Flashcards
Action potentials and muscles

Cards in this deck (64)
- 1What does the nervous system do?Regulates the major organs
e.g. heart, lungs, vasculature, skeleted muscle
-Pharmacological interference with this mode of regulation can be medically useful - 2What are the classifications of the nervous system?

- 3What is the resting membrane potential?-all living cells exhibit a RMP
-The RMP is established by ion channels and ion pumps
-its at -70mV
- 4What happens when excitable cells such as neurons and muscle/glands can alter the ion permeability of their membranes?can result in action potentials that travel along the neuron and transmit a signal
-the propagation of action potentials is how the nervous system signals over long distances - 5What are action potentials?it is the change in electrical potential that occurs across a cell membrane during the passage of a nerve signal
-a localised and transient switch in electrical potential across the plasma membrane [approx. -60mV or -70mV to +45mV] - 6What happens during an action potential?A cycle of membrane depolarisation, repolarisation, hyperpolarisation and return to the resting value
-lasts 1-2ms
-can be generated hundreds of times per second
- 7What causes an action potential?Electrical changes are due to voltage-gated Na+ and K+ channels that open and shut in response to changes in the membrane potential
-Once a threshold potential is attained the cell responds with an all-or-nothing depolarisation
-The cell responds in its own characteristic manner, irrespective of the magnitude of the stimulus
-Once it is initiated it will spread along the axon and will NOT decreases in amplitude - 8What are the five steps involved in action potential formation?1. Resting membrane potential
2. Depolarisation
3. Repolarisation
4. Hyperpolarisation
5. Return to resting membrane potential
- 9What causes resting membrane potential?-All voltage-gated Na+ channels are closed
-All voltage K+ channels are open
-All voltage-gated K+ channels are closed
- 10What causes Depolarisation?-A stimulus increases the membrane potential to a less negative value
-At a critical threshold potential, Depolarisation activates voltage-gated Na+ channels
-Changes in the conformation of these voltage-gated channels allow fast influx of Na+ into the cells
- 11What are the two driving forces (acting in the same direction) that cause depolarisation?1. Na+ concentration gradient (low Na+ in IC)
2. Resting membrane potential (negative IC) - 12What happens during depolarisation?The permeability of the stimulated membrane region becomes vastly greater for Na+ than for K+
-Thus the negative state inside the cell is reversed and the membrane potential reaches positive values
- 13What causes repolarisation?-Na+ channels become inactivated, so further net inward movement of Na+ ceases
-Delayed, voltage-gated K+ channels open, which repolarises the membrane (positive charge moves out)
- 14What causes Hyperpolarisation?-Before the efflux of K+ returns to resting level due to the inactivation of the voltage-gated K+ channels, a hyperpolarisation is observed

- 15What causes the return to resting potential?-The number of ions that move to cause the large changes in action potentials is small (1 in 100,000)
-Thus only small changes in total intracellular concentrations are produced
-Ionic concentration gradients are re-established by Na+-K+ ATPase
- 16Summary of the components of action potentials

- 17What are action potential thresholds?-Not all stimuli cause sufficient depolarisation to generate an action potential
-threshold is typically a stimulus of +15mV
-Stimuli above threshold result in sufficient opening of Na+ channels so that the movement of Na+ IC exceeds movement of K+ EC
-Above threshold stimuli initiate a positive feedback cycle
-The amplitude of the action potential is all or nothing
-dependent on initiating the positive feedback cycle not the stimulus strength
-Subthreshold stimuli fail to activate the positive feedback cycle
- 18How are action potential thresholds all or nothing?

- 19Where do refractory states develop?At a membrane site which has just fired an action potential

- 20What is the absolute refractory period?Nerve or muscle membrane can not be excited even by the strongest stimulus
- 21What is the relative refractory period?Nerve or muscle membrane can be excited only by a stimulus greater than the initial threshold stimulus
- 22What effect does refractory period have on AP direction?can only travel in the direction away from the neuronal cell body

- 23What causes the refractory periods?

- 24What are the two major ion channels in action potential formation?1. Voltage-gated e.g. voltage gated Na+ and K+ channels (AP) (open upon voltage change)
2. Ligand-gated e.g. nicotinic Ach receptor, glutamate receptors (open upon ligand-binding; ionotropic receptors) - 25How do the ion channels work in action potential formation?-Ion channels regulate the flux of ions across membranes by gating (open/closed) the channel pore
-Ion channels influence the rate, not the direction, of ion flow across membrane
-The rate and direction of ion flow, depend on both the concentration and electrical gradients across the membrane
-Pore size and charge interactions determine the ion selectivity of channels - 26What pharmacological agents act on ion channels?a) As drugs
e.g. Na+ channel blockers as local anesthetics
b) As research tools
-neurotoxins to characterise the pharmacological, electrophysiological and biochemical properties of ion channels
e.g. TTX (tetrodotoxin) to abolish Na+ current
- 27What are the sites of drug action at voltage-gated Na+ channels?

- 28How is an action potential signal transmitted?1) from neuron to neuron (synapse)
2) from neuron to muscle/gland - 29What are the two types of synaptic transmission?1. Electrical (minority)
2. Chemical (majority) - 30What can information be transmitted from to?1. Neuron to Neuron
2. Neuron to Muscle - 31How does neurotransmission work in the neuron?

- 32What are electrical synapse?-Direct flow of current from the presynaptic to the postsynaptic neuron through gap junctions
-Allows for rapid and synchronous firing of interconnected cells - 33What are chemical synapse?-Release of transmitter from presynaptic membrane, diffusion across synaptic cleft and bind to postsynaptic receptors
-Allows for amplification of the synaptic response, i.e. a single AP releases thousands of neurotransmitter molecules - 34Electrical synapse vs Chemical synapse

- 35What happens at chemical transmission?-At chemical synapses the pre- and postsynaptic elements are separated by a synaptic cleft
-Chemical synaptic transmission involves a delay between action potentials in the pre- and post synaptic cells
- 36What are the two processes of chemical transmission?1) The presynaptic transmitting process
2) The postsynaptic receptive process - 37What happens during the presynaptic transmitting process?

- 38What happens during the postsynaptic receptive process?

- 39What is the summary of chemical transmissions?

- 40What small molecules can serve as transmitters?-Ach (acetylcholine)
-GABA (y-aminobutyric acid)
-Glycine
-Glutamate
-Serotonin
-Dopamine
-Noradrenaline (norepinephrine)
- 41What does the action of a specific NT depend on?the properties of the receptors with which it binds e.g. ACh excites certain postsynaptic cells, while inhibiting others
-ACh produces synaptic excitation at nicotinic ACh receptors at the neuromuscular junction
-ACh slows heart at inhibitory muscarinic ACh receptors - 42What are the two possibilities when neurotransmitters bind with postsynaptic receptors?i) opens postsynaptic ion channels (Na+, K+) resulting in depolarisation
-excitatory postsynaptic potential (EPSP) (not an action potential)
ii) opens postsynaptic ion channels (K+, Cl-) resulting in hyperpolarisation
-inhibitory postsynaptic potential (IPSP)
- 43What do EPSP do in synaptic transmission?

- 44What do IPSP do in synaptic transmission?

- 45How do Chemical/Neurotransmitter receptors work?-Neurotransmitter receptors are membrane-spanning proteins
-The receptor region exposed to the external environment of the cell recognizes and binds the neurotransmitter released from the presynaptic cell
- 46What is the pharmacology at chemical synapses?

- 47What is Muscle?Muscle is an important regulator of many physiological systems
e.g. skeletal, heart, vasculature, respiratory tracts
-Thus it is a major target of drug action - 48What are the three types of muscles?1. Skeletal (supports and moves skeleton)
2. Cardiac (muscle of heart)
3. Smooth (surrounds intestinal, respiratory, blood vessel tracts, etc) - 49What is the structure of skeletal muscle?-The largest mass of somatic musculature
-Most attached to bone (by tendons)
-Responsible for movement and skeletal support
-Contraction is usually voluntary
-Muscle fibre (myocyte)- cylindrical, multinucleated muscle cell (80micrometers diameter, 20cm length
-Composed individual mononuclear cells (myoblasts) fuse together
-Arranged in parallel between tendons
-Surrounded by a cell membrane (sarcolemma)
-Muscle fibres bundle together to produce a muscle fascicle
-A group of fascicles form a muscle
- 50How is skeletal muscle excited?-The skeletal neuromuscular junction (NMJ)
-Junction between somatic neuron and skeletal muscle (motor end plate)
-Specialised sunapse
-Usually located in middle of muscle fibre
- 51How does the skeletal NMJ work?

- 52How does skeletal muscle organised?-Skeletal muscle fibres are straited
-Bundles of filaments called myofibrils run along axis of the cell
-A serries of perpendicular light and dark bands
-Due to an arrangement of thick and thin filaments in the cytoplasm
-Repeated to form the basic contractile unit (sarcomere).
- 53What does skeletal muscle look like (histology)?-Thick filaments: composed of the contractile protein myosin
-Thin filaments: contain proteins actin, troponin and tropomyosin
- 54How does skeletal muscle contract?-AP opens Na+ channels, propagates rapidly
-T-tubules connect plasma membrane and sarcoplasmic (SR)
-T-tubule contains dihydropyridine receptor (DHPR) (L-type Ca2+ channel)
-upon depolarisation DHPR activates Ryanodine Receptor (RyR) in SR
-release of Ca 2+ from SR into cytoplasm
-troponin/tropomyosin blocks actin-myosin interaction
-Ca 2+ binding to troponin release this block
-Actin-myosin bind ->contraction
- 55What is the diagram showing NMJ and muscle contraction fully?

- 56What is the sliding filament theory?-the way in which skeletal muscle contraction occurs upon binding of Ca2+ to troponin
- 57What is the structure of Cardiac muscle?-The walls of the heart (myocardium) are composed of cardiac muscle cells
-The cells (cardiomyocytes) are tightly-bound and arranged in layers surrounding the heart chambers
-Contraction enables blood to pump
-Cardiac muscle are striated
-Sarcomeres contains thick myosin and thin actin filaments
-Short (2 micrometers) cells with branching processes
-Separated from neighbouring cells by intercalated discs
- 58How does excitation of cardiac muscle work of a single unit?-A stimulus applied to any one part of the myocardium induces a wave of depolarisation, causing the entire myocardium to contract
-Gap junctions present in the intercalated discs allow this spread of excitation between adjacent cells
- 59How does cardiac tissue display automaticity?-displays automaticity (ability to initiate its own beat) and rhythmicity (regularity of activity)- does not require innervation
-Initial Spontaneous depolarisation occurs in specialised cardiac nodes (sinoatrial node) which act as the pacemaker= generates pacemaker potential due to spontaneous reduction in K+ permeability
-Action potential spreads through myocardial cells via gap junctions
-Pacemaker potential can be modulated by sympathetic and parasympathetic (autonomic) stimulation - 60How does the cardiac muscle contract?-AP dependent on voltage-gated Na+ and Ca 2+ channels
-No direct coupling between plasma membrane and SR
-Voltage-gated Ca2+ channels in plasma membrane open during repolarisation plataeu
-Ca2+ entry activates Ryanodine Receptors (RyR) in SR
-Release of Ca 2+ from SR into cytoplasm (positive feedback)
-Ca2+ binding to troponin releases block
-Actin-myosin bind ->contraction
- 61What is the structure of smooth muscle?-Major component of the airways, vasculature, digestive tract, urogenital tract,..
-Mononuclear, spindle-shaped cells (1-2 micrometers diameter)
-Smooth muscle cells are non-striated
-Actin and myosin are present, but not arranged in regular arrays (sarcomeres)
-Actin-containing filaments anchored to the cell membrane or dense bodies within the cytoplasm
- 62What controls smooth muscle contractions?-Innervated by sympathetic and parasympathetic (autonomic) stimulation
-Involuntary
-Do not have specialised motor end-plate region
-Autonomic neurons divide into varicosities filled with neurotransmitters
-Can act as a multi unit (multiple varicosities) or act as a single unit (one line of varicosities and gap junctions)
- 63What do neurotransmitters do?-can be excitatory (contract) or inhibitory (relax)
-Some smooth muscles have spontaneous pacemaker potentials- enable normal contraction without innervation
- 64How does smooth muscle contract?-AP not required (those present depend on voltage-gated Ca 2+ channels
-No direct coupling between plasma membrane and SR
-Ca 2+ enters by
>voltage-gated channels (AP)
>ligand-gated cation channels (transmitters e.g. P2XR and ATP)
>G-protein activation of IP3, activating IP3 receptors/channels on ER
-Elevated [Ca2+] binds calmodulin (CaM)
-Ca2+-CaM activates myosin light chain kinase (MLCK)
-MLCK phosphorylates myosin
-Actin-Myosin bind ->contraction
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- University Pharmacology Flashcards on Action potentials and muscles, created by Adrianna Bialecka on 19/02/2025.
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- Adrianna Bialecka
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