motor units and NM junction Flashcards
what is a motor unit
- a single alpha-motor neurone (nerve cell)
AND - all of the corresponding muscle fibres it innervates
muscle fibres + nerves/neurones (?) are interdependent
motor units in eye muscles vs hamstrings:
predict the muscle:nerve ratio
(can do as higher m:n and lower m:n)
explain why this may be
(EXPLAIN HOW THIS AFFECTS THE SIZE OF THE MOTOR UNITS - would MUs in eye or hamstring be bigger?)
- eye muscles have much lower muscle : nerve ratio than hamstrings
- meaning there are less muscle fibres innervated per nerve
- expected as this would increase sensitivity of movement/finer dexterity (?) LEVEL OF CONTROL
- and eye muscles need more control/finer/more sensitive control than hamstrings
- eye = smaller MUs (as each nerve innervates less muscle fibres)
the size of a motor uni (MU) dictates…?
the level of control (therefore dexterity?)
are the muscle fibres in motor units always made up of the same muscle fibre type e.g. 11a, 11b etc.?
YES
explain what happens at a NM (neuromuscular) junction:
- AP arrives, the wave of depolarisation in neurone activates VOLTAGE gated Ca2+ ion channels
- flow of Ca2+ into presynaptic neurone
- Ca2+ in neurone stimulates vesicles (in neurone) containing acetylcholine (ACh) to fuse with presynaptic membrane
- releasing ACh into synaptic cleft
- ACh binds to LIGAND-gated ion channels on postsynaptic membrane
- so Na+ flood into postsynaptic neurone
- depolarisation of Na+…blah blah…= AP and impulse along next neurone
enzyme that breaks down ACh (hydrolysis of ACh)
acetylcholinesterase
drugs that interact with ACh/ACh receptors and how/what they are used for:
NAME 3
- CURARE-RELATED DRUGS
- ANTICHOLINESTERASE DRUGS
- BOTULINUM TOXIN (BOTOX)
drugs that interact with ACh/ACh receptors and how/what they are used for:
Curare-related drugs
- function
- how
- Curare related drugs = muscle relaxation during surgery:
act at ACh receptor, so neuromuscular transmission blocked
drugs that interact with ACh/ACh receptors and how/what they are used for:
Anticholinesterase drugs
- function
- how
Anticholinesterase drugs = continuous/constant stimulation of muscle
prevent ACh hydrolysis, ACh no longer broken down, remains+build up in synaptic cleft, continuous/constant stimulation of muscle
drugs that interact with ACh/ACh receptors and how/what they are used for:
Botulinum toxin
- give informal name
- function
- how
-BOTOX
Botulinum toxin = flaccid paralysis/muscle spasm treatment:
stops ACh release (from vesicles?), muscles not able to contract as ACh not able to bind to ligand gated ion channels so no Na+ influx in postsyn. neurone, so no depolarisation/APs/muscle stimulation
injected locally = muscle spasm treatment (no voluntary OR involuntary control/movement of muscle SO muscle does not move at all
explain excitation-contraction coupling:
(T-tubule system)
- AP in T-tubule (invag. of sarcolemma)
- T-tubule in direct contact with SR (sarcoplasmic reticulum) which surrounds myofibrils
- voltage sensitive channels in SR membrane are coupled to ryanodine receptors (RR)
- RR = type of Ca2+ channel in membrane of SR
- upon depolarisation , voltage sensitive channels change conformation = open RR
- Ca2+ released
- Ca2+ induces more Ca2+ release
- Ca2+ pumped back into SR
what’s an/the other outcome of muscle contraction, other than force generation? (byproduct)
- is this beneficial or not (to animal)
HEAT - can be beneficial or deleterious to animal
muscle contraction - an example of when heat as a byproduct of of muscle contraction is negative:
name ONLY
malignant hypERthermia
muscle contraction - an example of when heat as a byproduct of of muscle contraction is negative:
MALIGNANT HYPERTHERMIA
- what is it (and what species)
- due to?
- explain what happens
- genetic disorder pigs/humans/horses
- usually due to mutation in RR (ryanodine receptors)
- certain gaseous anaesthesia
= XS Ca2+ release
= massive muscle contraction and release of heat
= can cause death
receptors in muscle - they may monitor: (2)
- length (stretch)
- tension
