Psychobiology: Learning & Memory, WEEK 4 Flashcards

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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
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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
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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
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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
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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.
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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
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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
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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.
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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
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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
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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
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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
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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
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14
Q

Chemical synapse

A
  • Communication across the synaptic cleft is a chemical synapse
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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
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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