Nervous coordination 2 The nerve impulse

NERVE IMPULSES The nerve impulse involves the movement of ions through the axon membrane When a neurone is not conducting an impulse it is in the Resting State and the inside has a slight negative charge When positively charged Na ions enter, the inside is briefly positive; Depolarised, generating an Action Potential.

The ions causing the resting state include sodium, potassium, chloride and large negatively charged organic ions The concs of these vary across the axon membrane due to its relative permeability to the ions During the resting state K+ ions can move out through protein channels (gates); but negative organic ions can’t move out so, negative inside keeps K+ inside Na+ ions are in high conc outside but membrane has low permeability with few sodium channels, those that do enter are expelled by ion pumps. This all results in a negative (-70mV) charge inside the axon during its resting state

Action Potential When nerve impulse generated, more sodium channels are opened so Na+ ions move in faster than can be expelled by pumps The charge inside briefly becomes positive (+40mV)and an action potential caused

The permeability to sodium ions is quickly decreased again; simultaneously potassium channels open allowing K+ ions to flood out This restores the negative charge inside the axon; Repolarised The potassium channel opening causes a slight “overshoot” causing a slightly too negative charge inside the axon; Hyperpolaristaion, but soon charge stabilises at resting state

Transmission speeds vary from 0.5msec-1 to over 100 msec –1 So the nerve impulse is caused by a wave of depolarisation travelling along the axon from each region of membrane to the next The ion channels are “voltage dependent” opening in response to depolarisation Impulses jump from one Ranvier node to the next in myelinated neurones, greatly increasing the speed of transmission; Saltatory Conduction Transmission speeds vary from 0.5msec-1 to over 100 msec –1 Controlled by: Diameter of the axon (greater=faster) Myelin sheath (myelinated=faster)

Resting potential The inside of a resting nerve fibre is about 60 mV negative compared to the surface of the cell This electrical potential difference across the fibre membrane (axolemma) is called the resting potential The resting potential is maintained by differences in the concentration of ions and other charged particles between the cytoplasm and the tissue fluid around the fibre

Resting potential Under normal conditions there is a greater concentration of sodium ions in the extracellular fluid than in the axon, and a greater concentration of potassium ions in the axon than outside. As a result there is a very slow inward diffusion of sodium ions, and a slightly faster outward diffusion of potassium ions. At rest this is balanced by the action of the sodium-potassium pump. As a result there is a very slow inward diffusion of sodium ions, and a slightly faster outward diffusion of potassium ions ... but a greater concentration of negatively charged protein molecules in the axoplasm keeps the inside negative with respect to the outside. There is also a very slow inward diffusion of chloride ions ... The membrane of the resting axon contains channels (gates) specific for sodium, potassium and chloride ions. At rest, more K+ channels are open than Na+ channels. Like most animal cell membranes, it also contains the sodium-potassium pump (Na+/K+-activated ATPase The result of all of these differences in concentration and permeability is the resting potential of -60 mV.

The action potential

The action potential The action potential is followed by a refractory period, when the sodium gates are inactivated. During the refractory period no stimulus, however strong, can trigger another action potential. The action potential is an all-or-nothing event: if the initial depolarisation reaches threshold value, a full action potential is triggered; if it does not, there is no action potential. When the initial depolarisation reaches threshold, Na+ gates open: Na+ ions flood in, causing rapid depolarisation 1 ms later Na+ gates are inactivated, and K+ gates open: K+ ions flood out The axon is hyper-polarised and refractory Oscilloscope trace Resting potential Resting potential restored 1 2 3 4 Time / ms Sodium gates inactivated K+ gates open Sodium gates closed Some K+ gates open Sodium gates reactivated and closed Sodium gates closed Events in the axon -60 +45 -70 -60 Some K+ gates open Most K+ gates open

The action potential: how much have you understood? What causes this sharp rise in potential? What causes this sharp fall in potential? What is this potential called? Oscilloscope trace What is this potential called? What is the state of the axon here? 1 2 3 4 Time / ms Events in the axon

Propagation of the action potential Repolarisation Threshold Local currents occur between the depolarised and resting regions of the membrane Initial depolar-isation At the trailing edge of the impulse local currents cannot open sodium gates because they are inactivated for the refractory period. At the leading edge of the impulse local currents cause initial depolarisation, which opens sodium gates when it reaches threshold. Hyperpolarised and refractory Resting Direction of impulse Sodium in Potassium out: refractory

Propagation of the action potential Na+ gates behind a.p. inactivated (refractory period), preventing backward propagation. Threshold depolarisation opens Na+ gates ahead of a.p., moving it forward. Action potential initiated by opening sodium gates Resting axon: sodium gates closed, some potassium gates open Local currents propagated, causing initial depolarisation

Propagation of the action potential The sodium inflow and potassium outflow at each action potential are restored by the sodium-potassium pump: the ion gradients maintained by the pump represent the energy store for action potential transmission The sodium and potassium ions exchanged at each action potential represent about one ten-millionth of those available: even if the sodium-potassium pump is stopped by metabolic inhibitors, the axon can still transmit thousands of action potentials

Properties of the action potential Action potentials are all-or-nothing: there either is one, or there isn’t; this is therefore a digital signalling system Action potentials are self-propagating: once initiated, an action potential propagates itself along the axon using the ion gradients maintained by the sodium-potassium pump Action potentials do not decay: unlike analogue signalling systems, there is no loss of signal strength with distance travelled

Properties of the action potential Frequency of action potentials conveys information about different intensities of stimulation Sensory neurones commonly have a resting transmission frequency: raising or lowering this frequency can therefore convey opposite kinds of information. E.g. hair cells in the inner ear: Hair bent to right Resting frequency Hair bent to left

Properties of the action potential The absolute refractory period following an action potential lasts about 1 ms, giving a theoretical maximum frequency of transmission approaching 1000 per second. In practice maximum frequencies observed are about 200 per second. Unmyelinated human nerve fibres conduct action potentials at about 1-2 ms-1; squid giant axons conduct at about 20 ms-1; the largest myelinated fibres in mammals conduct at over 100 ms-1. Myelination speeds up by transmission by allowing saltatory conduction (see next slide)

Saltatory conduction … so the action potential ‘jumps’ from one node to the next, greatly speeding up conduction. Insulation by myelin allows local currents to flow only between nodes …

Comprehension check Suppose that two action potentials have been generated at opposite ends of a fibre, and are travelling toward each other. What will happen when they meet? The membrane on both sides is refractory and incapable of being depolarised: both action potentials will therefore fade out. When the actions potentials merge, what is the state of the membrane on both sides? Make your prediction now …