Week 2 Flashcards
1
Q
Types of postsynaptic receptors
A
Ionotropic and Metabotropic
2
Q
What determines the effect?
A
Receptor, not the transmitter
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
3
Q
Duration of the PSP
A
20-40 ms
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)
4
Q
EPSP
A
Depolarizing (ion channel is specific for cations Na+ K+ etc)
5
Q
IPSP
A
Hyperpolarizing (Ion channel may be specific for Cl- or K- ions)
6
Q
Metabotropic effects
A
- Binding of a ligand to a postsynaptic receptor will activate an enzyme that is usually G protein-coupled
- the enzyme facilitation will result in increased production or destruction of 2nd messengers
- 2nd messenger will activate other enzymes
7
Q
2nd messengers
A
cAMP, cGMP, or InP3
8
Q
What effect is more immediate?
A
Ionotropic; metabotropic activation takes time
9
Q
How must PSS spread to get to the initial segment of an axon?
A
Passive conduction
9
Q
beta-adrenoreceptor
A
- beta-receptor is a metabolic receptor for noradrenalin.
- Binding of NA to beta receptor activates adenylyl cyclase via a G protein alteration
- adenylyl cylclase increases production of cAMP
- cAMP will then activate kinases which phophorylate Ca2+ channel
- the phosphorylation of the Ca2+ channel will increase the Ca2+ influx
9
Q
Where are PSPs generated?
A
They are generated in inexcitable membrane; neuronal dendrites and cell bodies
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+
11
Q
2 types of PSP summations
A
spatial and temporal
12
Q
Spatial summation
A
Minimum of 10-30 synchronous EPSPs in dendritic tree, generated at a different synapse
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
14
Q
IPSP (Cl- channel)
A
- they involve the opening of the Cl- channel
- the equilibrium potential for Cl- is very close to resting MP
- at result opening of Cl- causes little change
- when the membrane is depolarized, opening of the Cl- channel will
bring the MP back down to -70 mv - The net affect of Cl- is basically to ‘clamp’ the MP, which is preventing excitation,
thus preventing depolarization > inhibitory effect - These IPSPs are very strategically located and they completely block any signal
coming from EPSPs simply by positioning right on the soma
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
16
Q
Whats more imp IPSPs or EPSPs ?
A
IPSPs are generally more important than EPSPs
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
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’
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.
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
20
What can we generate due afterhyperpolarization
spike train
21
Receptor potential
Change in the membrane potential due to receipt of signal from exterior sensory cue
22
What happens when receptor proteins change shape?
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
23
What will happen when energy from the environment reacts with membrane proteins
Depolarization of sensory receptors
EXCEPTION: photoreceptors hyperpolarize
24
What happens when a chemical stimulus binds to a specific metabotropic receptor (G-protein coupled)
- 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
Categories of sensory cell transmission
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
What are the 2 stages of amplification
1. G protein can activate a number of different enzyme molecules
2. One stimulus can produce lots of 2nd messenger (cAMP)
27
Transmission of Signal (AP)
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
Transmission of Signal (Vesicles)
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
Adaptation
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
Types of adaptations
1. slowly adapting
2. rapidly adapting
30
Coding of stimulus intensity
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
Habituation
Response to successive stimuli in time.
Repeated stimuli (identical) in succession elicit progressively weaker
responses.
31
Slowly adapting
Receptor potential sustained for the duration of the stimulus. Interested in the total magnitude of the stimulus.
32
Rapidly adapting
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
Strategies to code for strength of stimulus
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
How do we continue coding for stimulus intensity after reaching the ceiling due to the refractory period?
Recruit additional neurons
34
How do we distinguish different modality of stimulus?
Labeled Line strategy
35
Population code
Population coding is coding using the ratio of activity from a restricted number of different receptor types
36
Receptive field
The spatial area the sensory neuron responds to; where a neuron can be activated
37
Why should the ionic composition of the extracellular fluid around the neuron be specifically controlled?
1. Cannot change the excitability of the membrane
2. Cannot have neurotransmitters floating around for no reason
Regulated by the BRAIN BLOOD BARRIER
38
Where is blood brain barrier located
Between Blood vessels and interstitial fluid and CSF
39
Parkinsons disease
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
MSG
Cannot cross BBB
they activate glutamate outside the brain and PNS
41
Why and where is BBB broken
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
Dura matter
Very tough membrane, sac containing the brain and spinal cord
43
Arachnoid membrane
More delicate tissue
44
Whats between the arachnoid membrane and pia matter
subarachnoid space filled with csf, the brain floats to protect from mechanical stress
45
Reticular formation
collection of lose nerve cells connecting brain to behaviour
45
Pia matter
Right on top of brain; tethered ton arachnoic by arachnoid 'trabeculae'
46
What is in the subarachnoid space
blood vessels, capillaries to the brain tissues, BBB in between capillaries and the brain tissue
46
Endothelial linings of blood vessels
Large gaps (fenstrations) to allows molecules to pass
47
Endothelial cells in brain
tightly bound leaving no gaps, constitues the BBB
48
Ventricles
deep cavities in the vrain
49
Lateral ventricle
large curved structure inside each cerebral hemisphere, paired structure across midline
50
Where does the lateral ventricle empty
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
Canal from 4th ventricle
central canal- goes to middle of the spinal cord
CSF produced in the ventricles drains through the ventricle of the central canal
52
After central canal where does csf move
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
Arachnoid villi
an outpouching of
the arachnoid tissue sticks out
through the dura mater into the
venous sinus > CSF drains into the
venous system
54
Where csf produced from
from the plasma by the 'choroid plexus' which lines the ventricles
come is produced from capillaries inside the brain
55
Choroid plexus
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
lumbar puncture
diagnostic rocedure to collect sample of CSF
57
CSF
osmolarity and Na+, same as blood
greatly reduced K+, Ca2+ and Mg2+
csf serves as a cushion - it fills ventricles and subarachnoid space
58
astrocytes
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
funcitons of astrocytes
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
How to astrocytes regulate local blood flow
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
What triggers Ca2+ release in astrocytes?
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
