Psychobiology: Learning & Memory, WEEK 4 Flashcards
1
Q
Electrical signalling
A
- how neurons communicate when they are far apart
- Neurons are large so axons can extend to reach different parts of the neuron to communicate
- We know communication is fast due to how quick reflexes are. (diffusion of chemicals is too time consuming, signal to communicate is electrical in nature)
- signals in neurons are electrical in nature
- Electrical signal allowing comm = action potential > this needs a resting membrane potential
2
Q
Resting membrane potential
A
- form of electrical excitability > RMP is when a neuron is inactive so energy is used to hold an unstable state
- as the neuron is unstable, when it’s triggered, the built up energy releases enabling the action potential signal > RMP has capacity to start action potential
3
Q
What happens in RMP?
A
- RMP depends on the cell membrane having a lipid bilayer (insoluble)>means ions don’t pass through the fatty molecule layer > is a bit leaky some ions can pass
- Membrane is a barrier between the inside + outside of the neuron, if we alter the structure of the outside compared to the inside, ions can get through > creates a ‘excitable + unstable’ RMP.
- Cell membrane have proteins which can serve functions like ion transporter
4
Q
Sodium-Potassium exchange transporter
ion transporter
A
- In the surface of cells of neurons, there is a sodium-potassium exchange transporter
- Moves Na+ ions out of the neuron + brings K+ ions into the neuron > leads to accumulation of + ions out of the cell, partially in exchange for K+ inside the cell.
- Partial exchange as more Na+ moves out than K+ moves in as theres more -ve charge inside.
- Outside is more +ve, inside is more -ve
- RMP difference is at -70mV (- as the inside is more -ve than outside)
- Na cations tend to move into the cell due to electrostatic pressure + diffusion but the transporter is pushing it back out
5
Q
Movement of ions
A
- Ion transporter: moves specific ions using energy from the whole body which maintains the RMP.
- Electrostatic pressure: ions w/ the same charge repel each other, + ions w/ the opposite charge attract
- Diffusion gradient: Regardless of the charge, they will want to move from areas of their own high concentration of the charge to low concentration of their charge.
6
Q
Cations at rest + activating action potential
A
- Diffusion + electrostatic pressure makes Na+ ions want to go in the cell, at rest the membrane is leaky so some Na goes in > if membrane became permeable, Na ions would flood in + make the inside more +ve than outside,
- Due to this, Na channels are the first mechanism in activating action potentials
- K+ wants to leave the cell because of diffusion (too much K in the cell) but electrostatic pressure makes it stay in as there is a high conc of cations outside the cell
7
Q
Stage 1: Action potential
A
- Na channels are voltage gated, approx threshold is -55mV (thresholds are not fixed but this is the average)
- If the membrane is depolarised (less -ve) + reaches -55mV from -70mV RMP, the Na channel opens
8
Q
Stage 2: Action potential
A
- Na channels open w/ K channels > Na channels flood into the cell > membrane potential gets more +ve
- When K channels open, there is little movement of K+ due to balance from diffusion gradient + electrostatic pressure.
9
Q
Stage 3: Action potential
A
- More Na cations will be on the inside than outside so membrane potential is more +ve than outside > allows K+ ions to move out as there is no more electrostatic pressure + moves w/ diffusion
- Na channel closes when it reaches 40mV
10
Q
Stage 4: Action potential
A
- Na channel close but K channels stay open as K ions keep leaving the cell due to diffusion + electrostatic p
- This makes the membrane potential more -ve as there are less cations inside the cell > this is called membrane repolarisation
11
Q
Stage 5: Action potential
A
- K cations keep leaving the cell past original RMP > membrane potential gets more -ve past -70mV
- K channels close eventually + combination of processes lead to balance of membrane potential
12
Q
Relevance of action potentials for brain function
A
- Action potentials are basic code for info in the brain > this code is specific in nature (same shape + size)
- They follow an ‘all or nothing’ law, they either will occur or do not (nothing in between)
- Size of the action potential doesn’t contain info
- Frequency (rate) of action potentials contain info
13
Q
Transmission of the electrical signal
A
- The signal cannot jump from one neuron to another as the synaptic cleft in only 20nm but isn’t wide enough to allow it to jump
- Recipient neuron needs to be depolarised
- Membrane may depolarise to begin with as a action potential may have been generated nearby > creates localised movement of ions + membrane change which can breach threshold of excitation
14
Q
Chemical synapse
A
- Communication across the synaptic cleft is a chemical synapse
15
Q
Chemical synapses : pre-synaptic neuron
A
- Input neuron brings info to the synapse
- Terminals > end of axon are axonal terminals where there are vesicles containing neurotransmitters
- Neurotransmitters get released by the pre-synaptic neuron into the synaptic cleft > done by fusing vesicle into membrane at axonal terminal
16
Q
Chemical synapse: post-synaptic neuron
A
- Output neuron receives info at the synapse
- Receptors (many which are ion channels) > the released neurotransmitters bind to the receptor, binding opens the channels > allows ions to flow through + change voltage + conductance of output neuron > creates a post synaptic potential as potential of membrane changes
17
Q
Post-synaptic potentials (PSPs)
A
- Hypopolarisation > essentially the same as depolarisation, allows opening of cation channels, excitatory (EPSP = excitatory post synaptic potential)
- Hyperpolarisation > is inhibitory and allows opening of anion channels, (IPSP = inhibitory post synaptic potential) > becomes permeable to anion channels (Cl-) > would make RMP more -ve than -70mV > less likely to fire potential
18
Q
Why is communication within a neuron fast?
A
- Speed of action potentials are facilitated by the myelin sheath made from glial cells
- AP’s decreases while travelling under sheath due to insulating properties, but it fully regenerates at nodes of Ranvier (gaps between) > allows AP to jump from nodes to nodes
- This speeds communication through the axon but also conserves energy as AP is only regenerated between the myelin sheath + not all through the axon
19
Q
Neural integration
A
- communication between synapses allow neural integration
- where each pre-synaptic neuron may contact other different post-synaptic neurons > post-synaptic neurons can get inputs from several different pre-synaptic neuron
> means post-synaptic neurons integrate across many inputs. > these several inputs combine to affect the probability of the post-synaptic neuron firing. - PSP’s are small + opening of a channel isnt enough for depolarisation or hypopolarisation > means summation of many PSP’s enhance ability of post-synaptic neuron firing - likely basis of brains computing power
20
Q
Post-synaptic receptor (ligand)
A
- Ligand = chemical interacting w/ a receptor > neurotransmitter + drugs are ligands
- the binding site on the receptor is where the ligand interacts
21
Q
Binding ligands to receptors
A
- Selectivity of binding: only specific ligands fit in a binding site due to 3D shape of receptor. Some drugs bind to more than one receptor (means there are more receptor types than neurotransmitters)
- Affinity: describes how well a ligand binds to a receptor > high affinity ligand means receptors are completely bound by small amounts of ligand
22
Q
Iontropic receptors
A
- directly paired to an ion channel (receptor is an ion channel in a way) > means it has a direct effect on neuron as when ligand binds to the receptor, the ion channel opens
23
Q
Metabotropic receptors
A
- Metabotropic receptor: begins w/ ligand binding to receptor + neurotransmitter released into cleft > binds to outside of post-synaptic membrane
- This changes the 3D shape of receptor as receptor proteins span lipid bilayer of membrane
- Receptor proteins are connected to other proteins > the changed shape of receptor proteins activates G proteins
- Activation of G proteins initiates intracellular signalling cascade > results in many effects such as altering iontropic receptors to make them more/less excitable
24
Q
Receptors on pre-synaptic neurons
A
- Receptors here allow many functions such as negative feedback > release of neurotransmitter can stop its own further release to avoid wasting neurotransmitter + is stored in pre-synaptic neuron
- Another function is retrograde signalling > signal from post synaptic neuron to pre synaptic neuron
25
Q
2 broad types of neurotransmitter based on chemical nature
A
- Amino acid derivatives
- Monoamines
26
Q
Amino acid derivatives
A
- Glutamate: comes from glutamic acid + are usually seen in brains of mammals > excitatory neutrotransmitter as receptors it binds to tend to make ESPS
- Glutamate binds to at least 8 different receptors (ionotropic+metabotropic+NMDA+AMPA)
- GABA: synthesised from glutamate but most abundant inhibitory neurotransmitter > makes post-synaptic neuron less likely to fire
- Glycine: unusual as it is an amino acid itself + binds to inhibitory receptors in spinal cord > co-agonist w/ glutamate at NMDA receptors
27
Q
Monoamines
A
- Mostly bind to metabotropic receptors + found in specific groups in neurons
- Includes dopamine, seratonin and neuropeptides (eg: opiods)
- Peptides are proteins which act as neurotransmitters
28
Q
Factors affecting Na+ and K+ channels
A
- increasing Na+ channels reduce the threshold of action potential
- increasing K+ channels delays initiation of action potential
- High amplitude can reduce threshold
- High density of Na+ channels reduce threshold
29
Q
Blocking sodium channels with TTX
A
- TTX is a toxin binding to Na+ channels and blocks the flow of sodium ions through a channel
- This prevents the production of an action potential
30
Q
Blocking potassium channels with TEA
A
- TEA is a potassium-selective ion channel blocker
- TEA only affects voltage dependant changes in K+ permeability
- This increases the duration of an action potential > because K+ is responsible for cell repolarisation, when it is blocked, it takes longer to repolarise, increasing AP time
