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ICCP Yr1 SEM 1 > Session 6 LT2 CHANGING MEMBRANE POTENTIAL > Flashcards

Session 6 LT2 CHANGING MEMBRANE POTENTIAL Flashcards

1
Q

WHAT IS THE CONNECTION BETWEEN CHANGING THE MEMBRANE POTENTIAL AND SIGNALLING?

A
  • The changes in membrane potential underlie many forms of signalling in cells.
    Eg. Action potentials in nerve cells
  • Triggering and controlling muscle contraction
  • Control of secretion of hormones and neurotransmitters ( action potential insulin and synaptic cleft)
  • ## Post synaptic actions of Fast synaptic transmitters
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2
Q

Define Depolarisation

A
  • DECREASE in the size of membrane potential from its normal value
  • Cell interior becomes less negative ( more positive)
  • eg from -70 mV to -50 mV
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3
Q

DEFINE HYPERPOLARISATION

A
  • INCREASE in the size of a membrane potential from its normal value.
    -Cell interior becomes more Negative
    Eg from -70 mV to -90 mV
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4
Q

OPENING OF WHAT CHANNELS CAUSE DEPOLARISATION AND HYPERPOLARISATION?

A

Depolarisation - caused by Opening of Na+ and Ca2+
Hyperpolarisation - caused by Opening Cl- and K+ channels

Therefore changes in MP are caused by changes in activity of ION CHANNELS

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5
Q

How long does an action potential last?

A

4-5 milli seconds

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6
Q

What is the connection between membrane potentials and ion permeability?

A
  • You have membrane potentials because of selective permeability
  • Therefore changing the permeability of these ions will consequently change the MP
  • Changes in membrane potential occur due to change in activity of IC
  • Increasing the membrane permeability of a ion will mean MP will move towards the EP of that ion.
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7
Q

Describe the relation ship between membrane permeability, EP and MP:

A
  • MP - due to selective permeability
  • increasing permeability to a particular ion means MP moves towards EP of that ion.
  • Eg. At resting state the membrane is more permeable to k+ therefore MP closer to EK but not exactly the same because other channels are open.
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8
Q

WHAT DO WE MEAN WHEN WE SAY REAL MEMBRANES HAVE IMPERFECT SELECTIVITY?

A
  • Real cell membranes are not permeable to just one Ione they have channels open for more than one type of ion
  • Therefore the contribution of each ion to membrane potential will be dependent on the permeability of ion. (= conductance) dep no channels open- GHK equation the permeability coefficient for ion moving in likely to be different to moving out - basis of Nernst eq
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9
Q

Explain conductance

A
  • Real cell membranes more than one ion channel open therefore the contribution each ion plays on the MP depends on permeability of the ion
  • Depends on the number of channels open.
  • Resting state membrane more perm to K+ therefore MP closer to EK
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10
Q

GIVE AN EXAMPLE OF LESS SELECTIVE RECEPTOR

A
  • Nicotinic Ach
    -NMJ motor neurone terminals release Ach that binds to receptors on Muscle membrane
  • NAchR - Have an intrinsic ion channel
  • Opening via the binding of 2x Ach
  • Let’s Na+ and K+ flow through not anions
    Moves MP towards 0 intermediate betwe ENa and EK
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11
Q

NAchR - Describe its features and non selectivity

A
  • NAchR- Intrinsic ion channel, open via the binding of two Ach, channel lets Na+, K+ through
  • Moves MP towards 0 intermediate between ENa and EK
  • Nicotine also binds - so very active in smokers
  • Opiates also bind such as morphine, cannabinoids such as Marijuana increase activity so effects muscle see SHAKES
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12
Q

HOW DO WE CONTROL CHANNEL ACTIVITY?

ESPECIALLY THAT WE KNWO THAT MEMBRANE PERMEABILITY- THEREFORE CHANNEL ACTIVITY AFFECTS MP

A
  • Channels can open or close- Gated
    3 types of gating
  • Ligand eg NAchR and Serotonin receptors
  • Voltage gated - channels involved in AP
  • Mechanical - Mechanoreceptors receptors, carotid stretch receptors and hair cells in the inner ear
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13
Q

What is ligand gating?

A
  • Channels open and close in response to binding of a CHEMICAL ligand.
  • E.g. Channels at synapse which respond to extracellular signals eg Ach and Serotonin
  • Channels that respond to intracellular messengers
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14
Q

What is Mechanical Gating:?

A
  • Channels open and close in response to MEMBRANE DEFORMATION
  • Channels in mechanoreceptors , carotid sinus receptors and hair cells in the inner ear
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15
Q

What is Voltage gating?

A
  • Open and close in response to changes in membrane potential
  • e.g. channels involved in action potentials
  • Propagation of a nerve signal at a synapse.
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16
Q

Give an example of sensory mechanical gating

A
  • Cochlear Fluid filled structure with hair cells within them
  • In the cuticular plates there are a number of Na+ and K+ channels
  • Stop the K+ channels from opening, depolarisation occurs , Vg Ca2+ opens , influx Calcium causes vesicles with NT ( dopamine and Dynorphin) fuse with bMEMBRANE close to Afferent nerve
  • NT binds to receptor on post synaptic membrane which generates an AP which goes to CNS for interpretation
17
Q

Where can synaptic connections occur?

A
  • Nerve cell- nerve cell
  • Nerve cell - Muscle cell
  • Nerve cell - gland cell
  • Sensory celll - Nerve cell- e mechanoreceptors
    Synapse Chem transmitter release presynap binds to receptors post synaptic
18
Q

WHAT TYPES OF SYNAPTIC TRANSMISSION CAN WE HAVE?

A

-Fast and slow synaptic transmission

19
Q

What is Fast synaptic transmission?

A
  • The receptor channel is also the ION CHANNEL
  • eg NACHR - intrinsic ion channel activity
  • Transmitter binding causes the channel to open
20
Q

What two types of synapse do we have?

A
  • Excitatory synapses - Membrane depolarisation - Ach, Dopamine and Glutamate - Permeable to Na+, Ca2+- NAchR - Cations in general
  • Inhibitory synapse- Membrane hyperpolarisation- GABA, and Glycine
  • Permeable to K+ and Cl-
21
Q

Describe excitatory synapses:

A
  • Excitatory transmitters open ligand gated channels which cause membrane depolarisation
  • Can be permeable to Na+, Ca2+ , NAchR- cations in general
  • RESULTING IN MEMBRANE POTENTIAL = EPSP
  • Which has a longer time course than AP 20 milliseconds delayed propagation
  • Graded with the amount of transmitter
  • Transmitters include Dopamine , Glutamate and ACH
22
Q

What transmitters involved in EPSPs?

A
  • Dopamine
  • Ach
  • Glutamate
    ( Transmitters open ligand gated channels which cause membrane depolarisation)
23
Q

Describe Inhibitory synapse

A
  • Inhibitory transmitters open ligand gated channels which causes hyper-polarisation.
  • Permeable to K+ and Cl_
  • Transmitters GABA and glycine
24
Q

What transmitters are involved in IPSPs?

A
  • GABA

- Glycine

25
Q

WHAT TWO PATTERNS ARE SEEN IN SLOW SYNAPTIC TRANSMISSION?

A
    1. Direct G protein Gating: eg Cannabinoid receptor
  • Localise and quite rapid comp to 2.
  • Within the membrane
  • Gating via intracellular messengers
  • Throughout the cell , amplification by cascade - slower because ENZYME AND CASCADE INVOLVED
26
Q

WHAT TWO FACTORS AFFECT MEMBRANE POTENTIAL

A
  1. CHANGES IN ION CONCENTRATION:
    - Most important changes in extracellular k+
    - Some times altered in clinical situations- Hyperkalemia - End stage renal failure
    - Can alter membrane excitability - in the heart Hyperkalemia where RMP higher so Na+ channels are not activated affects depol= bradycardia
    - 2. Electrogenic pumps
    - Na/K+ ATPASE contributes few mV in some cells 5 mV making more negative
    - Sets up and maintains the ionic gradients required to generate MP
27
Q

Explain the role of Na+ K+ ATPASE

A
  • it does not generate the mp
  • some cells it contributes directly to the MP generate few mV - making more negative
  • Indirectly through Active transport it setts up and maintains the ion gradients which generate the resting membrane potential.
28
Q

Insulin release process explain:

A
  • 1.Blood glucose increased
    2. Glucose transported in to beta cell via facilitated diffusion through a glucose transported
    3. Elevated concentration of glucose within B cell causes ATP into cell via metabolism which bind to ATP sensitive cell - K+ ATP sensitive cell - Closes the channel so k+ can no no longer leave have depolarisation
    4. Causes Vg Ca2+ channels to open which causes influx ca2+ - which causes vesicles containing insulin o fuse with the membrane and release Insulin in to the blood stream via exocytosis.
    5. Insulin decreases blood glucose levels
29
Q

What drugs is used to treat type 2 diabetes and how does it work?

A
  • Sulfonylureas
  • Widely used to treat type two diabetes.
  • Because they stimulate insulin secretion from pancreatic B cells
  • They act by binding to the SUR site of ATP sensitive K+ channels inducing channel closure causing the depolarisation
  • Does not work on type 2 diabetes because B cells destroyed
30
Q

Membrane potentials of the heart

A

NO CHLORIDE CHANNELS SO NO CHLORIDE IONS
YoU HAVE THREE PHASES THE RAPID DEPOLARISATION WHERE FAST Na+ channels operate
- The Plateu is caused by Calcium entry L type
- Repolarisation
The MP of the heart -90mv held at this point because Na+ and Ca2+ channels are closed

31
Q

Change in membrane potential in the anterior pituitary

A
  • Calcium release is required for prolactin secretion
    TRH- Gq and IP3 causing Ca2+ release, calcium binds to calcium sensitive k+ channels calcium leaves have hyper-polarisation you then have another G protein which binds o the ERG channel prevents K+ leaving
  • Have depolarisation calcium channels open calcium in causes prolactin release

ICCP Yr1 SEM 1 (4 decks)

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