Nerve and Muscle Flashcards
what do each of the cells do multipolar unipolar bipolar neurogllia astrocytes oligodendrocytes microglia ependyma
motor neurones, can be pyramidal or stellate
PNS - in sensory ganglia cell body attached at the side
retinal - found in sensory structures
glial cells - considered supporting cells for neurones
involved in metabolic exchange between neurones and blood
militate the axon
less common immune defence
lining cells for ventricles have cilia on lumen
difference between dendrites axons and neuritis
neuritis are dendrites and axons
dendrites are shorter and thicker giving rise to small spins
axons are long and thin usually only one axon
difference between nerves and ganglia
nerves are axons and ganglia are cell bodies
what are nerves made up of
bundles (fascicles) of myelinated and non-myelinated axons plus blood vessels and shwwan cells
what are the two types of ganglia
sensory and autonomic (efferent neurones from ANS)
what is the structure of a peripheral nerve
epineurim - covers whole nerve
perineurium - covers whole fascicle
endoneruim covers individual nerve axons
what do satellite and schwaan cells do
satellite - surround nerve body and may aid in controlling chemical envirmoent of neurones
schwaan cells for myelin sheath around large nerve fibres and are phagocytic
what is the difference between oligodendrocytes and schwaan cells
oligo - myelin sheath in CNS (around several axons)
Schwaan cells - myelin sheath in PNS (one single axon)
difference between somatic and autonomic
somatic - voluntary
auto - involuntary - heart beat, lungs, BP etc
autonomic is split into what
sympathetic and parasympathetic
what is the difference in structure and neurotransmitter between pre ganglionic and postganlionic
Preganglionic fibres long, myelinated (p.) short, myelinated (s.)
Postganglionic fibres short, few branches (p.) long, many branches (s.)
Location of ganglia near/in target tissue (p.) close to spinal cord (s.)
Preganglionic transmitter Ach (p.) Ach (s.)
Postganglionic transmitter Ach (p.) Noradrenaline (s.)
When active rest, sleep (p.) stress, exercise (s.)
Physiological effect slow things down (p.) speed things up (s.)
what are the classifications of nerve fibres
it is based on nerve fibre diameter and conductance 1st class is A (fastest) B and C - motor fibres and some non-muscle sensory 2nd class = I (fastest), II, III, IV
what are non myelinated sensory fibres referred to as
C fibres
what do proprioreceptors do
concerned with position of muscles tendons and joints
what are the 4 receptors endings
free endings - connective tissues/ muscle/ skin - slow or fats adapting - pain, touch, light, pressure
Pacinian corpuscle = deep dermis/tendons/joints/genitalia, vibration/deep pressure, fast adapting
Meissner’s or krause’s bulbs = oral mucosa/lips/genitalia/fingertips, touch/vibration/light pressure, rapid adapting
Ruffini organs = deep dermis/ligaments/joint capsules, stretch/deep pressure, very slow adapting
what is a simple spinal reflex pathway
- Sensory receptor = site of stimulus action
- Sensory neurone = transmits afferent info to the CNS
- Integration centre = one or more synapses within CNS (may also signal up to brain)
- Motor neurone = conducts efferent impulses to effector organ
- Effector = muscle fibre (or gland) that responds to impulses
what is the role of proteins on the resting potential
large negatively charged proteins can’t exit the cell and help maintain a -65 mV resting potential
what is the definition of the nerviest equation and what is it used for
cell resting membrane potential close to but not equal to K+ equilibrium potential, also small leak for Na+, equation determining equilibrium potential for any ion, determined using conc. of ion inside/outside and cell temp.
what are the 4 phases of an action potential
Phase 1 = Na+ channels open, Na+ enters nerve cell, membrane potential rises towards 0
Phase 2 = if threshold potential reached, voltage gated Na+ channels open, cell depolarises, Na+ ions flow into cell, action potential spike results
Phase 3 = Na+ channels close when Na+ equilibrium potential reached, voltage gated K+ channels open and K+ ions flow out of cell, membrane potential reverses
Phase 4 = K+ ions continue to flow out of cell while Na+ channels closed, hyperpolarisation results for brief period before normal resting potential restored, during this period (refractory period) another action potential cannot be generated, so action potentials only travel one way
what are the benefits of the refectory period
no further action potentials can be elicited, ensures action potential propagation is unidirectional, action potential can only travel along axon from cell body to terminal, during relative refractory period, larger stimulus can result in action potential
what is sensory transduction
conversion of environmental or internal signals into electrochemical energy
receptors in muscles are varied what are they
sensory, proprioceptors and mechanoreceptors
how and where are muscle spindle fibres stimulated
located within muscle and stimulated when muscle passively stretched, bundle of modified skeletal muscle fibres enclosed in connective tissue capsule
what is the golgi tendon organ
located in tendon and responds to tension (stimulated when associated muscle contracts), small bundles of tendon (collagen) fibres enclosed in layered capsule with terminal branches of large diameter afferent fibre intertwined with collagen bundles, active during passive stretch and active contraction, tension director that protects muscle against excess load
how does the spindle protect the muscle
When muscle is stretched passively the spindle is activated and initiates a reflex, when muscle contracts and shortens it is switched off, protects muscle being overstretched
describe the knee jerk pathway
monosynaptic stretch reflex, stretching of muscle stretches spindle resulting in increased discharge of sensory nerves, results in increased firing of motoneuron, muscle contracts, no spinal interneuron is involved, effect is to dampen stretch of the muscle, specific for muscle stretched
what are the differences in chemical vs electrical transmission
Electrical = more common in invertebrate nervous system, do occur in human brain and involved in epileptiform activity, formed by interlocking connexon channels of adjacent neurones, connexons comprise connexin proteins, present at points of contact between neurones with no synaptic cleft, only very narrow gap, direct, very fast electrical transmission, unidirectional in mammalian CNS but bidirectional in invertebrates Chemical = interface for chemical communication between neurones, release of transmitter from synaptic vesicles on arrival of an action potential in the terminal bouton of neuronal axon
what are the structural differences between ionotrophic and metabotrophic
ionotrophic receptor = cluster of similar subunits forming ion channels, that depolarise or hyperpolarise the postsynaptic cell (fast responses),
metabotrophic receptors = 7-transmembrane molecule coupled to intracellular proteins that transduce a signal to cell interior (slow responses)
what is a neuromuscular junction
synapse between a motor neurone and skeletal muscle fibres
where are neurotransmitter receptors concentrated
in post junctional folds
what neurotransmitter is released at NMJ
ACh
in a NMJ which receptors does ACh bind to
nicotinic receptors
where is AChE found
in the cleft and attached to the basal lamina
what happens to ACh after it is broken down
into acetate and choline
choline reabsorbed to pre synapse
acetate binds with CoA to for acetyl c A which then reacts with choline to make more ACh
what causes the concentrated vesicles full of ACh in the cell
Antiporter H+ / ACh - into vesicle
how are vesicles reserved and blocked
Reserve vesicles anchored near active zone by synapsin that tethers them to actin filaments
Docking of vesicles, v-snare protein on vesicle binds to t-snare on membrane at active zone
how is choline taken up
Na + co transporter
what are synaptic vesicle pools
multiple, readily releasable, undergo exocytosis in response to single action potential as have been primed by docking at active zone, recycled synaptic vesicle pool, reserve pool ensures neurotransmitter is available even for highest physiological demands
what does Curare do
comes from plants found in s. America, tribes used it to hunt and kill animals, causes muscle paralysis, so animals die from asphyxiation, If create artificial respiration for around 2 hours can recover
what does tubocurarine do
non-depolarising competitive nAChR antagonist, competes with ACh for nicotinic receptor binding sites, muscle paralysis occurs gradually, reversed by AChE inhibitors, as ACh is around for longer so eventually outcompetes, hydrolysed by circulating esterases, therapeutic use in surgery, adverse effects are decreased DP and bronchospasm
what does succinylcholine do
depolarising nAChR agonist, persistent depolarisation of NMJ, phase 1 = membrane depolarised causing brief period of muscle twitching as fibres firing off all of a sudden, phase 2 = end plate eventually repolarises, but as drug not metabolised as rapidly as ACh it continues to occupy receptor, causes flaccid paralysis, hydrolysed by circulating esterases, therapeutic use in surgery given continuously, adverse effects in halothane susceptible people experience malignant hyperthermia
what does neostigtme/edrophonium do
cholinesterase inhibitors, therapeutic use as antidote for non-polarising blockers e.g. tubocurarine, treatment for and diagnosis of myasthenia gravis, adverse effects are generalised cholinergic activation (muscarinic and nicotinic), abdominal cramping, diarrhoea, salivation, incontinence, other uses nerve gas as weapon of war
what does sarin do
liquid and gas, inhibits AChE, highly toxic and volatile agent, can linger on clothes so spread easily, causes muscle convulsive contractions, nose and eyes watering, drooling, nausea, vomiting, constriction of pupils to pinpoints, loss of control of bladder and bowel, chest pain, shortness of breath, collapse, seizures, death end result due to asphyxia
what are tetanus and botulin toxins
reduce probability of neurotransmitter release by preventing vesicles binding to pre-synaptic membrane
what does tetrodoxin do
binds to Na+ channel to block activation
what is lambert-eaton syndrome
Reduced ACh release as autoantibodies stop Ca influx
associated with lung cancer
cancer symptoms, abnormal reflexes, lack of saliva
doesn’t usually affect respiratory/face/eyes
diagnosed with electromyography and test for antibodies
treatment - immunosuppressants or amifampridine - blocks K so action potential duration is bigger
what does these types of muscle mean pennate fusiform parallel convergent circular skeletal cardiac smooth
feather like arrangement, unipennate (hands), bipennate (legs/thighs), multipennate (shoulders)
spindle shaped
fascicles lie parallel to axis of muscle, flat muscles (often have aponeuroses)
broad attachment from which fascicles converge to a single tendon
surround body opening/orifice, constricting when contracted
striated, multinucleated, voluntary, non-branching, attached to skeleton
striated, single nucleus, involuntary, branched, heart muscle
non-striated, single nucleus, involuntary (stimulus), tapered, forms walls of organs
what is the basic muscle structure
sarcolemma inside of is sarcoplasm, which surrounds myofibril, which contains filaments made up of actin and myosin
what is the difference between actin and myosin
Actin = major component of I-band, extend into A-band Myosin = bipolar, extend throughout A-band, major component of H-zone, crosslinked at centre by M-band
what do these refer to Z line I band A band H zone M line Titin
disc between I-bands appears as series of dark lines
Surrounds Z line zone of thin filaments not superimposed bu thick filaments - ie only actin present
a band - section contain whole of myosin
H zone - within A band, paler region, zone of thick filaments (myosin only)
M line - inside H zone middle of sarcomere - formed of cross connecting elements
connecting protein extends from Z line which binds to actin and M band which interacts with myosin
what is the mechanism of muscle contraction
Troponin complex moves tropomyosin
This exposes myosin-binding sites on actin
Unblocking the binding sites
1. Action potential arrives at NMJ
2. ACh is released, binds to receptors, opens Na+ channels leading to action potential in sarcolemma
3. Action potential travels along T-tubule
4. Ca2+ released from sarcoplasmic reticulum
5. Ca2+ binds to TnC region of troponin
6. Troponin changes shape, moves tropomyosin, exposing binding site on actin filament
7. Myosin head with ADP + Pi binds actin and attaches
8. Myosin head bends, pulling along actin filament, ADP + Pi released during power stroke
what happens to the bands in contraction of muscle
ATP and Ca2+, A-band remains unchanged, H-zone gets shorter, distance between Z-lines gets shorter
what are isotonic contractions
causes muscle to change length as it contracts
what is the differences between
concentric
eccentric
isometric
muscle shortens
muscle lengthens as it contracts such as a slow relation rep at the end of a set
no change in length as the muscle contracts
what are the stages of a muscle twitch
1 = latent period, delay of a few milliseconds between action potential and start of contraction, reflects time for excitation-contraction coupling 2 = contraction phase, starts at end of latent period and ends when muscle tension peaks, cytosolic calcium levels increasing as released calcium exceeds uptake 3 = relaxation phase, time between peak tension and end of contraction, when tension returns to 0, cytosolic calcium is decreasing as reuptake exceeds release
what is the difference between fast twitch and slow twitch
fast twitch - type II fibres, white, lots of mitochondria, myoglobin less dense, contract quickly and powerfully, fatigues easily
slow twitch
red as lots of myoglobin, dense capillaries, contract slowly but little force, very resistant to fatigue, large amounts mitochondria, produces low amount of power, used in aerobic activities e.g. long distance running
difference between type IIb and IIa
Type IIa = red as lots of myoglobin, resistant to fatigue, contains large amounts mitochondria, contracts relatively quickly, produces moderate amount of power when contracted, used in long-term anaerobic activities e.g. swimming, fast twitch A fibres
Type IIb = white as low myoglobin, fatigue very easily, contains low amounts mitochondria, contracts very quickly, produces high amount of power when contracted, used in short-term anaerobic activities e.g. sprinting and heavy lifting, fast twitch B fibres
what does the force of muscle contraction rely on
the number of action potentials per second
what happens when the muscle is stretched beyond the amount normal
number of cross bridges decreases as overlap between filaments decreases
what are some examples of injury or oversuse of muscles
sprain/cramps/strain/tendinitis
what is a genetic muscular disease
muscular dystrophy, more difficult to treat and diagnose, testing will happen and family history taken
what are some neurological muscular disorders
multiple sclerosis/myasthenia gravis/Parkinson’s disease, as muscles require action potentials, can cause many issues
what is myositis/polymyalgia rheumatica
short/long term condition, consequence of autoimmune condition (myositis), self-limiting treated with medication
describe the structure of cardiac muscle
Striated with characteristic A and I bands, contains actin and myosin filaments in myofibrils
Branched, interconnected, small
Rich in myoglobin and mitochondria
Forms thick layer in the heart called myocardium
Each cell contains 1-2 centrally located nuclei
Mitochondria comprise 30% of volume of cell, require lots of energy
what do intercalated discs do
specialised cell-cell contacts, cell membranes interlock, function for mechanical coupling (desmosomes – macula adherens – which hold cells together to stop separation during contraction) (and fascia adherens – actin anchoring sites connect to closest sarcomere) and electrical coupling (gap junctions allow action potentials to spread quickly to adjoining cells, permit passage of ions between cells allowing depolarisation
what are the phases of ventricular action potential
Phase 0 = cell depolarisation, greatly increased membrane permeability to Na+ ions, rush in through fast channels, down conc. gradient reversing cell polarity
Phase 1 = partial repolarisation, loss of Na+ conductance and decrease in K+ conductance
Phase 2 = plateau, due to slow inward flow of Ca2+ ions through slow channels, also some inward movement of Na+ through slow channels and a decrease in membrane K+ conductance
Phase 3 = repolarisation, decreased Ca2+ conductance and increased K+ conductance, inside of cell again becomes negative relative to outside, Na+/K+ pump re-establishes distribution of ions
Phase 4 = interval between action potentials when the ventricular muscles are at their stable resting membrane potential
Long refractory period, no summation as refractory period lasts as long as twitch, so prevents tetanus
what happens during complete heart block
no transmission through AV node, Purkinje fibres take over pacemaker, slower pacemaker activity in distal parts of conducting system allow heart to continue breating if SA node fails, patients have bradycardia and reduced cardiac output
what is wolf parkinson white
disorder of conduction of the heart, pre-excitation syndrome, caused by presence of abnormal accessory electrical conduction pathway between atria and ventricles, electrical signals travel down abnormal pathway (bundle of Kent) may stimulate ventricles to contract prematurely, resulting in unique type of supraventricular tachycardia referred to as AV reciprocating tachycardia
what are the 4 classes of anti arrhythmic agents and give examples
Class 1 = sodium channel blockers, treat ventricular ectopics
Class 2 = beta blockers (block effects of catecholamines in beta1-adrenergic receptors, decreasing sympathetic activity on the heart), slow conduction in the SA and AV nodes
Class 3 = potassium channel blockers, treat ventricular tachycardia and atrial fibrillation
Class 4 = calcium channel blockers, slow conduction in the SA and AV nodes, shorten plateau of action potential but allow body to retain adrenergic control of heart rate and contractility
what does digoxin do
foxglove plant digitalis, inhibits Na+/K+ ATPase pump, increases intracellular Na+ causing less Ca2+ to be secreted, so intracellular Ca2+ conc. remains high, used to treat heart failure, causes decrease in heart rate, increased force of contraction as there is more release of Ca2+ from the SR so another increase in release of Ca2+ during each action potential
describe the process of excitation contraction curling in the heart
Ca2+ enters through voltage-gated L-type Ca2+ channels in T-tubule membrane
Triggers further Ca2+ release from adjacent sarcoplasmic reticulum
Each L-type channel controls only one SR release channel, so tight local control
Ca2+ binds to troponin-C and contraction proceeds
After contraction, relaxation occurs when Ca2+ unbinds from troponin
Ca2+ pumped back into SR for storage
Ca2+ exchanged with Na+ at the membrane
Na+ gradient maintained by Na+/K+ ATPase
how does noradrenaline affect excitation contraction coupling in the heart
Noradrenaline increases contractile force of the heart, acts through beta-type adrenergic receptor to increase cAMP, to activate PKA which phosphorylates L-type channel increasing passive Ca2+ influx
Amplifies Ca2+ (calcium-induced calcium release)
what regulates heart and force of contraction
ACh from parasympathetic acts on SA from vagus nerve and decreases HR
NA from symp nerves increases rate of pacemaker cells
what is the structure of smooth muscle
2 sheets - one circular and one longitudinal more actin than myosin no troponin no sarcomeres no striations no t tubules or SR have caveolae - act like T tubules actin attached to dense bodies
what is the mechanism of action of contraction of smooth muscle
Ca2+ binds to calmodulin, interacts with enzyme myosin kinase to phosphorylate myosin
Once phosphorylated generates tension
Cytoplasmic Ca2+ falls, Ca2+ calmodulin complex dissociates, inactivating myosin kinase
Cross bridges dephosphorylated by enzyme myosin phosphatase
which type of muscle can stay contracted for longer
smooth muscle
Reduced ATP consumption, so takes long time for each cross bridge to detach from actin
Rate of Ca2+ removal from cytoplasm is slow, so prolonging duration of contraction
what is the difference between single unit and multi unit smooth muscle
Single unit = most common, gap junctions, located in GI, respiratory, urinary and reproductive tracts, in walls of small arteries, electrical activity may arise spontaneously due to presence of pacemaker cells, action potentials developed, nervous regulation via ANS, contract in response to stretch
lack gap junctions so cells innervated individually, allows fine control, examples include ciliary muscle of the eye, controlling size of pupil and piloerector muscles of hair follicles, not spontaneously active, innervation autonomic, no inherent response to stretch, contractions slow and sustained
what is dilated cardiomyopathy
enlarged heart - sudden death poor function
weak muscles, short breath, heart failure
can be due to viral infection, autoimmune, exposure t toxic compound
what is hypertrophic cardiomyopathy
thickening of muscle due to athetoid performance
myocardial disarray
can have genetic causes
common in young adults
what is leiomyoma
fibroids of smooth muscle
heavy uterine bleeding
unknown genetic cause more common in afro-carribean race
