10. Behavioural Neuroscience: Structure & action of neurons Flashcards
what are the 5 key features of a neuron?
- Soma (cell body)
- Dendrites
- Myelin sheath
- Axon (inside myelin sheath)
- Terminal buttons
which direction does messages flow?
from Soma > Terminal buttons
what is the action potential caused by?
changes in flow of ions across the neuron’s cell membrane
- RAPID change in the membrane potential of the neuron (caused by ion movement)
what is the membrane potential?
charged difference b/w inside & outside of the cell
what is the membrane potential of a neuron at rest?
polarised at -70mV
how does the membrane potential DEPOLARISES
- Na+ flow INTO cell, membrane potential becomes less -ve (-70 > 0mV)
when will an action potential be triggered?
when the membrane potential reaches -50mV
what does triggering of action potential cause?
triggers cascade of other seq of events
what happens when Na+ flow into the cell’s membrane?
- K+ from inside the cell will FLOW OUT (K+ channels open)
- Na+ still entering the cell, so membrane potential CONT to DEPOLARISE
what happens AFTER the action potential is FINISHED
- K+ channels take LONGER to close (so some K+ cont to leave cell)
- membrane potential is HYPERPOLARISED (more -ve)
- further from threshold (<-70mV)
CONSEQ: subseq action potential req GREATER Na+ INFLUX IMMEDIATELY AFTER neuron fired (becuz currect membrane potential is more -ve than before)
what is the REFRACTORY period? what happens?
- when action potential reaches its PEAK
- charge inside neuron is more +ve so Na+ channels CLOSE
- will not open until membrane potential RETURNS to RESTING POTENTIAL (-70mV)
what happens after the PEAK in action potential?
- K+ channels STILL OPEN
- K+ cont to EXIT cell
- charge becomes MORE -ve
- membrane potential RETURN to RESTING LVL (-70mV)
what happens when the action potential reaches the RESTING MEMBRANE POTENTIAL AGAIN?
- K+ channels close
- Na+ channels RESET (another depolarisation can cause them to repoen)
what is the rate law of action potentials?
- neuron firing is ALL OR NONE
- SAME action potential EVERY TIME (size is UNCHANGED)
- STRONG stimulus = reach threshold for activation FASTER = MORE FREQ action potential
what enables communication b/w neurons?
synapses (area where 2 neurons come together)
what are the key structures of a synapse? (4)
- terminal button
- synaptic clef (gap b/w neurons)
- pre & post synaptic membrane
- synaptic vesicles
desc how signals are sent through the synapse
- many # of points of contact b/w 2 neurons
- contact @ end of terminal button
- from pre > post synaptic neuron
what are the chemical messengers & where are they synthesised?
- neurotransmitters
- synthesised w/in brain/neuron
desc how action potential moves from the pre > post synaptic neuron
- action potential in PRE triggers synaptic vessels to move > cell membrane
- vesicle & membrane FUSE
- Neurotransmitters w/in vesicle RELEASED
- Neurotransmitters flow > Synaptic Clef & BIND > RECEPTORS on post membrane
desc neurotransmitter RELEASE
- synaptic vesicle (w/ NEUROTRANSMITTER) fuses w/ presynaptic membrane
- CONTENTS RELEASED to clef
- “exocytosis”
desc neurotransmitter REUPTAKE
- synapse can RECYCLE & REUSE neurotransmitter molecules AFTER release
- REABSORPTION into synapse
- endocytosis
what are EPSP & what do they do? & e.x
- Excitatory postsynaptic potential
- DEPOLARISES the postsynaptic cell membrane
- ^ likelihood that action potential WILL BE TRIGGERED in postsynaptic neuron
- GLUTAMATE = primary EPSP
what are IPSP & what do they do? & e.x
- Inhibitory postsynaptic potentials
- HYPERPOLARISES the postsynaptic cell membrane
- DECREASE likelihood that action potential will be TRIGGERED
- makes cell membrane potential MORE -VE THAN -70mV
- GABA = primary IPSP
what is the combined effect of EPSP & IPSP?
Neural integration
under what circumstances will a neuron FIRE?
if the sum of the EXCITATORY inputs is SUFFICIENTLY GREATER than the INHIBITORY inputs
- causes the membrane potential to PASS the threshold of activation (-50mV)
what are the 4 neuromodulators?
- dopamine
- noradrenaline
- histamine
- serotonin
what do AGONISTS do
- activate the receptor like the natural compound
- similar molecular structure & can bind to the receptor
what do ANTAGONISTS do?
- block the receptor & prevent the natural compound from activating it
- still able to bind to the receptor
what are the impacts of DRUGS on NEUROTRANSMITTER FUNC?
- mimic chemical struc of neurotransmitter
- impact every stage (synthesis > release > receptor binding)
what is the primary means of communication b/w neurons?
synaptic transmission (transmission of messages 1 neuron > another across synapse)
what are post synaptic potentials?
- brief depolarisations/hyperpolarisations
- increase/decrease rate of axon firing of postsynaptic neuron
what struc are located in the cytoplasm of terminal buttons & what is their func?
- mitochondria : ATP prod
- synaptic vessels : contain neurotransmitters 4 transport
- microtubules : transport material b/w soma & terminal button
why is there a high # of synaptic vesicles near the presynaptic membrane that faces the clef?
because that is the region where neurotransmitters are released from pre > post via clef
