Action potentials are self ________

A

propagating
The same type of AP regenerates along the route of conduction - runs the same amplitude the entire length of muscle fiber or nerve fiber

152
Q

Phases of an action potential

A
  1. Upstroke (depolarization)
  2. Overshoot (when membrane potential is positive)
  3. Downstroke (repolarization) and after the Vm goes below 0 again
  4. Afterpotential (after hyperpolarization) when membrane potential is more negative than resting membrane potential (RMP,Vm)
    Then returns to resting membrane potential.
153
Q

What occurs during depolarization of an AP?

A

Voltage gated Na+ channels open allowing in influx of Na+ ions into the cell - increased membrane conductance to sodium ions.

154
Q

What happens during repolarization of an AP?

A

There is an increase in K conductance when K+ gates open allowing an efflux of K+ out of the cell.

155
Q

What occurs at the peak of the action potential?

A

It reaches a voltage that closes voltage gated Na+ channels and opens voltage gated K+ channels. These have already begun to open prior to repolarization.

156
Q

PNa/PK and significance

A

Conductance of sodium relative to potassium.

As we raise this ratio (essentially increasing sodium conductance/permeability of the membrane to Na), the membrane potential increases

157
Q

What happens with the ratios Na/K conductance is zero?

A

As we increase EC K concentration, the membrane potential becomes less negative/increases.

RESTING MEMBRANE POTENTIAL INCREASES WITH INCREASED EXTRACELLULAR K CONCENTRATION. PARTICULARLY WHEN THE NA/K CONDUCTANCE IS ZERO.

158
Q

What causes the membrane potential changes during an action potential?

A

Na influx and K efflux

159
Q

What occurs during the upstroke/depolarization?

A

An increase in Na+ conductance (and lack of K+ conductance) leads to Na+ rushing into the cell (influx) and moves the membrane potential towards its very positive equilibrium (ENa+)

160
Q

What happens during the downstroke/repolarization?

A

An increase in K+ conductance (and diminishing Na+ conductance) leads to K+ rushing out of the cell (efflux) and moves the membrane potential towards its very negative equilibrium potential (EK+)

161
Q

Vm and Vna or Vk relationship during AP

A

Depolarization: Na+ open and Vm moves toward VNa

Overshoot: Na+ channels inactivate and Vm moves back toward Vk

Repolarization: K+ channels open and Vm moves faster toward Vk

Hyperpolarization: Na+ channels deinactivated, K+ channels open, Vm moves close to Vk

162
Q

Phases of an action potential beginning with resting (5)

A
  1. Resting state: The activation gates on the Na+ and K+ channels are closed, and the membrane’s resting potential is maintained
  2. Depolarization: A stimulus opens the activation gates on some Na+ channels. Na+ influx through those channels depolarizes the membrane. If the depolarization reaches the threshold, it triggers an AP.
  3. Rising phase of the AP: Depolarization opens the activation gates on most Na+ channels, while the K+ channels’ activation gates remain closed. Na+ influx makes the inside of the membrane positive with respect to the outside.
  4. Falling phase of the AP: The inactivation gates on most Na+ channels close, blocking Na+ influx. The activation gates on most K+ channels open, permitting K+ efflux which again makes the inside of the cell negative.
  5. Undershoot: Both gates of the Na+ channels are closed, but the activation gates on some K+ channels are still open. As these gates close on most K+ channels, and the inactivation gates open on Na+ channels, the membrane returns to its resting state.
163
Q

Subthreshold potentials only elicit…

A

graded/local potentials

164
Q

The peak of an AP is shaped by…

A

the ionic movements in and out of the cell, and how long it takes to do that.

The density of ionic channels determines the slope and peak of an AP

165
Q

How does resting membrane potential change with respect to EC K+ concentrations?

A

Resting Vm changes if extracellular K+ concentration changes (because K+ conductance is high even at rest).

Increased EC K+ will increase resting membrane potential. This brings Vm closer to threshold meaning that we will need a small stimulus to elicit an AP. This makes it easier to depolarize tissues.

Decreased EC K+ will decrease resting membrane potential. This brings Vm further from threshold meaning that we will need a stronger stimulus to elicit an AP. This makes it more difficult to depolarize tissues.

166
Q

Hypokalemia will lead to …

A

Muscle weakness - brings Vm further from threshold making it more difficult/need a stronger AP to elicit an AP.

167
Q

Increasing/decreasing ____ conductance can alter membrane potential.

A

K+

Increasing K+ conductance causes K+ to leave the cell resulting in hyperpolarization of the cell because we are decreasing membrane potential.

Decreasing K+ conductance causes K+ to stay in the cell.

This is DIFFERENT than manipulating EC K+ concentrations. The number of ions needed to move out of the cell for repolarization will never affect the EC K concentrations enough because the number is relatively small compared to EC K+ levels.

168
Q

Increasing K+ conductance (g) results in:

A

K+ leaving the cell resulting in hyperpolarization. Recall that increasing g for an ion causes the Em to move toward the equilibrium potential for that ion. Thus, the cell will move from -70 mV to -95mV.

169
Q

Decreasing K+ conductance (g) results in:

A

depolarization of the cell - the cell moves away from K+ equilibrium.

170
Q

Which changes the EC K+ concentration - K+ leak channels or voltage gated K+ channels?

A

K+ leak channels!!!

increasing permeability of the membrane to K+ by opening voltage gated K+ channels will not have an effect on EC K+ concentrations.

171
Q

Is conductance the same as EC K+ concentrations?

A

NO -they are not the same!!!!!!!!

172
Q

Hypokalemia

A

Decreased EXTRACELLULAR K+ concentration

This HYPERPOLARIZES the membrane

Vm is decreased - moves closer to Vk (-95)

Makes depolarization more difficult and a larger depolarizing current will be required

Can lead to asystole (failure of contraction)

173
Q

Hyperkalemia

A

Increased EXTRACELLULAR K+ concentration

The membrane is “depolarized”

Vm is increased - moves farther away from Vk and closer to VNa

Makes it easier to initiate an AP. Once an AP is fired, it may not be able to repolarize. This is because if resting membrane potential is too high then it may never get low enough for enough K+ channels to open to repolarize the cell. May also never move the Na+ channel from inactive to closed.

174
Q

What will happen when you decrease EC Na+ concentrations?

A

This will change the AP peak.

Decreasing EC Na+ concentrations will produce an AP with a smaller peak.

Increasing EC Na+ concentrations will produce an AP with a larger peak because there is more sodium to rush into the cell causing in increase in Na+ conductance.

175
Q

Which has a more significant effect on the cell - changing EC Na+ or EC K+ concentrations?

A

K+ concentration because the scale is much smaller so making smaller changes to K+ has a larger effect than make the same change to Na+ concentrations

176
Q

Which has refractory periods - Graded potential or action potential?

A

Action potentials. Graded potentials DO NOT have refractory periods.

177
Q

Which can be summed - graded or action potentials?

A

Graded - AP can NOT be summed.

178
Q

What are action potentials initiated by? Graded potentials?

A

AP: Graded potentials

Graded potentials: environmental stimulus (receptor), by neurotransmitter (synapse) or spontaneously.

179
Q

Graded potentials and AP depend on what types of mechanisms?

A

Graded: ligand-gated ion channels or other chemical or physical changes

AP: voltage-gated ion channels

180
Q

Absolute refractory period

A

Due to inactivated Na+ channels. While voltage-gated Na+ channels are inactive but not closed, the cell can NOT produce another action potential.

Axon membrane is incapable of producing another AP NO MATTER HOW LARGE THE STIMULUS IS.

This period lasts just about until the end of repolarization.

181
Q

Relative refractory period

A

Due to continued outward diffusion of K+.

Once the Na+ channel closes, you can produce another AP, but the stimulus has to be greater.

Voltage gated ion channel shape alters at the molecular level.

Voltage gated potassium channels are open.

Axon membrane can produce another action potential but requires a stronger stimulus.

The stimulus needed to produce an AP is increase initially and eventually will decrease down to normal.

182
Q

Excitability of the cell during refractory periods

A

Absolute: Zero

Relative: Increasing

Resting: High

183
Q

Most Na+ channels are __________ during an absolute refractory period.

A

Inactivated!!

184
Q

Some Na+ channels are still ______ and most K+ channels are _______ during a relative refractory period.

A

Inactivated
Open

185
Q

Changes in plasma Ca2+ change _____ _____ of excitable cells.

A

membrane excitability

186
Q

Hypocalcemia

A

Decreased plasma Ca2+ concentrations leading to INCREASED excitability.

This increases THRESHOLD!!!!

Spontaneous alpha MN firing –> spasm (tetanus)

Cardiac arrhythmias

Seizures

187
Q

Hypercalcemia

A

An increase in plasma Ca2+ concentrations leading to DECREASED membrane excitability.

This decreases THRESHOLD!!!

CNS depression and coma

Decreased myocardial excitability (anti-arrhythmogenic effect)

188
Q

Plateaus in action potentials occur when…

A

repolarization does not begin immediately following depolarization. Occurs because calcium (and Na) is coming into the cell at the same time that K+ is leaving the cell. These can occur in the cardiac myocyte.

189
Q

The causes (2) of a plateau in an action potential are:

A

1) Depolarization occurs because of the opening of voltage-gated sodium channels (fast) and the secondary opening of calcium-sodium channels (slow). The Ca/Na channels prolong the depolarization time as positively charged Ca flows into the interior of the cell.

2) Myocardial voltage-gated potassium channels are particularly slow in opening and are typically not open until the end of the plateau further delaying repolarization.

190
Q

Action potentials in nonneural tissue: skeletal muscle

A

The AP in skeletal muscle is similar to that of an alpha moron neuron, only slower conducting and longer time to complete a cycle.

191
Q

Action potentials in nonneural tissue: cardiac myocytes

A

The AP in cardiac myocytes is generally similar to that of an alpha MN, but has a plateau due to Ca2+ coming into the cell (depolarization) at the same time that K+ is leaving the cell.

The AP of a cardiac nodal cell is different still.

192
Q

The ANS is primarily responsible for managing what?

A

phasic/acute deviations of homeostasis.

193
Q

The endocrine system is primarily responsible for managing what?

A

more chronic/permanent management of homeostasis.

It can respond phasically particularly at the prompting of the ANS - norepinephrine stimulates the adrenal glands to release epinephrine

194
Q

Information from the brain travels via (2)

A

Somatic motor neurons to skeletal muscle

Autonomic neurons innervating smooth muscle, cardiac muscle, secretory epithelia and glands

195
Q

Three divisions of the ANS

A

Parasympathetic (PANS)
Sympathetic (SANS)
Enteric nervous system (ENS): Also called the “little brain” and specific to the digestive tract

196
Q

Are ANS branches weighted equally in each organ/organ system?

A

No! Some have more or predominant input from one branch or the other. Ex: the SANS causes blood vessels to constrict. When they are dilated it doesn’t mean that there is more parasympathetic drive than sympathetic. It just means there is less sympathetic drive. Same with the GI system and parasympathetic input.

197
Q

Parasympathetic effects on organs/systems:

A

Pupillary constriction
Tear secretion
Airway constriction
Slows heartbeat
Stimulates digestion
Stimulates gallbladder to release bile
Stimulates GI function
Contracts urinary bladder
Relaxes urinary sphincter
Induces penile erection
Induces engorgement and secretions of female genitalia

198
Q

Sympathetic effects on organs/systems:

A

Dilates pupil and elevates eyelid
Ciliary body
Stimulates salivation
Modulates blood vessel tone
Relaxes airways
Causes erection of hair
Stimulates secretion by sweat glands
Accelerates and strengthens heartbeat
Inhibits digestion
Stimulates glucose production and release from liver
Stimulates secretion of epinephrine
Inhibits GI function
Relaxes urinary bladder
Contracts urinary sphincter
Induces ejaculation
Stimulates contraction of smooth muscle in female genitalia

199
Q

Primary neurotransmitter of SANS

A

Norepinephrine (stimulates epinephrine release from adrenal glands)

200
Q

Primary neurotransmitter of PANS

A

Acetylcholine

201
Q

What can change the effect of ANS input in an organ system?

A

The amount of neurotransmitter can have different effects in the same organ

202
Q

Examples of the same branch of ANS eliciting opposite effects in different organ systems

A

In vasculature, norepinephrine and epinephrine cause constriction. In the lungs they cause dilation. This is because the same neurotransmitter is binding to different receptors in different tissues eliciting different effects.

203
Q

Which systems have sympathetic input ONLY (2)?

A

Vascular smooth muscle cells - vasoconstriction
Sweat glands - secretion

204
Q

Which organ has parasympathetic input ONLY?

A

Stomach - stimulates acid secretion

205
Q

Sympathetic/parasympathetic effects on the SA/AV nodes

A

Parasympathetic: Decrease HR
Sympathetic: Increase HR

206
Q

Sympathetic/parasympathetic effects on cardiac muscle

A

Parasympathetic: Decrease (atrial) contractility
Sympathetic: Increase contractility

207
Q

Sympathetic/parasympathetic effects on the lung smooth muscle cells

A

Parasympathetic: constriction
Sympathetic: dilation

208
Q

Sympathetic/parasympathetic effects on the pancreas

A

Parasympathetic: Increases secretion
Sympathetic: Decreases secretion

209
Q

Sympathetic/parasympathetic effects on the GI tract

A

Parasympathetic: increase motility & sphincters relax
Sympathetic: decrease motility & sphincters contract

210
Q

Somatic nervous system target organ, neurotransmitter and receptor

A

Skeletal muscle
Acetylcholine
N1 (nicotinic acetylcholine receptor)

211
Q

Norepinephrine binds which type of receptors?

A

alpha and beta adrenergic receptors

212
Q

Acetylcholine binds which type of receptors?

A

N1 (nicotinic) and muscarinic Act receptors

213
Q

Parasympathetic target organ, neurotransmitters and receptors

A

Preganglionic fiber synapses at N2 receptor via acetylcholine
Postganglionic fiber synapses at M (muscarinic acetylcholine) receptor innervating smooth muscle, cardiac muscle and glands.

214
Q

Which nicotinic receptors does the ANS use?

A

N2 receptors (with acetylcholine) - preganglionic fiber synapse

215
Q

Which nitotinic receptor does the somatic nervous system use?

A

N1 with acetylcholine on skeletal muscle

216
Q

Sympathetic neurotransmitters, receptors and target organs

A

Norepinephrine: preganglionic fiber synapses at N2 receptor in ganglion releasing acetylcholine. Post ganglionic fiber synapses at alpha/beta receptors using norepinephrine

Epinephrine: preganglionic fibers synapse at N2 receptors of chromaffin cells of adrenal glands using acetylcholine. This causes release of epinephrine that travels through the blood to reach target cells using alpha/beta adrenergic receptors.

217
Q

Acetylcholine binds what types of receptors?

A

Nicotinic (N1 and N2) and muscarinic receptors

218
Q

Epinephrine will bind what receptors most preferentially?

A

Beta adrenergic receptors

219
Q

Norepinephrine will bind which receptors more preferentially?

A

Alpha adrenergic receptors

220
Q

As norepinephrine increases, it will also stimulate release of more….

A

epinephrine via the adrenal gland stimulation

221
Q

Epinephrine receptor selectivity, high and low dose-dependent actions

A

Receptor: B1 = B2 > a1 = a2
Low dose: cardiac stimulation, vasodilation, bronchodilation
High dose: greater cardiac stimulation, vasoconstriction, bronchodilation

222
Q

Norepinephrine receptor selectivity, high and low dose-dependent actions

A

Receptor: a1 = a2 > B1 = B2
Low dose: some cardiac stimulation, vasoconstriction
High dose: Reflex bradycardia and extensive vasoconstriction

223
Q

Dopamine receptor selectivity, high and low dose-dependent actions

A

Receptor: B1 = B2 > a1
Low dose: cardiac stimulation, vasodilation
High dose: vasoconstriction

224
Q

Degradation of norepinephrine and epinephrine

A
  1. 50-80% reuptake
  2. Diffusion (into blood)
  3. MAO or COMT in heart, glands, smooth mm cells
225
Q

Muscarinic receptors are primarily found in the _______ nervous system.

A

Parasympathetic (but M1 are also found in sympathetic postganglionic neurons)

226
Q

M1 receptor location, second messenger/cascade and action

A

Location: CNS and sympathetic postganglionic neurons
Second messenger/cascade: Form IP3 and DAG, increase intracellular calcium concentrations
Action: Cellular excitation

227
Q

Potassium channels are always hyperpolarizing except for in the _______.

A

Pancreas

228
Q

M2 receptor location, second messenger/cascade and action

A

Receptor location: Cardiac and coronary smooth muscle
Second messenger/cascade: Open K+ channels, inhibits adenylyl cyclase and reduce cAMP
Action: hyperpolarization, vasodilatory effects on coronary smooth muscle cells

229
Q

M3 receptor location, second messenger/cascade and action

A

Receptor location: glands and visceral smooth muscle, vascular smooth muscle
Second messenger/cascade: Form IP3 and DAG, increase intracellular calcium concentrations
Action: Secretion and contraction, relaxation

230
Q

Sympathetic vs parasympathetic

A

Never “all or none”
More of which is predominating at any given point in time.

Heart rate is predominantly one or the other

Cardiac output are regulated BEAT TO BEAT

In arterioles VSMCs vasodilation is really a decreased sympathetic tone

GI tract has a lot of parasympathetic input (probably the most of the entire body), but sympathetic control is massive, particularly regarding arterioles.

231
Q

Another name for neuromuscular junction is…

A

Motor end plate

232
Q

The motor end plate/NMJ is…

A

the synaptic connection between the alpha motor neuron axon and the skeletal muscle fiber

233
Q

What is the most studied synaptic connection?

A

The NMJ/neuromuscular junction

234
Q

Which part of the motor end plate has invaginations? Why?

A

The muscle fiber at the NMJ. To increase the surface area for acetylcholine receptors

235
Q

Sarcolemma is the…

A

postsynaptic membrane of the NMJ. Folded to increase surface area for AchR

236
Q

What prevents the NMJ from sliding away from one another?

A

The presynaptic bouton is anchored to the postsynaptic membrane by the ECM (proteins and proteoglycans). These two things NEVER touch but need to stay close to one another for synaptic transmission.

237
Q

Events at the NMJ

A
  1. Neurotransmitter (Ach) is packaged into vesicles transported to presynaptic terminal
  2. AP arrives at the presynaptic terminal
  3. Depolarization of nerve membrane at presynaptic terminal OPENS voltage gated Ca2+ channels
  4. Increased presynaptic Ca2+ concentration triggers fusion of vesicles to the presynaptic membrane and release of neurotransmitter (QUANTA) into synaptic cleft. About 150 quanta per vesicle.
  5. Neurotransmitter (Ach) molecules diffuse across the synaptic cleft and bind to specific (Act) receptors on the postsynaptic cell.
  6. Binding of neurotransmitter (Ach) to (Ach) receptor activates postsynaptic cell. 2 Ach/AchR at NMJ for activation of AchR
  7. Termination of process: 1. Enzymatic destruction of neurotransmitter. 2. Uptake of neurotransmitter by presynaptic cell of other cells (usually Na+ mediated). 3. Diffusion of neurotransmitter away from receptor
238
Q

What type of receptor is the AchR? Inotropic or metabotropic

A

Inotropic (nicotinic)

239
Q

What type of receptor is a muscarinic receptor? Inotropic or metabotropic?

A

Metabotropic

240
Q

How many Ach molecules are required for activation of 1 AchR?

A

2

241
Q

What happens once an AchR is activated by 2 Ach molecules?

A

The pore on the receptor opens allowing movement of ions through the pore. The Ach receptor is non-specific and Na+ primarily moves into the postsynaptic cell but can also let K+ out (not at the same time)

242
Q

How is an action potential triggered at the motor end plate?

A

Ach binds to AchR opening the pore and allowing sodium into the muscle cell and potassium out of the muscle cell. This causes a change in the local membrane potential that, if large enough, can cause a change in membrane potential opening voltage gated sodium channels (that are located in the folds of the sarcolemma) depolarizing the cell and triggering an action potential.

243
Q

Thin filaments are

A

actin

244
Q

This filaments are

A

myosin

245
Q

Muscle arrangement from largest to smallest

A

Fascicle —> fiber —> myofibril —> myofilaments —> thick and thin filaments (repeating units make up the sarcomere)

246
Q

A sarcomere spans from ____ to ____.

A

Z line to Z line

247
Q

Actin/thin filaments only in a sarcomere are represented by the ______ which spans the _____.

A

I band
Z line

248
Q

The H band is where there is no _____ overlap with _____.

A

Actin
Myosin
Right in the middle of the sarcomere

249
Q

The A band…

A

spans the length of myosin filaments

250
Q

The M band…

A

Is right in the center of the sarcomere and is where myosin is anchored

251
Q

T tubule location and function

A

invaginations in the myofibril usually where there are a lot of sarcoplasmic reticulum

It conducts the action potential that is occurring along the surface of the muscle fiber down into the muscle fiber so that it can be depolarized in unison

252
Q

Actin structure and function

A

Thin filaments
Double stranded alpha helices of F(filamentous) actin.

Contains 2 regulatory proteins: tropomyosin and troponin

253
Q

Tropomyosin structure and function

A

2 alpha helices that fit in the groove of the actin helix
Regulates the binding of myosin to actin

254
Q

Troponin structure and function

A

Heterotrimer bound to tropomyosin

Troponin T (TnT): binds to tropomyosin
Troponin C (TnC): binds 2 Ca2+ molecules
Troponin I (TnI): binds actin and inhibits myosin interaction

255
Q

Myosin structure and function

A

Thick filaments
Made up of heavy chains and light chains

Heavy chains form cross bridge and hydrolyze ATP

Light chains stabilize and regulate ATPase activity (smooth muscle mostly) - located on the hinge region of the heads of the myosin heavy chain

256
Q

Excitation-Contraction Coupling is where you take the ________ from the sarcolemma and produce ______.

A

Electrical impulse
Work

257
Q

Sarcolemmal resting membrane potential

A

-85 mV
Some can be closer to -70 mV

258
Q

Why may there be variation in resting Vm in striated muscle fibers?

A

The diameter of the muscle fiber will affect the Vm

Thinner diameter muscle fiber in motor neurons = higher resting membrane potential

Thicker diameter tends to have much lower (more negative) resting membrane potentials.

259
Q

At what Vm does a sarcolemmal action potential propagate?

A

-55 mV (this is pretty universal but some texts quote -45 mV)

260
Q

How long does a muscle AP last and how does this compare to a neuronal AP?

A

Lasts much longer than neuronal AP!

Muscle AP lasts 1-5 ms

Neuronal AP lasts 0.1 ms

261
Q

How fast does muscle AP travel compared to neuronal AP?

A

Much slower than neuronal!!

Muscle AP travels 3-5 m/sec

Neuronal AP travels 50-130 m/sec for large myelinated neurons

262
Q

What happens after the sarcolemmal AP is initiated?

A

It propagates along the sarcolemma and into the core of the fiber via transverse tubules (invaginations in the sarcolemma and is still the membrane/conducts AP)

263
Q

What is a triad?

A

Forms these where the T-tubules interface with the sarcoplasmic reticulum at the A-I juncture on the sarcomere. It is made up of one T-tubule and a SR on either side. Tetrad? called this in lecture but shows triad in the diagram.

264
Q

Where is the DHP receptor located? What does it stand for? What type of receptor is it? What is it connected to? What is its function?

A

On the sarcolemma in the T-tubule of the muscle cell.
Dihydropyridine receptor
L-type calcium receptor
It is connected to the ryanodine receptor located on the sarcoplasmic reticulum
An action potential causes a conformation shift in the DHP receptor which then causes a conformational shift in the ryanodine receptor allowing calcium to be released from the sarcoplasmic reticulum into the cytoplasm.

265
Q

What happens to the DHP and ryanodine receptor during repolarization?

A

They return to their original conformation and no more calcium leaves the sarcoplasmic reticulum

266
Q

What form of calcium is released from the sarcoplasmic reticulum?

A

Ionic/free form which is incredibly biologically active

267
Q

What is calsequestrin?

A

A protein in the sarcoplasmic reticulum of muscle cells that loosely binds calcium to aid in calcium sequestration in SR.

268
Q

What is SERCA?

A

A calcium pump found on the membrane of the sarcoplasmic reticulum of muscle cells that pumps calcium from the cytosol back into the SR

269
Q

How does calcium get released from and back into the SR in muscle cells?

A

It is released in response to depolarization of the muscle cell which changes the conformation of DHP receptor that then causes a conformational shift in ryanodine receptor on SR membrane. This conformational shift in the ryanodine receptor allows calcium to rush out of the SR. After the AP, the SERCA pump pumps calcium back into the SR.

270
Q

What is the DHP receptor inhibited by?

A

DHP class of drugs for hypertension and arrhythmias

271
Q

What is the ryanodine receptor inhibited by?

A

A class of plant alkaloids (ryanodine)

272
Q

Excitation Contraction Coupling process

A

Need an AP to release calcium from SR increasing cytosolic Ca2+ to lead to contraction.

Depolarization of the sarcolemma leads to a shift in conformation of DHPR which leads to a conformational shift in ryanodine receptor causing calcium release from SR.

Ionic calcium is released from the SR causing a 500 fold increase in intracellular calcium concentrations in about 50 milliseconds (only about a 10 fold increase is needed for contraction).

This duration is longer in cardiac myocytes!

2 calcium molecules bind to troponin C that rotates troponin I off of the myosin binding site allowing myosin to bind actin forming a cross bridge and subsequent contraction.

273
Q

What happens if you don’t have IONIC calcium to be released from the SR in a muscle cell?

A

Contraction will cease!!!!

274
Q

Muscle contraction occurs as long as there is …

A

ionic calcium present in the cytosol. No calcium = no contraction

275
Q

Why is the “calcium pulse” from the SR releasing 500 fold calcium when only about 10 fold is needed for contraction?

A

We need ATP for muscle contraction, SERCA pump function. Calcium can also be used to bind enzymes in glycolytic pathway increasing glycolysis and subsequent production of ATP so that we can replace ATP as efficiently as possible during and after muscle contraction.

276
Q

Where do the two calcium molecules bind during muscle contraction?

A

On troponin C

277
Q

Resequestration by SR during excitation coupling contraction

A

SERCA pump - ATPase hydrolyses ATP

Concentrates calcium about 10,000 times the amount inside the SR

Calsequestrin and sacalumenin (in longitudinal SR, facilities SERCA activity by loosely binding Ca2+).

Phospholamban, sarcolipin & myoregulin also affect SERCA activity
These generally DECREASE SERCA pump activity
PLN can be phosphorylated (PKA dependent pathway) to remove inhibition and is predominantly in cardiac, slow twitch sk mm.

278
Q

What proteins help to sequester calcium in the SR?

A

SERCA ATPase

Calsequestrin

Sacalumenin - in longitudinal SR, facilitates SERCA activity by loosely binding Ca2+

279
Q

What proteins generally decrease SERCA pump activity?

A

Phospholamban (PLN): can be phosphorylated (PKA dependent pathway) to remove inhibition of SERCA pump. This occurs predominantly in cardiac, slow twitch sk. muscle and works to decrease cardiac muscle rate and strength.

Sarcolipin

Myoregulin

280
Q

Ca2+ resequestration and removal of primary importance in cardiac muscle

A

Na-Ca and exchanger and Ca2+ pump in the plasma membrane both extrude Ca2+ from the cell.

281
Q

Ca2+ resequestration and removal of primary importance for skeletal muscle

A

Ca2+ pump sequesters Ca2+ within the sarcoplasmic reticulum (SERCA-ATPase)

Ca2+ is bound in the sarcoplasmic reticulum by calreticulin and calsequestrin.

282
Q

Calcium binding and dissociation from actin and what occurs

A

When cytosolic Ca2+ rises and binds to troponin C (TrC), conformational changes cause TnT to pull tropomyosin and TnI out of the way, exposing myosin binding sites on actin so that myosin can bind to actin.

As long as Ca2+ is present, multiple cross-bridge cycles occur.

when cytosolic Ca2+ concentrations fall, Ca2+ dissociates from TpC and the subsequent movements of TnT, tropomyosin and TnI once again block further myosin-actin interactions.

283
Q

The cross bridge cycle in muscle contraction

A
284
Q

What is the force output per cross bridge?

A

2-5 pN - big for one cross bridge!

285
Q

What is the importance of maintaining ATP levels in skeletal muscle fibers?

A

The myosin head releases the actin binding site when ATP replaces the ADP molecule. If you let ADP accumulate and let ATP diminish, ADP will remain bound to myosin and the muscle fiber won’t be able to relax = RIGOR MORTIS.

Maintaining high ATP levels relative to ADP levels allows the cross bridge cycle to repeat indefinitely

286
Q

When does cross bridge cycling stop?

A

Death (low ATP and buildup of ADP leading to rigor mortis)

when calcium is resequestered/dissociates from troponin C

287
Q

Crossbridge cycle

A
  1. Binding of ATP to the myosin head
  2. The myosin head then detaches from actin
  3. ATP is hydrolyzed to phosphate and ADP
  4. The myosin now bound to ADP becomes weakly bound to actin
  5. The binding of Ca2+ to troponin causes tropomyosin to slide over actin and enables the two myosin heads to close
  6. This results in the release of of inorganic phosphate and the extension of the myosin neck leading to the power stroke of the cross bridge cycle
  7. Each cross bridge exerts a force about 2 pN during the structural change
  8. The release of ADP
288
Q

How do we transmit the crossbridge force out of the sarcomere?

A

By using proteins like dystrophin which connect the sarcomere to the sarcolemma and out to the collagen that makes up the tendon that connect to bone.

289
Q

Muscular dystrophy is an issue with…

A

dystrophin which prevents the transmission of force from the sarcomere out the to sarcolemma to tendon and then to bone.

290
Q

Skeletal muscle fiber contraction lasts…

A

20-200 ms depending on the muscle fiber type

291
Q

Sarcolemmal AP only lasts….

A

1-5 ms BUT it is possible to initiate another AP BEFORE twitch contraction is over

292
Q

What is it called when another CONTRACTION (not just AP) is initiated before previous contraction has ended?

A

Summation
This will greatly increase force/tension development of a fiber/muscle

Tension is higher when APs occur at a higher frequency = frequency summation

This is the most energetically efficient way to increase force output/tension

293
Q

What is tetanus and why does it happen?

A

When stimulation frequency is increased sufficiently so NO drop in force is seen between twitches.

This occurs when ionized Ca2+ is being released into the cytosol to create contraction

294
Q

Which contraction is longer? Cardiac or skeletal?

A

Cardiac

295
Q

What needs to occur every time there is an AP in order to have a muscle contraction?

A

The release of calcium from the SR into the cytosol. It doesn’t matter if there is already a lot of calcium present in the cytosol - if more isn’t release then there won’t be a contraction

296
Q

If the SERCA pump is inhibited, what will happen?

A

Muscle contraction will cease. It won’t be taking ionic calcium back up into the SR to then be released again for contraction. None taken up = none released!!

297
Q

Temporal summation

A

introduce another impulse before the precious contraction was finished and begin to build a larger force.

More calcium is release before the previous calcium has been sequestered

298
Q

Tetanic state types

A

Unfused and fused - the force never returns to zero and all cross bridges are always engaged.

299
Q

A non-tetanus state has a _________ appearance.

A

Stair step

300
Q

What determines a single muscle twitch, temporal summation, or fused/unfused tetanus?

A

The amount of ionized calcium in the cytosol and how much continues to be released

301
Q

Purpose of myoglobin

A

Acts as facilitative diffusion to move oxygen to the mitochondria in muscle cells. When the muscle isn’t being used then it’ll bind oxygen, but is mainly there to move O2 to mitochondria very quickly from sarcolemma

302
Q

How are skeletal muscle fiber types determined?

A

Usually done by myosin heavy chain phenotyping

303
Q

Myoglobin heavy chain phenotypes (3 main ones)

A

Type I
Type IIa
Type IIb

Others exist (type IId/x

304
Q

Other typing nomenclature for skeletal muscle fibers (other than phenotypes I, IIa and IIb)

A

Twitch and oxidative characteristics
- Slow oxidative (type I)
- Fast oxidative (IIa)
- Fast glycolytic (IIb)

Both twitch and appearance (color - myoglobin content) characteristics
-Slow red (type I)
- Fast red (type IIa)
- Fast white (type IIb)

305
Q

Postural muscles in humans are what kind of fiber type?

A

slow twitch/type I/oxidative

306
Q

Relationship between conduction velocity and alpha motor neuron diameter

A

increased conduction velocity with increased diameter

307
Q

Ocular muscles are what type of fiber?

A

IIb

308
Q

Gastrocnemius muscles fiber type and contraction time compared to other types

A

Type IIa and in between I and IIb for contraction time

309
Q

Ocular muscle fiber type and contraction time compared to other types

A

Type IIb and the shortest contraction time - easily fatiguable

310
Q

Soleus muscles fiber type and contraction time compared to other types

A

Type I and the longest contraction time compared to the other fiber types

311
Q

What constitutes force output? How do the different fiber types compare?

A

The number of cross bridges engaged.

Type I (slow) has the least force output and is fatigue resistant

Type IIa (fast, fatigue resistant) is higher than type I for force output

Type IIb (fast, fatiguable) has the highest force output. The rate of rise in this type is the fastest but is not as sustained as the other two

312
Q

Length-tension relationship in sarcomere

A

Very long and very short fibers produce less force output. You want a little bit of overlap with actin and myosin but not too much and they can’t be too far apart.

Short fibers: Actin starts to overlap

Long fibers: too far apart

There is an optimal length of muscle fiber/sarcomeres that will produce near maximal force.

313
Q

Force Velocity Curve

A

As we lengthen the muscle, we have greater force output because dystrophin and associated proteins act as a spring connecting the contractile apparatus to the basement membrane. If you stretch the spring then you can get more force with lengthening contraction than shortening contraction

314
Q

Types of muscle contractions (3)

A

Isometric
Isotonic (everything we do)
Isokinetic (doesn’t occur naturally)

315
Q

Isometric muscle contractions

A

NO change in muscle length, as defined by change in joint angle

Fiber lengths often change with no change in joint angle

316
Q

Isotonic Muscle contractions

A

Muscle length changes against fixed load (velocity varies)

2 Types:
-Shortening (concentric)
-Lengthening (eccentric; primarily responsible for muscle injury and DOMS)

317
Q

Isokinetic muscle contractions

A

Muscle length changes against fixed VELOCITY (load varies)

Also shortening and lengthening but does NOT HAPPEN NATURALLY

318
Q

A motor unit is…

A

a single alpha motoneuron and ALL the muscle fibers it innervates

319
Q

Motor unit innervation ratios

A

Range from 1:5-10 to 1:2000+

Those with very low ratios and found in muscles that cause precise movements such as finger muscles

Those with high innervation ratios are large muscles like leg muscles

320
Q

Generally, fibers of a single motor unit are …

A

dispersed throughout the muscle, not clustered. This aids with control of movement.

There are exceptions in cases of deinnervation and rein nervation

321
Q

Motor unit recruitment in cases of deinnervation and reinnervation

A

If the motor neuron dies then the muscle nerves from adjacent muscles will reinnervate that muscle. Then single motor neuron will be innervating many muscle fibers. There will be less control in this case and occurs in polio, ALS, MS, etc.

Jerky movements

322
Q

T/F: A muscle fiber can be innervated by many motor neurons

A

FALSE: a muscle fiber can only be innervated by ONE motor neuron

323
Q

Large motor neurons typically innervate type _____ fibers and have ____ innervation ratios. These are designed for _____ output and very _____ durations.

A

IIb
high
maximal
short

Explosive movements with short duration recruit by IIb fibers from large motor neurons that recruit many muscle fibers

324
Q

Types of motor units and what they are based on

A

Based on n’conduction velocity and fatigue resistance during isometric contraction

-FR (fast, fatigue resistant) Type I
- FF (fast, fatiguable) Type IIb
-FI (fatigue intermediate, fatigue resistant) Type IIa

Correlates with number of fibers innervated

Also correlates with fiber twitch mechanics, oxidative capacity

325
Q

Spatial summation

A

Also called multiple fiber summation

Mechanism by which whole muscle can develop relatively constant force over time

Achieved by activating individual MOTOR UNITS asynchronously
-More efficient that bringing fewer motor units to tetanus
-Allows for most control over force output
-ESSENTIAL FOR FINE MOTOR CONTROL involving low innervation ratios

326
Q

What is the most important way for skeletal muscle to resequestrate calcium?

A

SERCA pump (L-type calcium channel that is inhibited by phospholamban - this is more important in cardiac muscle).

The SERCA pump is also important in cardiac muscle, but since skeletal muscled doesn’t have the membrane ion exchanger pumps that cardiac muscle does, it relies on SERCA pumps to get calcium out of the cytoplasm

327
Q

Membrane ion exchanger pumps are more important in _____ muscle than they are in _____ muscle.

A

Cardiac
Skeletal

328
Q

Myosin releases from the actin binding site when…

A

ATP replaces the ADP molecule on the myosin head

329
Q
A

Fundamentals of Physiology (1 decks)

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