Synaptic Transmission & Muscle Physiology Flashcards

1
Q

Differentiate between a chemical and electrical synapse.

A

Synapse: functional connection between neuron and a second cell
Electrical Synapse: action potential is passed directly from one cell to the next via connections known as gap junctions
Chemical Synapse: release of neurotransmitters from the presynaptic cell, which bind to receptors on the postsynaptic cell; action potential

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2
Q

Identify different neuronal connections including: axodendritic, axosomatic, and axoaxonis.

A

Axodendritic Synapse: a synaptic connection between the axon of one neuron and the dendrite of a second neuron
Axosomatic Synapse: a synaptic connection between the axon of one neuron and the cell body (soma) of a second neuron
Axoaxonic Synapse: a synaptic connection between the axon of one neuron and the axon of a second neuron

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3
Q

Identify components of the synapse including: neurotransmitters, pre-synaptic membrane, post-synaptic membrane, synaptic cleft, terminal bouton, synaptic vesicles.

A

Neurotransmitters: stored within synaptic vesicles located in the presynaptic axon terminals
Pre-synaptic Membrane: membrane with which synaptic vesicles fuse to allow for exocytosis of neurotransmitter into the synaptic cleft
Post-synaptic Membrane: membrane in which neurotransmitter receptors are found
Synaptic Cleft: space between the pre- and post-synaptic membrane
Terminal Bouton: name given to the presynaptic axon endings from which neurotransmitters are released
Synaptic Vesicles: storage vesicles for neurotransmitters

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4
Q

Describe electrical synapses and the role of gap junctions.

A

-electrical synapse involved direct conduction of action potential from one cell to the next via gap junctions
-cell membranes of the 2 neurons are very close together (2nm) allowing for channels formed by connexins to exist between them
-channels allow for movement of ions and molecules from one cell to the next

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5
Q

Describe the steps involved in chemical synapse nervous impulse transmission.

A

-chemical synapses are more prevalent than electrical synapses in the nervous system
-when an action potential reaches the terminal bouton; cascade, which leads to the exocytosis of neurotransmitter vesicles
-cross the synaptic cleft to bind to receptors on the postsynaptic cell
-causes specific ion channel to open and can lead to either excitatory postsynaptic potentials (EPSP) or inhibitory postsynaptic potentials (IPSP) in the postsynaptic cell

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6
Q

Discuss the roles of calcium, synaptogamin, calmodulin, synaptobrevin, syntaxin, SNARE complex in exocytosis of neurotransmitter vesicles.

A

Calcium: opened by the action potential reaching the terminal bouton; Ca2+ enters the cell and forms a complex synaptogamin
Synaptogamin: is the calcium sensory, and complexes with Ca2+; complex displaces components of the SNARE, or fusion, complex allowing for neurotransmitter release via exocytosis
Calmodulin: activated by calcium, calmodulin activates protein kinase that is responsible for phosphorylating other proteins involved in the cascade leading to exocytosis
Synaptobrevin: one of the SNARE proteins
Syntaxin: one of the SNARE proteins
SNARE Complex: responsible for holding docked vesicles to the presynaptic membrane to allow for exocytosis

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7
Q

Describe how neurotransmitters function on the post-synaptic membrane in conducting nerve impulses.

A

-neurotransmitters bind to specific receptor proteins on the postsynaptic membrane
-binding causes ion channels to open in the postsynaptic membrane
-opening of these channels produces are graded change in the membrane potential

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8
Q

Differentiate between voltage-gated and ligand gated ion channels.

A

Voltage-Gated: found primarily in the axon; open in response to depolarization
Ligand (chemically) Gated: found primarily in the postsynaptic membrane; open in response to the binding of ligands to receptors

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9
Q

Define graded potentials.

A

-change in the membrane potential (depolarization or hyperpolarization) with amplitudes that are varied, or graded, by gradations in the stimulus intensity
-stimuli for graded potentials in postsynaptic neurons are neurotransmitters, and the degree of depolarization or hyperpolarization produced depends on the amount of neurotransmitter released by the presynaptic axon

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10
Q

Differentiate between excitatory postsynaptic potential (EPSP) and inhibitory postsynaptic potential (IPSP).

A

EPSP: when Na+ or Ca2+ channels are opened in the postsynaptic membrane leading to a depolarization; cell becomes less negative; stimulate the cell to produce action potentials
IPSP: occurs when Cl- channels are opened in the postsynaptic membrane leading to a hyperpolarization; cell becomes more negative; inhibit the cell’s ability to produce action potentials

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11
Q

Identify the 4 major classes of neurotransmitters and identify key members of each family.

A
  1. Acetycholine: acetylcholine
  2. Bioamines: norepinephrine, epinephrine, dopamine, serotonin
  3. Amino Acids: gamma-amino butyric acid (GABA), glutamate, aspartate and histamine
  4. Neuropeptides: substance P, enkephalins, beta-endorphin and cholecystokinin
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12
Q

Differentiate between nicotinic and muscarinic acetylcholine receptors and identify where they are found in the body.

A

Nicotinic Receptors: found is specific regions of the brain; in autonomic ganglia and in skeletal muscle fibres
-activated by nicotine
Muscarinic Receptors: found in the plasma membrane of smooth muscle cells, cardiac muscle cells, and the cell of particular glands and in brain
-can be activated by muscarine

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13
Q

Define agonist and antagonist.

A

Agonist: drug that can bind to and thereby activate receptor proteins
Antagonist: drug that can bind to and thereby reduce the activity of receptor proteins

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14
Q

Describe the steps involved in G-protein receptor activation and cAMP secondary signal transduction.

A

G-protein Receptor Activation:
1. Membrane receptor doesn’t have neurotransmitter bound; alpha, beta, and gamma G-protein subunits are aggregated together and attached to the receptor; the alpha subunit binds GDP
2. When neurotransmitter binds to the receptor, the alpha subunit releases GDP and binds GTP; this allows the alpha subunit to dissociate from the complex
3. Either the alpha subunit or the beta-gamma complex moves through the membrane and binds to a membrane effector protein (ex. ion channel)
4. Deactivation of the effector protein is caused by the alpha subunit hydrolyzing GTP to GDP
5. Subunits then reaggregate and bind to the unstimulated receptor protein cAMP Secondary Signal Transduction
-when a neurotransmitter binds to its receptor, it stimulated the release of the alpha subunit from the G-protein complex
-alpha subunit then diffuses in the membrane until it binds to an enzyme known as adenylate cyclase
Adenylate Cyclase: converts ATP to cAMP and pyrophosphate
-cAMP activated protein kinase; ion channels are opened in the postsynaptic membrane

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15
Q

Discuss the fate of neurotransmitters secreted into the synaptic cleft including acetylcholinesterase and monoamine oxidase.

A

Acetylcholinesterase (AChE): enzyme on the postsynaptic membrane or immadiately outside the membrane
-hydrolyzes acetylcholine into acetate and choline, which prevents further activation of ACh receptors on the postsynaptic membrane
Monoamine Oxidase (MAO): degrades monoamines within axon terminal after they have been reuptaken from the synaptic cleft

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16
Q

Describe the catecholamine family of neurotransmitters.

A

Catecholamines are a family including dopamine, norepinephrine, and epinephrine. All derived from the amino acid tyrosine. A catechol refers to a common six-carbon ring structure.

17
Q

Define divergence, convergence, spatial summation, temporal summation in regards to synaptic integration.

A

Divergence: when one neuron makes synaptic connections with many neurons
Convergence: when a number of neurons make synaptic connection with one neuron
Spatial Summation: occurs due to the convergence of axon terminals from different presynaptic neurons on the dendrites and cell body of a postsynaptic neuron; allows EPSPs (or IPSPs) to summate at the axon hillock
Temporal Summation: rapid bursts of activity of a single presynaptic axon can cause corresponding bursts of neurotransmitter release resulting in successive waves of EPSPs (or IPSPs) that summate with each other as they travel to the initial segment of the axon

18
Q

Describe synaptic plasticity.

A

Synaptic Plasticity: ability of the synapses to change in response to activity

19
Q

Define agonist muscle, antagonistic muscle, flexion, extension, insertion, origin.

A

Agonist Muscle: prime mover of any skeletal movement
Antagonist Muscle: flexors or extensor muscles that act on the same joint to produce opposite reactions
Flexion: bending movement that decreases the angle at a joint
Extension: straightening movement that increases the angle at a joint
Insertion: more moveable attachment of the muscle to bone
Origin: less moveable attachment of muscle to bone

20
Q

Describe the anatomical organization of skeletal muscle: periosteum, tendon, fascia, epimysium, perimysium, fasciculus, endomysium, muscle fibre.

A

Periosteum: membrane that covers the outer surface of bones
Tendon: tough connective tissue used to connect muscles to bones
Fascia: connective tissue structure that surrounds muscles
Epimysium: fibrous connection tissue proteins within tendons extend around the muscle in an irregular arrangement; subdivides the muscles into columns
Perimysium: surrounds each of the fascicles; a connective tissue sheath
Fasciculus: grouping of muscle fibres
Endomysium: thin connective tissue layer, surrounds each muscle
Muscle Fibre (myofibre): skeletal muscle cell

21
Q

Describe the structure of skeletal muscle at the cellular level: sarcolemma, sarcoplasm, myofilaments, myofibrils, motor end-plate, T-tubule.

A

Sarcolemma: PM surrounding each muscle fibre
Sarcoplasm: the cytoplasm of striated muscle cells
Myofilaments: thick and thin filaments in a muscle fibre
Myofibrils: subunit of striated muscle fibre that consists of successive sarcomeres
Motor Endplate: specialized region of the sarcolemma of the muscle fibre at the neuromuscular junction
T-tubule: transverse tubules, narrow membranous tunnels formed from and continuous with the sarcolemma, separate sarcoplasmic reticulum

22
Q

Describe the structure of the sarcomere: Z disc, H zone, I band, A band, M line, thick filaments, thin filaments, actin, myosin, titan.

A

Z Disc: boundary of sarcomere
H Zone: region of the sarcomere containing only the thick filaments
I Band: extend from the edge of one stack of thick filaments to the edge of the next stack of thick filaments
A Band: extends the length of the thick filament
M Line: protein filaments in the middle of the A band that join thick filaments together
Thick Filaments: 110-angstrom filament composed of myosin
Thin Filaments: 50-60 angstrom filament composed of actin
Actin: structural protein of muscle, composing the thin filament
Myosin: protein that forms the A bands of striated muscle cells
Titan: largest protein of the human body, extends from a Z disc of a sarcomere to its M line

23
Q

Define syncytium.

A

Syncytium: fused mass of cells which shared continuous cytoplasm

24
Q

Identify the components of a motor unit.

A

Motor units consists of a somatic motor neuron and the muscle fibres it innervates.

25
Q

Discuss the sliding filament theory of contraction and identify specific steps.

A
  1. Myofibre, with all its myofibrils shortens by movement of the insertion toward the origin of the muscle
  2. Shortening of the myofibrils is caused by shortening of sarcomeres; distance between Z lines is reduced
  3. Shortening of sarcomeres is accomplished by sliding of myofilaments
    -length of each filament remains same during contraction
26
Q

Describe cross-bridge formation and the role of calcium, troponin, tropomyosin, ATP, actin, and myosin.

A

-sliding of filaments is produced by the action of numerous cross bridges
-cross bridges are part of the myosin proteins, extend towards the actin filament and terminate in a globular head
-reaction must occur before the myosin head can bind to actin
-ATP is hydrolyzed to ADP and Pi, the phosphate binds to the myosin head, leading to a change in conformation
-following binding to actin, the phosphate is lost and the cross bridge produces a power stroke
-to relax, ADP is released and is replaced by ATP
-before the cross bridge can form, binding sites must be exposed on actin; facilitated by calcium
-calcium entering the cell attaches to troponin, causing a conformational change that moves the troponin complex and its attached tropomyosin out of the way so that the cross bridges can attach to actin
-tropomyosin is a filamentous protein that winds along the actin filament and covers up the myosin binding sites

27
Q

Discuss excitation-contraction coupling.

A

Process by which action potentials cause contraction is termed excitation-contraction coupling.

28
Q

Identify the role of the sarcolemma, T-tubule system, and sarcoplasmic reticulum in excitation-contraction coupling.

A

Sarcolemma: contains nicotinic ACh receptors which are activated by motor neuron ACh release; Na+ channels are opened leading to depolarization and action potential production
Transverse T-tubule System: action potentials are conducted along the transverse tubules and calcium channels are opened
Sarcoplasmic Reticulum: calcium channels are opened and calcium leaves the sarcoplasmic and enters the sarcoplasm

29
Q

Identify the role of dihydropyridine and ryanodine receptors in excitation-contraction coupling.

A

DHP Receptors: voltage-gated calcium channels located in the transverse tubules that respond to depolarization
Ryanodine Receptors: calcium release channels in the sarcoplasmic reticulum that are opened via conformational changes in DHP receptors of the transverse tubules

30
Q

Discuss the fate of calcium during muscle relaxation.

A

-calcium release will continue until action potentials cease
-Ca2+-ATPase pumps, pump calcium back into the sarcoplasmic reticulum to sequester calcium from the cytoplasm

31
Q

Compare and contrast skeletal, cardiac, and smooth muscle in regards to: anatomical location, nervous control (voluntary VS involuntary), tissue structure and excitation-contraction coupling.

A

Skeletal Muscle: attached to bones, voluntary, contain striations, composed of longitudinal muscle fibres grouped into fascicles, ACh release, Na+ channels open, AP produces, Ca2+ channels open, contraction
Cardiac Muscle: heart, involuntary, contains striations, myocardial cells are short, branched and interconnected, joined to adjacent cells by gap junctions, slower than skeletal muscle, calcium-induced calcium release
Smooth Muscle: in organs (blood vessels, uterus), involuntary, not striated, contain actin and myosin but aren’t arranged into sarcomeres, less extensive sarcoplasmic reticulum, extracellular Ca2+ complexes with calmodulin, MLCK activation

32
Q

Describe calcium induced calcium release in cardiac muscle.

A

-in myocardial cells, voltage-gated Ca2+ channels in PM and Ca2+ release channels in sarcoplasmic reticulum don’t directly interact
-calcium that enters the cytoplasm through the voltage-gated channels in the transverse tubules stimulates opening of the Ca2+ release channels of the sarcoplasmic reticulum
-calcium serves as a second messenger from voltage-gated calcium channels to calcium release channels

33
Q

Describe the role of the pacemaker in cardiac muscle contraction.

A

Cardiac action potentials normally originate in a specialized group os cells called the pacemaker; therefore, cardiac muscle is able to produce action potentials automatically. However, rate of this spontaneous depolarization is regulated by autonomic innervations

34
Q

Discuss the role of calmodulin, myosin light-chain kinase and myosin phosphatase in smooth muscle cross-bridge formation.

A

-sarcoplasmic reticulum is less extensive in smooth muscle; therefore, sustained muscle contractions are produced in response to extracellular calcium that diffuses into the smooth muscle cells
-greater membrane depolarization leads to more calcium entering the cell
-calcium combines with calmodulin-calcium-calmodulin complex combines with and activates myosin light-chain kinase (causes the phosphorylation of myosin light chains), a component of myosin cross bridges
-phosphorylation is a regulatory event that allows binding to actin
-phosphorylation event can be reversed by myosin phosphatase, and this loss of phosphate inhibits cross bridge formation