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PSL300 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Types of postsynaptic receptors

A

Ionotropic and Metabotropic

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2
Q

What determines the effect?

A

Receptor, not the transmitter

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3
Q

Postsynaptic potential (PSP)

A

The binding of the transmitter to the post-synaptic membrane results in a change of the post-synaptic membrane potential called PSP

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3
Q

Duration of the PSP

A

20-40 ms

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4
Q

Ligands for ionotropic/metabotropic receptors

A

ionotropic and metabotropic: Acetylcholine (Ach), Glutamate, GABA, Glycine
metabotropic: Ach (muscarinic receptor), peptides (substance P, beta endorphin, ADH)
catecholamines (noradrenaline, dopamine)
serotonin
purines (adenosine, ATP)
Gases (NO, CO)

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4
Q

EPSP

A

Depolarizing (ion channel is specific for cations Na+ K+ etc)

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5
Q

IPSP

A

Hyperpolarizing (Ion channel may be specific for Cl- or K- ions)

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6
Q

Metabotropic effects

A
  1. Binding of a ligand to a postsynaptic receptor will activate an enzyme that is usually G protein-coupled
  2. the enzyme facilitation will result in increased production or destruction of 2nd messengers
  3. 2nd messenger will activate other enzymes
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7
Q

2nd messengers

A

cAMP, cGMP, or InP3

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8
Q

What effect is more immediate?

A

Ionotropic; metabotropic activation takes time

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9
Q

How must PSS spread to get to the initial segment of an axon?

A

Passive conduction

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9
Q

beta-adrenoreceptor

A
  1. beta-receptor is a metabolic receptor for noradrenalin.
  2. Binding of NA to beta receptor activates adenylyl cyclase via a G protein alteration
  3. adenylyl cylclase increases production of cAMP
  4. cAMP will then activate kinases which phophorylate Ca2+ channel
  5. the phosphorylation of the Ca2+ channel will increase the Ca2+ influx
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9
Q

Where are PSPs generated?

A

They are generated in inexcitable membrane; neuronal dendrites and cell bodies

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10
Q

Can PSPs generate an AP?

A

No they cannot as the areas they are generated do not have a high density of voltage-gated Na+

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11
Q

2 types of PSP summations

A

spatial and temporal

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12
Q

Spatial summation

A

Minimum of 10-30 synchronous EPSPs in dendritic tree, generated at a different synapse

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13
Q

Temporal summation

A

Only a few active synapses, but each generating EPSPs at high frequency; summated potentials reach threshold over a period of time.
they last about 30-40 ms before dying out

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14
Q

IPSP (Cl- channel)

A
  1. they involve the opening of the Cl- channel
  2. the equilibrium potential for Cl- is very close to resting MP
  3. at result opening of Cl- causes little change
  4. when the membrane is depolarized, opening of the Cl- channel will
    bring the MP back down to -70 mv
  5. The net affect of Cl- is basically to ‘clamp’ the MP, which is preventing excitation,
    thus preventing depolarization > inhibitory effect
  6. These IPSPs are very strategically located and they completely block any signal
    coming from EPSPs simply by positioning right on the soma
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15
Q

Where are IPSPs located?

A

Cell soma, they are half way between the site where EPSP is generated and the trigger zone. they can shunt depolarizing EPSPs out of the cell

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16
Q

Whats more imp IPSPs or EPSPs ?

A

IPSPs are generally more important than EPSPs

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17
Q

Spike train

A

Depolarizing the trigger zone to threshold and sustaining that depolarization for 500 ms, turns powerful input to be translated into continuous stream of APs

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18
Q

Generating a Spike train

A
  • If we depolarize the membrane above threshold and keep it there, you’ll get one
    AP and the voltage-gated Na+ channels will inactivate (refractory period) and you
    can not get another AP until the membrane repolarizes
  • Therefore, after each ‘spike’ we need to get the membrane ‘hyperpolarized’ to
    restore the Na+ channels to re-open them for the next one
  • We must have Hyperpolarization to generate another AP, otherwise we’ll never
    generate a ‘Spike Train’
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19
Q

After hyperpolarization

A
  • Voltage-gated K+ channels at trigger zone.
  • Hyperpolarization after each spike ensures that Na+ channels reconfigure, and membrane excitability is restored.
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20
Q

What happens after after-hyperpolarization fades away?

A

The Membrane potential will shoot right back up where EPSP is taking and crossing the threshold again and a whole new spike gets generated

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20
Q

What can we generate due afterhyperpolarization

A

spike train

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21
Q

Receptor potential

A

Change in the membrane potential due to receipt of signal from exterior sensory cue

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22
Q

What happens when receptor proteins change shape?

A
  1. Directly open ion channels
  2. enzyme is activated via G protein coupling > leading to production of 2nd messenger (cAMP, cGMP, INP3) > lots of 2 nd messenger proteins > leads to signal amplification
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23
Q

What will happen when energy from the environment reacts with membrane proteins

A

Depolarization of sensory receptors
EXCEPTION: photoreceptors hyperpolarize

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24
Q

What happens when a chemical stimulus binds to a specific metabotropic receptor (G-protein coupled)

A
  • the G protein is activated
  • Adjacent enzyme (adenylyl cyclase) is activated
  • 2nd messenger proteins are produced (cAMP)
  • cAMP activates kinases
  • they directly interact with ion channels or phosphorylate other proteins
25
Q

Categories of sensory cell transmission

A
  1. sensory cell generates an action potential at a spike generating zone
  2. sensory cell releases vesicles when depolarized; impulses in post synaptic neuron
26
Q

What are the 2 stages of amplification

A
  1. G protein can activate a number of different enzyme molecules
  2. One stimulus can produce lots of 2nd messenger (cAMP)
27
Q

Transmission of Signal (AP)

A

Located at the axon terminal (e.g. in the sensory axon innervating the skin). First patch of excitable membrane will generally be at the branch point; thus, the receptor potential will have to travel and generate summation at a branch point to reach threshold to get an AP

28
Q

Transmission of Signal (Vesicles)

A

The depolarizing current don’t produce any AP > travel throughout the membrane and at the other end > they depolarize the membrane sufficiently > influx of Ca++ ions and trigger exocytosis vesicles > sensory cell is releasing vesicles and not producing an AP

28
Q

Adaptation

A

Membrane potential can decay over time and lead to adaptation.
The original voltage is not sustained and its dropped over time, even though the stimulus may be constant

29
Q

Types of adaptations

A
  1. slowly adapting
  2. rapidly adapting
30
Q

Coding of stimulus intensity

A

The receptor potential will vary directly in proportion to the intensity of the stimulus.
The greater the stimulus intensity > the greater the receptor depolarization (graded potential) > More transmitter released and higher AP frequency
* The more eminent the depolarization > the faster the membrane will be brought up from hyperpolarization to generate a new spike
* The Impulse frequency will always be limited by the refractory period

30
Q

Habituation

A

Response to successive stimuli in time.
Repeated stimuli (identical) in succession elicit progressively weaker
responses.

31
Q

Slowly adapting

A

Receptor potential sustained for the duration of the stimulus. Interested in the total magnitude of the stimulus.

32
Q

Rapidly adapting

A

Receptor potential elicited by change in stimulus energy, decays to zero when stimulus is constant.
Interested in how the stimulus is being delivered, and velocity of stimulus

33
Q

Strategies to code for strength of stimulus

A

Increase frequency of AP at excitable membrane ( increasing intensity of stimulus > increasing frequency
of AP)
– With increasing stimulus strength, we recruit an additional receptor , which has a higher threshold

33
Q

How do we continue coding for stimulus intensity after reaching the ceiling due to the refractory period?

A

Recruit additional neurons

34
Q

How do we distinguish different modality of stimulus?

A

Labeled Line strategy

35
Q

Population code

A

Population coding is coding using the ratio of activity from a restricted number of different receptor types

36
Q

Receptive field

A

The spatial area the sensory neuron responds to; where a neuron can be activated

37
Q

Why should the ionic composition of the extracellular fluid around the neuron be specifically controlled?

A
  1. Cannot change the excitability of the membrane
  2. Cannot have neurotransmitters floating around for no reason
    Regulated by the BRAIN BLOOD BARRIER
38
Q

Where is blood brain barrier located

A

Between Blood vessels and interstitial fluid and CSF

39
Q

Parkinsons disease

A

Problems with dopamine, lack of dopamine, etc.
Causes muscle stiffness, contractions, etc.
We cannot inject the patients with dopamine and it doesn’t cross BBB, so they’re injected with L-dopa instead, which does cross the barrier.

40
Q

MSG

A

Cannot cross BBB
they activate glutamate outside the brain and PNS

41
Q

Why and where is BBB broken

A

Most of the brain is protected by BBB, but it is not continuous
* At some places it is essential for neurons to communicate freely with the blood stream (e.g. hypothalamus)
* The pituitary gland (releases hormones) is directly connected to the hypothalamus > thus, BBB is purposely broken to allow release of hormones
* In ‘Circumventricular organs’ (around 3rd ventricle) the BBB is broken so neurons can sense specific chemical [ ]
* Generally, BBB is broken in areas that interact with endocrine system or require sensitivity to metabolites in plasma

42
Q

Dura matter

A

Very tough membrane, sac containing the brain and spinal cord

43
Q

Arachnoid membrane

A

More delicate tissue

44
Q

Whats between the arachnoid membrane and pia matter

A

subarachnoid space filled with csf, the brain floats to protect from mechanical stress

45
Q

Reticular formation

A

collection of lose nerve cells connecting brain to behaviour

45
Q

Pia matter

A

Right on top of brain; tethered ton arachnoic by arachnoid ‘trabeculae’

46
Q

What is in the subarachnoid space

A

blood vessels, capillaries to the brain tissues, BBB in between capillaries and the brain tissue

46
Q

Endothelial linings of blood vessels

A

Large gaps (fenstrations) to allows molecules to pass

47
Q

Endothelial cells in brain

A

tightly bound leaving no gaps, constitues the BBB

48
Q

Ventricles

A

deep cavities in the vrain

49
Q

Lateral ventricle

A

large curved structure inside each cerebral hemisphere, paired structure across midline

50
Q

Where does the lateral ventricle empty

A

Into the 3rd ventricle, right in the middle, deep in the brain under the cerebral hemisphere
3rd ventricles communicated with a channels called Aqueduct of sylvius to 4th ventricle

51
Q

Canal from 4th ventricle

A

central canal- goes to middle of the spinal cord
CSF produced in the ventricles drains through the ventricle of the central canal

52
Q

After central canal where does csf move

A

to outer parts of the brain (subarachnoid space) and finally exits at the top of the brain into large vinous sinus (on the midline).
about half the csf drains through arachnoid villi into venous system

53
Q

Arachnoid villi

A

an outpouching of
the arachnoid tissue sticks out
through the dura mater into the
venous sinus > CSF drains into the
venous system

54
Q

Where csf produced from

A

from the plasma by the ‘choroid plexus’ which lines the ventricles
come is produced from capillaries inside the brain

55
Q

Choroid plexus

A

it produces most of the CSF.
it is made of epithelial cells connected by tight junctions
it is a dense network of capillaries ballooning out into the ventricular wall with tight junctions so that everything has to be transported

56
Q

lumbar puncture

A

diagnostic rocedure to collect sample of CSF

57
Q

CSF

A

osmolarity and Na+, same as blood
greatly reduced K+, Ca2+ and Mg2+

csf serves as a cushion - it fills ventricles and subarachnoid space

58
Q

astrocytes

A

The walls of the capillaries are plastered with the ‘end feet’ of glial cells, particularly the astrocytes
Astrocytes provide a bridge between neurons and blood vessels.

59
Q

funcitons of astrocytes

A

Astrocytes are efficient at glycolysis
* Astrocytes produce lactate as an end-product
* Lactate is a substrate for ATP production
- Remove neurotransmitters
– Provide energy substrates for neurons and more
- regulate local blood flow

60
Q

How to astrocytes regulate local blood flow

A

Astrocytes are already bridging the gap between BV and neurons, so they are in a good spot to signal BV when to dilate and to constrict (increase or decrease blood flow)
* Astrocytes have a connection with the neuron at the synapse and when they detect increased signaling, they can send a metabolic signal outward to BV (opposite to nutrient flow), signaling neuronal activity level

61
Q

What triggers Ca2+ release in astrocytes?

A

Glutamate in synapses triggers Ca2+ release within astrocytes; Ca2+ wave travels through astrocytes and triggers prostaglandin (PGE2) release at end-foot
* PGE2 causes vasodilation > increased blood flow

62
Q
A

PSL300 (9 decks)

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