structure and action of neurons

action potential

rapid change in membrane potential of the neuron caused by the movement of ions. 

key ions

• Na+ Sodium, Cl- Chloride, K+ Potassium 

Cytoplasm + extracellular space. More sodium on inside. More potassium outside 

resting membrane potential

-70mV

what happens when positive Na⁺ ions flow into the cell?

membrane potential depolarises, (potential moves from -70mV to 0mV

refractory period

membrane potential is hyperpolarised. becomes even further from the threshold of activation. neuron will be less likely to trigger another action potential

rate law of action potentials

neuron firing is ‘all or none’. thus frequency of firing determines strength of neural signal

• strong stimulus → faster threshold of activation → more frequent action potential

synapse

allows for communication between neurons

terminal button

projections from the axon that send excitatory or inhibitory messages to the next neuron. small bulb like structure. release neurotransmitters into synaptic cleft

synaptic cleft

microscopic gap between neurons that facilitates chemical communication (~20-40 nm). separates pre-synaptic and post-synaptic neuron

pre synaptic membrane

specialised plasma membrane of the axon terminal that releases neurotransmitters into the synapses. cell membrane of an axon terminal that faces the recieving cell

post-synaptic membrane

specialised thickened region of receiving cell’s surface. contains high densities of receptors, ion channels and signalling molecules

synaptic vesicles

~35-50 nm membrane-bound sacs in presynaptic axon terminals. store, transport and release neurotransmitters

neurotransmitters

chemicals that are synthesised within the brain/neurons. often referred to as ‘chemical messengers’

steps of chemical signalling in the brain

1. action potential is PRESN triggers synaptic vesicles to move towards membrane

2. fusion of two membranes

3. neurotransmitters released

4. neurotransmitters flow in synaptic cleft, where they bind to receptors on the post synaptic membrane (lock and key)

neurotransmitter release

when synaptic vesicle merges with presynaptic membrane, contents released in the synaptic cleft. ‘kiss and run’

neurotransmitter re-uptake

synapse has ability to reuse neurotransmittes molecules after release

endocytosis

process of reabsorption into synapse

neural excitation

excitatory post-synaptic potentials depolarise post-synaptic membrane

• ESPS (excitator post-synaptic potentials) increase the likelihood that an action potential will be triggered in post-synaptic neuron (eg. glutamate)

neural inhibition

inhibitory post-synaptic potentials (IPSP) hyperpolarise post synaptic cell membrane

• decrease likelyhood that an action potential will be triggered in the post-synaptic neuron (eg. glutamate)

neural integration

combined effect of EPSP + IPSP

• a single neuron can simultaneously receive excitatory and inhibitory inputs, with impact flow of ions into the neurons

THE NEURON WILL ONLY FIRE IF THE SUM OF THE EXCITATORY INPUTS IS SUFFICIENTLY GREATER THAN THE INHIBITORY INPUTS IN ORDER TO CAUSE THE MEMBRANE POTENTIAL TO PASS THE THRESHOLD OF ACTIVATION

neuromodulators

substances or devices that alter nerve activity and synaptic transmission in the body

examples of neuromodulators

serotonin, dopamine, histamine

action of neurotransmitters at receptors

transmitters don’t usually enter PSN directly. to cause effect on PSN, chemical message recieved by attaching to binding site of receptor sensitive to tranmitter

→ opening ion chanel is one example of the effect caused by neurotransmitter binding to receptor. ‘

lock and key mechanism

how do drugs work?

mimick natural neurotransmitters and neuromodulators

agonists

activating receptor like the natural compound

antagonist

blocking receptor + preventing natural compound from activating

why do drugs impact psychological processes?

ONLY because they mimic. trigger same biological responses triggered by naturally occuring substances