Neuroanatomy Lecture #14: Resting Excitable Cells

Front 1

Define the Equilibrium Potential

Back 1

It is the value of the membrane potential where there is not net positive transport of a permeant ion into or out of a cell.

Front 2

The direction of current in an ionic solution follows the movement of these ions

Back 2

It follows the movement of cations in an electric field

Front 3

The equilibrium potential can vary based on these factors (2)

Back 3

Temp and [ionic]

Front 4

The equilibrium potentials for the following ions in a neuron:
Ca2+:
Na+:
Bicarbonate:
Cl-:
K+:

Back 4

The equilibrium potentials for the following ions in a neuron:
Ca2+: +123
Na+: +62
Bicarbonate: -14
Cl-: -65
K+: -80

Front 5

The equilibrium potentials for the following ions in a muscle cell:
Na+
K+
Cl-
Ca2+
Bicarbonate

Back 5

The equilibrium potentials for the following ions in a muscle cell:
Na+: +65
K+: -95
Cl-: -90
Ca2+: +132
Bicarbonate: -26

Front 6

General description of an ion channel (3 components)

Back 6

1. Consists of protein subunits surrounding
2. a central aqueous pore
3. with an ion selectivity filter

Front 7

An example of a symport at the synaptic cleft

Back 7

Neurotransmitters use the energy created by Na+ to re-enter nerve terminals

Front 8

An example of an antiport with synaptic vesicles

Back 8

Neurotransmitters are allowed to enter the vesicle in exchange for Na+

Front 9

Typical mean values of Vm for:

• Photoreceptors:
• Neurons:
• Skeletal muscle fibers:

Back 9

Typical mean values of Vm for:

• Photoreceptors: - 40mv
• Neurons : - 65mv
• Skeletal muscle fibers: - 90mv

Front 10

Compare/Contrast the relative number of K+, Cl- and Na+ channels open in the Neurons and Skeletal muscle and why this is significant

Back 10

---------------- K+ Cl- Na+
Neurons Large some Few
Skeletal Large Large Few

The significance is K+ contributes greatly to the Vm of neurons where as in Skeletal muscle, both K+ and Cl- are contributing

Front 11

A stable resting membrane potential is dependent on this (2)

Back 11

Ion pump activity and Ion channels

Front 12

All excitable cells have resting membrane potentials dependent on this

Back 12

Outside [K+]

Front 13

The reason why raising outside [K+] causes depolarization and possible subsequent signaling failure in excitable cells

Back 13

• Raising outside [K+] causes less K+ to flow out of the cell

• This leads to a less negative cell interior (Vm becomes less negative)

• The depolarization and can lead to a "depolarization-induced closure" of voltage-sensitive Na+ channels ---> this closure is called inactivation

Front 14

In the scenario of depolarization-induced closure of voltage-sensitive Na+ channels, which gate on the channel is closed?

Back 14

The inactivation gate

Front 15

These factors will affect the cell's transmembrane potential (4)

Back 15

• The type of open ion channels
• The number of open ion channels
• The amount of current passing through the channel when it is open
• The time the channel spends in an open state

Front 16

Define Po and how it is measured

Back 16

Po is the probability of a channel opening

It is calculated as a fraction of the observed time a channel is open. Another way to look at it is:

Po = (the # of open ion channels in a time period) / (the total # channels available for opening at that same time period)

Front 17

The relationship of conductance and resistance and their units

Back 17

Conductance (g) is the inverse of Resistance (r).

Conductance is measured in Siemens
Resistance is measured in Ohms

Front 18

Ohm's Law

Back 18

V = Ir = I/g

Front 19

The total membrane conductance for an ion is dependent on this

Back 19

The number of open channels for the ion, Nx

Front 20

Calculating the membrane conductance, g(x), for an ion X

Back 20

g(x) = Nx (γx)

where γ = the single channel conductance for that ion

Front 21

Voltage-gated channels and transmitter-gated channels have there Po values dependent on this (one each)

Back 21

V-gated: Po dependent on Vm
Transmitter- gated: Po dependent on [transmitter] in their vicinity

Front 22

Electrochemical gradients drive this type of flux

Back 22

Passive ion

Front 23

What is the general form of the Nernst equation and what does it tell us

Back 23

It tells us the value of the Vm that exactly counterbalances the ion's [gradient] across the membrane

Front 24

The only ion that has an equilibrium potential close to Vm for neurons and skeletal muscle

Back 24

Chloride (-65mV)

Front 25

The relationship btwn the equilibrium potential for an ion and its concentration gradient

Back 25

The equilibrium potential and the concentration gradient is equal and opposite

Front 26

Calculating the Electrochemical gradient for an ion

Back 26

(Vm - Ex) mV

Front 27

The significance of calculating the electrochemical gradient using the equilibrium potential of an ion

Back 27

The value calculated gives the driving force as produced by the electrochemical gradient that an ion would use to passively leave/enter a cell. However, an equal and opposite force will be matching this value which represents what an active (ATP-driven) pump is doing to ensure there is no net flux of the ion

Front 28

Equating a cell to a circuit, this represents the capacitor and conductor

Back 28

Capacitor = plasma membrane
Conductor = open ion channel

Front 29

The value of the total ionic current, Im, when the cell is at rest

Back 29

Im = zero, ** however, its components are non-zero

Front 30

How the resting membrane potential is calculated when there are >1 ion channels present

Back 30

The Potential is the weighted sum of all the equilibrium potentials

Front 31

Channelopathies:
• definition
• what the episodes involves
• how it can be acuired (3 possible sources)

Back 31

Channelopathies:
• d/o caused by dysfxnal ion channel activity
• episodes of disturbed nerve or muscle cell excitability
• autoimmune attack, nerve damage, after use of drug tx or toxins

Front 32

Ischaemic cerebral edema:
• what it can cause
• another name for this type of edema
• why the edema occurs
• the secondary edema that can follow

Back 32

Ischaemic cerebral edema:
• irreversible cellular damage due to cellular swelling
• cytotoxic edema
• Na/K pump is no longer supplied w/ ATP and the gradient dissipates. The influx of Na and Cl into the cell leads to cellular swelling from water
• Vasgogenic edema - blood vessels become more permeable and water flows out of them and into the extra cellular space

Front 33

Aquaporins:
• their fxn
• two prominent fxns in the CNS
• The name of the primary channel in the brain and where its found (2 sites)

Back 33

Aquaporins:
• selectively allow water through the plasma membrane
• production of CSF, regulation of water at the BBB
• AQP-4
> astrocyte foot processes at the BBB
> brain-CSF interface

Front 34

Relationship of Lethal injection and cardiac muscle

Back 34

The increase in extracellular [K+] causes many muscles, particularly cardiac, to fail to generate APs because v-gated Na+ channels become inactivated (depolarization-induced closure)

Front 35

Channelopathies:
• definition
• what the episodes involves
• how it can be acuired (3 possible sources)

Back 35

Channelopathies:
• d/o caused by dysfxnal ion channel activity
• episodes of disturbed nerve or muscle cell excitability
• autoimmune attack, nerve damage, after use of drug tx or toxins

Front 36

Ischaemic cerebral edema:
• what it can cause
• another name for this type of edema
• why the edema occurs
• the secondary edema that can follow

Back 36

Ischaemic cerebral edema:
• irreversible cellular damage due to cellular swelling
• cytotoxic edema
• Na/K pump is no longer supplied w/ ATP and the gradient dissipates. The influx of Na and Cl into the cell leads to cellular swelling from water
• Vasgogenic edema - blood vessels become more permeable and water flows out of them, into the extra cellular space

Front 37

Aquaporins:
• their fxn
• two prominent fxns in the CNS
• The name of the primary channel in the brain and where its found (2 sites)

Back 37

Aquaporins:
• selectively allow water through the plasma membrane
• production of CSF, regulation of water at the BBB
• AQP-4
> astrocyte foot processes at the BBB
> brain-CSF interface

Front 38

Relationship of Lethal injection and cardiac muscle

Back 38

The increase in extracellular [K+] causes many muscles, particularly cardiac, to fail to generate APs because v-gated Na+ channels become inactivated (depolarization-induced closure)