Neuron leak channels
Pores for K+, constutively active.
High permeability for K+ = resting potential negative.
Depolarisation
Na+ permeability increase, equilibrium shifts to Na+
Hyperpolarisation
K+ permeability increase, equilibrium shifts to K+
Neuron variations
Purkinje cells - coordination of movement in cerebellum, lots of dendrites
Pyramidal cells - cognition & vision guided movement
Graded potentials
For integrate information, not for long distance.
Dendrite signal receptors lead to change in ion channel activity & membrane potential.
Allows responding with polarisation changes.
Polarisation change depends on:
in/out ion concentrations
equilibrium potentials
ion channels selectivity
The stronger the stimmuli, the stronger the effect on the membrane potential of dendrite.
Spatial summation
sum of EPSPs that come at the same time to axon hillock
Temporal summation
sum of postsynaptic potentials from the same synapse
Action potential phases
Resting - channels closed, resting state of the membrane.
Depolarisation - axon membrane potential reaches treshold potential, Na+ gate opens, ion depolarise the membrane.
Repolarisation - Na gate closes, K+ channels open. K+ ions leave & repolarise.
Repolarisation continues- membrane potential decrease, K+ equilibrium bring hyperpolarisation.
Refractory periods
Absolute - no action potentials due to inactive Na+ channels
Relative - after hyperpolarisation; lower membrane potential require depolarising power to reach treshold.
Due to those periods action potentials travel only away from the soma & towards the synapse.
Graded potentials - properties
Vary in magnitude & duration
Decay with distance
Occur in dendrites & cell body
Caused by opening & closing of various ion channels
Action potentials - properties
Always the same size, shape, duration
Occur in axons of neurons & muscle cells
Caused by opening & closing of voltage-gated ion channels
Dendrite
receive information from other neurons
Cell body
Contains nucleus + organelles
Axon hillock
Information gets collected and integrated, generating action potentials
Axon
Conducts action potentials away from cell body
Axon terminals
Synapse with target cell
Glial cells
Surround neurons, provide support and insulation between them.
Astrocytes - homeostasis
Microglial cells - macrophage-like
Oligodendrocytes (PNS-Schwann cells) - wrap axons for insulation
Nodes of Ranvier
Non-insulated parts of axon, the only place with voltage gated Na+/K+ channels so action potential will jump on nodes.
Saltatory conductions
In nodes of ranvier;
Action potential generated in node, fastly jumps on nodes.
Electrical synapse
Fast, allow for synchronisation of neuronal activity
Chemical synapse
Excitatory or inhibitory, only link cells.
Acetylcholine
EPSP
Acetylocholine opens cation channel, K+ leaves the cell, Na+ enter
Postsynaptic membrane depolarise
EPSP created
Easier to trigger action potential by crossing the treshold
IPSP
Metabotropic acetylocholine receptor activates G-protein, opening K+ channel
K+ leaves, postsynaptic membrane hyperpolarise
IPSP created
More difficult to trigger action potential by crossing the treshold
Neurotransmitter receptors
Ionotropic receptors - ion channels open by binding to neurotransmitter. Simple crossing.
Metabotropic receptors - coupled with intracellular signal proteins that open ion channels.
Depending on which ion channel it opens it will hyper/depolarise postsynaptic membrane.
Excitatory neurotransmitters
lead to EPSP = graded action potential
Glutamate, Serotonin
Inhibitory neurotransmitters
lead to IPSP = no potential
GABA, Glycine
Excitatory & Inhibitory
Depends on type of receptors it activates on the neuron.
Acetylcholine, adrenaline, dopamine, endorphins
GABA
Synthesized from glutamate
A receptors: chloride channels (ionotropic receptors). Binding opens the channel, Cl goes in, hyperpolarisation of the membrane = IPSP.
Low GABA = axciety, irritiation
Glutamate
Subtypes: AMPA, Kainate, NMDA - different agonists
Activation leads to cation influx = depolarisation = EPSP
Acetylcholine receptors
nAChR are cation channels, activated by nicotine & inhibited by alkaloid arrow poisons.
In skeletal muscle & ANS.
mAChR coupled to G-proteins that activate K+ channels; inhibited by atropin.
In PNS & iris (control pupil size. Inhibited = big)
Noradrenaline & adrenaline
adrenaline hormone; noradrenaline neurotransmitter;
both acts on the same receptors - metabotropic, multiple function.
Adrenaline triggers stress response.
Tetrodotoxin TTX
Accumulated in the body of animal, block Na+ channels = no depolarisation.
Does not work on venomous animals due to insensitivity of their channels.