PNS 3.docx

Somatic nervous system- the efferent division Somatic nervous system in the conscious part that controls the skeletal muscle. 1 neurone Motor neurone localised in the ventral hole of the spinal cord. Myelinated axon sends action potential down to the skeletal muscle. Axon terminals release Ach to st...

Somatic nervous system- the efferent division Somatic nervous system in the conscious part that controls the skeletal muscle. 1 neurone Motor neurone localised in the ventral hole of the spinal cord. Myelinated axon sends action potential down to the skeletal muscle. Axon terminals release Ach to stimulate muscle contraction. *One exception being the muscles that control our head is not localised in the spinal cord, instead localised in the brain* Motor neurones are the final common pathway- all the upper areas in the brain such as primary motor cortex, basal nuclei etc can influence the activity of our muscle by acting at the end on the motor neurones. For somatic, it is ONLY excitation whereas for autonomic, it can be either excitation or inhibition. Neuromuscular junctions (NMJ) Motor neurones send fibres to innervate the skeletal muscle fibres. The axon branches into different axon terminals When the axon terminals are close to skeletal muscle fibres, it loses its myelin sheath and divides into branches and ends in terminal buttons. The structure when the terminal button ends on the skeletal muscle fibres are called motor end plate and is part of the muscle. NMJ has 2 parts: Neural component= terminal button Muscular component= motor end plate Each skeletal muscle fibre can be only innervated by one single motor neurone. Can’t have 1 single muscle fibre with 2 NMJ. 1 motor neurone can innervate more than 1 skeletal muscle fibre. Motor unit= a motor neurone + all skeletal muscle fibres it innervates. Process of how information is carried from nerve to the muscle fibre. Nerve and the muscle fibre doesn’t come into direct contact at the NMJ, a chemical messenger (Ach) carries the information. An action potential travels along the axon fibre of the motor neurone When an axon arrives closer to the muscle fibre, it loose sits myelin sheath and ends in a structure called terminal button. There is a gap between the muscle fibre and the axon terminal therefore action potential can’t jump. The action potential causes voltage gated Ca2+ channels to open resulting in an influx of Ca2+ causing the vesicles containing Ach to release via exocytosis. Ach enables communication between the axon terminal and the skeletal muscle fibre. Receptors at the motor end plate are nicotinic receptors (membrane channel proteins). Ach with nicotinic receptors always causes depolarisation (excitation). Ach binding to nonspecific cation channels on the motor end plate causes large movement of Na+ into the muscle cell and smaller movement of K+ outwards. This results in an end plate potential (EPP) (depolarisation of motor end plate) which isn’t an action potential) due to a large difference in electrochemical gradient. The EPP is large enough to open voltage gated sodium channel that are localised in an adjacent area of plasma membrane of skeletal muscle fibre. This causes influx of Na+ which causes an action potential to form which is propagated throughout the muscle fibre. A NMJ consists of multiple terminal buttons, each terminal button contains thousands of vesicles to store Ach. To prevent constant stimulation of the muscle, Ach is degraded/hydrolysed by an enzyme called acetylcholinesterase. EPP vs EPSP One NMJ has multiple terminal buttons, and each terminal button contains Ach. Whereas in EPSP there is only a single pre and post synaptic neurones. More neurotransmitter is released from a single terminal button than from a pre-synaptic bulb in response to action potential. Motor end plate has a higher surface area and has more density of receptor than a post synaptic membrane therefore greater influx of + ions and larger depolarisation. = EPP is much larger than EPSP Chemicals/ agents that act on NMJ’s. Black widow spider venom causes explosive release of Ach therefore the muscle contracts constantly which ends up in respiratory failure hence death. Botulinum toxin blocks release of Ach therefore muscle can’t contract therefore respiratory failure hence death. Curare blocks action of Ach at receptor channels Organophosphates prevents inactivation of Ach therefore constant muscle contraction. Myasthenia gravis inactivates Ach receptor-channels.