Unit 9 Flashcards

1
Q

Differentiate between a chemical and electrical synapse

A

The synapse is a functional connection between a neuron and a second cell. In electrical synapses, the action potential is passed directly from one cell to the next via connections known as gap junctions. Chemical synapses involve the release of neurotransmitters from the presynaptic cell, which bind to receptors on the postsynaptic cell. This bind facilitates the production of a new action potential.

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2
Q

axodendritic

A

a synaptic connection between the axon of one neuron and the dendrite of a second neuron

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3
Q

axosomatic

A

a synaptic connection between the axon of one neuron and the cell body (soma) of a second neuron

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4
Q

axoaxonic

A

a synaptic connection between the axon of one neuron and the axon of a second neuron

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5
Q

Identify components of the synapse

A

Neurotransmitters: Neurotransmitters are stored within synaptic vesicles located in the presynaptic axon terminals.

Pre-synaptic membrane: The membrane with which synaptic vesicles fuse to allow for exocytosis of neurotransmitter into the synaptic cleft

Post-synaptic membrane: the membrane in which neurotransmitter receptors are found

Synaptic cleft: the space between the pre- and post-synaptic membranes

Terminal bouton: a name given to the presynaptic axon endings from which neurotransmitters are released

Synaptic vesicles: Storage vesicles for neurotransmitters

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6
Q

Describe electrical synapses and the role of gap junctions

A

The electric synapse involves direct conduction of action potential from one cell to the next. This is accomplished by gap junctions. The cell membranes of the two neurons are very close together (2 nm) allowing for channels formed by connexins to exist between them. These channels allow for movement of ions and molecules from one cell to the next.

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7
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, it sets about a cascade, which leads to the exocytosis of neurotransmitter vesicles. Once the neurotransmitters are released, the cross the synaptic cleft to bind to receptors on the postsynaptic cell. This 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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8
Q

calcium

A

Calcium channels are opened by the action potential reaching the terminal bouton. Calcium enters the cell and forms a complex with synaptotagmin.

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9
Q

synaptotagmin

A

Synaptotagmin is a calcium sensor and complexes with calcium. This complex then displaces components of the SNARE, or fusion, complex allowing for neurotransmitter release via exocytosis.

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10
Q

calmodulin

A

Activated by calcium, calmodulin activates protein kinase that is responsible for phosphorylating other proteins involved in the cascade leading to exocytosis.

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11
Q

synaptobrevin

A

one of the SNARE proteins

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12
Q

syntaxin

A

one of the SNARE proteins

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13
Q

SNARE complex

A

responsible for holding docked vesicles to the presynaptic membrane to allow for exocytosis

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14
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. This binding causes ion channels to open in the postsynaptic membrane. The opening of these channels produces are graded change in the membrane potential.

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15
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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16
Q

Define graded potentials

A

A change in the membrane potential (depolarization or hyperpolarization) with amplitudes that are varied, or graded, by gradations in the stimulus intensity. The 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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17
Q

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

A

membrane leading to a depolarization, and the cell becomes less negative. They stimulate the cell to produce action potentials.

IPSP: Occur when Cl- channels are opened in the postsynaptic membrane leading to a hyperpolarization, and the cell becomes more negative. They inhibit the cell’s ability to produce action potentials.

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18
Q

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

A

1) Acetylcholine: acetylcholine (ACh)
2) Bioamines: norepinephrine (NE), epinephrine, dopamine and serotonin
3) Amino acids: gamma-amino butyric acid (GABA), glutamate, aspartate and histamine
4) Neuropeptides: substance P, enkephalins, beta-endorphin and cholecystokinin (Course notes: Neurotransmitter action)

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19
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 fibers. Nicotinic receptors are named as such as they can be activated by nicotine.

Muscarinic receptors: Found in the plasma membrane of smooth muscle cells, cardiac muscle cells, and the cell of particular glands. They are also found in the brain. Muscarinic receptors are named as such as they can be activated by muscarine.

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20
Q

Define agonist and antagonist

A

Agonist: a drug that can bind to and thereby activate receptor proteins

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

21
Q

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

A

G-protein receptor activation

1) When the membrane receptor does not have neurotransmitter bound, the 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 (ie. Ion channel)
4) Deactivation of the effector protein is caused by the alpha subunit hydrolyzing GTP to GDP
5) The subunits then reaggregate and bind to the unstimulated receptor protein (Ch. 7.4)

cAMP secondary signal transduction

When a neurotransmitter binds to its receptor, it stimulates the release of the alpha subunit from the G-protein complex. This alpha subunit then diffuses in the membrane until it binds to an enzyme known as adenylate cyclase. This enzyme converts ATP to cAMP and pyrophosphate. Cyclic AMP in turn activates another enzyme, protein kinase, which phoshporylates other proteins. Through this action, ion channels are opened in the postsynaptic membrane

22
Q

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

A

Acetylcholinesterase (AChE) is an enzyme present on the postsynaptic membrane or immediately outside the membrane. AChE hydrolyzes acetylcholine into acetate and choline, which prevents further activation of ACh rececptors on the postsynaptic membrane. Monoamine oxidase (MAO) degrades monoamines (ie. Dopamine, norepinephrine, epinephrine and serotonin) within the axon terminal after they have been reuptaken from the synaptic cleft.

23
Q

Describe the catecholamine family of neurotransmitters

A

The catecholamines are a family including dopamine, norepinephrine, and epinephrine. They are all derived from the amino acid tyrosine. A catechol refers to a common six-carbon ring strucure.

24
Q

divergence

A

when one neuron makes synaptic connections with a number of neurons

25
Q

convergence

A

when a number of neurons make synaptic connection with one neuron

26
Q

spatial summation

A

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 (see figure 7.33, 13th edition)

27
Q

temporal summation

A

successively 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

28
Q

Describe synaptic plasticity

A

The ability of synapses to change in response to activity

29
Q

agonist muscle

A

the prime mover of any skeletal movement (ie. Flexor in flexion)

30
Q

antagonistic muscle

A

flexors or extensor muscles that act on the same joint to produce opposite actions

31
Q

flexion

A

A bending movement that decreases the angle at a joint

32
Q

extension

A

A straightening movement that increased the angle at a joint

33
Q

insertion

A

The more moveable attachment of the muscle to bone

34
Q

origin

A

The less moveable attachment of the muscle to bone

35
Q

Describe the anatomical organization of skeletal muscle

A

Periosteum: a membrane that covers the outer surface of bones

        Tendon: a tough connective tissue used to connect muscle to bones

        Fascia: a connective tissue structure that surrounds muscles

Epimysium: the fibrous connection tissue proteins within tendons extend around the muscle in an irregular arrangement; (epi = above; my = muscle) this sheath subdivides the muscle into column (fascicles)

Perimysium: surrounds each of the fascicles; a connective tissue sheath

Fasciculus: a grouping of muscle fibers

Endomysium: a thin connective tissue layer known as the endomysium surrounds each muscle fiber

Muscle fiber: also known as a myofiber, this is a skeletal muscle cell

36
Q

Describe the structure of skeletal muscle at the cellular level

A

Sarcolemma: a plasma membrane surrounding each muscle fiber

        Sarcoplasma: the cytoplasm of striated muscle cells

        Myofilaments: the thick and thin filaments in a muscle fiber

Myofibrils: a subunit of striated muscle fiber that consists of successive sarcomeres

Motor end-plate: the specialized region of the sarcolemma of the muscle fiber at the neuromuscular junction

T-tubule: transverse tubules, narrow membranous tunnels formed from and continuous with the sarcolemma; separate sarcoplasmic reticulum

37
Q

Describe the structure of the sarcomere

A

Z disc: also known as Z lines; the boundary of the sarcomere

        H zone: region of the sacromere containing only the thick filament

I band: extend from the edge of one stack of thin 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: a 110-angstrom filament composed of myosin

Thin filaments: a 50-60 angstrom filament composed of actin

Actin: a structural protein of muscle, composing the thin filament

Myosin: the protein that forms the A bands of striated muscle cells

Titan: the largest protein of the human body, extends from a Z disc of a sarcomere to its M line

38
Q

Define syncytium

A

A fused mass of cells which shares continuous cytoplasm

39
Q

Identify the components of a motor unit

A

A motor unit consists of a somatic motor neuron and the muscle fibers it innervates

40
Q

Discuss the sliding filament theory of contraction and identify specific steps

A

1) A myofiber, together 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 the sarcomeres –the distance between Z lines is reduced
3) Shortening of the sarcomeres is accomplished by sliding of the myofilaments –the length of each filament remains the same during contraction
4) Sliding of the filaments is produced by asynchronous power strokes of myosin cross bridges, which pull the thin filaments of the thick filaments
5) The A band remains the same length during contraction, but are pulled toward the origin of the muscle
6) Adjacent A bands are pulled closer together as the I bands between them shorten
7) The H bands shorten during contraction as the thin filaments on the sides of the sarcomeres are pulled toward the middle

41
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. The cross bridges are part of the myosin proteins, extend towards the actin filament and terminate in a globular head. A reaction must occur before the myosin heads can bind to actin. When 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. This is 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.

42
Q

Discuss excitation-contraction coupling

A

The process by which action potentials cause contraction is termed excitiation-contraction coupling

43
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 alone the transverse tubules and calcium channels are opened

Sarcoplasmic reticulum: calcium channels are opened and calcium leaves the sarcoplasmic reticulum and enters the sarcoplasm

44
Q

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

A

Dihydropyridine (DHP) receptors: voltage-gated calcium channels located in the transverse tubules that respond to depolarization (via action potential)

Ryanodine receptors: calcium release channels in the sarcoplasmic reticulum that are opened via conformational changes in DHP receptors of the transverse tubules

45
Q

Discuss the fate of calcium during muscle relaxation

A

Calcium release will continue until action potentials cease. Active transport pumps, termed Ca+2-ATPase pumps, pump calcium back into the sarcoplasmic reticiulum to sequester calcium from the cytoplasm.

46
Q

Compare and contrast skeletal, cardiac and smooth muscle

A
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47
Q

Describe calcium induced calcium release in cardiac muscle

A

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In myocardial cells, the voltage-gated Ca+2 channels in the plasma membrane and the Ca+2 release channels in the sarcoplasmic reticulum do not directly interact. The calcium that enters the cytoplasm through the voltage-gated channels in the transverse tubules stimulates opening of the Ca+2 release channels of the sarcoplasmic reticulum. Thus, calcium serves as a second messenger from voltage-gated calcium channels to calcium release channels.

48
Q

Describe the role of the pacemaker in cardiac muscle contraction

A

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

49
Q

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

A

The 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. A greater membrane depolarization leads to more calcium entering the cell. Here, calcium combines with calmodulin. This calcium-calmodulin complex combines with and activates myosin light-chain kinase, and enzyme that causes the phosphorylation of myosin light chains, a component of myosin cross bridges. This phosphorylation is the regulatory event that allows binding to actin. This phosphorylation event can be reversed by myosin phosphatase, and this loss of phosphate inhibits cross bridge formation.