Neurons and myocytes Flashcards

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1
Q

Neurons

A

Long lived, non dividing cells that can last from the fetal stages until elderly. They can be of enormous length, the longest axon in humans runs from the base of the spine to the big toe. They transmit signals through action potentials (a transient change in the charge of the membrane) and the signal is transmitted across a synapse

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2
Q

Cell body

A

Where the normal cellular processes are taking place- cellular metabolism, protein transport, and others. This is where the nucleus and other organelles are located.

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3
Q

Axon

A

Extended part of the neuron connected the cell body to the axon terminals. It does not have organelles, mainly just cytoplasm. Action potentials travel across the surface

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4
Q

Astrocytes

A

Most abundant glial cell in the CNS. They help to form the blood brain barrier and regulate the fluid composition of the brain by regulating what fluid can get in (interstitial fluid). They form a structural network, which acts as scaffolding for neurons to grow and rest. Therefore, some extensions of one astrocyte can contribute to forming the blood brain barrier while its other extensions are bound to neurons

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5
Q

Blood brain barrier

A

Regulates what can get in and out of the brain compartment. Astrocytes help to form the BBB using their processes (extensions) which wrap around brain capillaries and form a physical barrier that coats the outside of the blood vessel. Astrocytes can be bound to the basement membrane (ECM) which is bound to the endothelium, connected with tight junctions. All of these cells/layers of tissue surround the walls of the blood vessels going into the brain

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6
Q

Astrocytes functions (6)

A
  1. Form the blood brain barrier
  2. Regulate tissue fluid composition
  3. Form a structural network
  4. Replace damaged neurons
  5. Provide nutrients like lactate and glucose
  6. Very concentrated at synapses
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7
Q

Oligodendrocytes

A

Glial cells that form the myelin sheath around neurons in the CNS only. It has cellular processes (layers of membrane) that extend out and wrap around the axons of neurons. One oligodendrocyte may provide myelin for several different neurons

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8
Q

Microglia

A

Glial cells specific to the CNS- they are the motile and resident macrophages of the CNS. They are responsible for repairing damaged neural tissue, remove dead cells, and provide a defense against pathogens. They are an important source of chemokines and cytokines, helping to recruit other cells to the damaged areas

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9
Q

2 types of microglia activated states

A
  1. M1- microglia that produces more proinflammatory cytokines, can create collateral damage
  2. M2- microglia that produces anti-inflammatory cytokines, associated with protective functions
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10
Q

Schwann cells

A

Form myelin sheath around neurons in the PNS, similar in function to oligodendrocytes in the CNS. However, Schwann cells do not have extensions, one Schwann cell wraps one portion of one neuron w/ myelin. The myelin sheath is still basically created by layers of membrane

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11
Q

Myelin sheath

A

Layers of membrane wrapped around neuron- it insulates the axonal membrane, prevents current leakage, and increases the speed & efficiency of the action potential. The myelin sheath is interrupted by the nodes of Ranvier (non myelinated sections of the axon). All voltage dependent Na+ channels are concentrated here. They are responsible for propagating the action potential down the axon- promotes rapid depolarization from node to node, allows for saltatory conduction

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12
Q

Saltatory conduction

A

Increases action potential rate. When the concentration of sodium channels are activated in the node of Ranvier, the action potential rapidly “jumps” to the next unmyelinated portion of the axon

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13
Q

Action potential steps (6)

A
  1. A stimulus depolarizes the axonal membrane, voltage gated Na+ channels open, there is a sodium influx into the cytoplasm of the axon
  2. Sodium influx allows for further depolarization, which opens other channels. Membrane potential goes from -70mV to +50mV, becoming more positive
  3. Na+ reaches the equilibrium state
  4. Channels inactivate, which helps bring the membrane potential back to original neg value. Ensures that action potentials only travel in one direction
  5. Cycle of closed, open, inactivated channels transmits electrical signal
  6. Voltage-gated K+ channels activate in response. Help bring membrane potential back to normal via K+ efflux- membrane potential becomes more negative
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14
Q

Action potential

A

A transient change in membrane potential- basically a traveling wave of electrical excitation that has a “domino effect”. Voltage gated cation channels are responsible for action potentials occurring- the positive change in membrane potential is due to a sodium influx. Since the channels are voltage changed, the change in membrane potential is causing them to open

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15
Q

When do sodium channels become inactive?

A

When local sodium concentrations reach equilibrium across the membrane. This ensures that the action potential is only moving in one direction

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16
Q

What happens to the action potential when it reaches the terminus of the axon?

A

It can be sent to another neuron (axon branch-dendrite, axon branch-cell body) or to a myocyte (neuromuscular junction). It can be sent by one of 2 types of synapses- electrical or chemical

17
Q

Electrical synapse

A

Direct , 3.5 nm distance. Typically found when the pre- and post-synaptic cells are both neurons. These 2 neurons are directly connected through gap junctions. In this case, the action potential can immediately travel from the pre-synaptic cell over to the post-synaptic cell.

18
Q

Chemical synapse

A

Indirect, 20-40 nm distance. Can be located between two neurons or between a neuron and a muscle cell. When there is an increase in cytoplasmic calcium, the secretory vesicles in the axon terminal release neurotransmitters into the synapse through exocytosis. The neurotransmitters act on channels in the post-synaptic cell to create another action potential

19
Q

Chemical synapses

A

A membrane potential change in the axon triggers the exocytosis of neurotransmitters, which are stored in synaptic vesicles. Voltage-gated Ca2+ channels are triggered to open by this change in membrane potential. Ca2+ disrupts the interaction of secretory vesicles with cytoskeleton, so the secretory vesicles are no longer locked in place. They fuse with the axon membrane via SNAREs, allowing for the exocytosis of neurotransmitters

20
Q

Transmitter-gated ion channels

A

Channels located on the post-synaptic neuron in synapses. Called transmitter gated because specific neurotransmitters open them. Neurotransmitters diffuse across synapse and bind to/open these channels, which creates a change in membrane potential. This triggers the voltage-gated sodium ion channels and results in a continuation of the electrical signal as a sodium influx occurs

21
Q

What happens to neurotransmitters once the postsynaptic cell is stimulated?

A

Neurotransmitters are either rapidly degraded in the synapse or rapidly taken up by the presynaptic neuron, where they can be reused for another action potential

22
Q

Reuptake of neurotransmitters

A

Synaptic vesicles that take up unused neurotransmitters reform in the presynaptic neuron via a modified endocytic pathway. The unused neurotransmitters are endocytosed, but they do not acidify/turn into lysosomes because we do not want them to be degraded.

23
Q

Myocytes

A

Muscle cells, filled with myofibrils

24
Q

Myofibrils

A

Bundles of thick and thin filaments. The thick filaments are bundles of myosin 2 and the thin filaments are bundles of actin

25
Q

Sarcoplasmic reticulum

A

A modified endoplasmic reticulum found in muscle cells. It forms a web-like sheath around myofibrils. It stores intracellular calcium, which is important for muscle contraction

26
Q

Transverse (T) tubules

A

Intracellular folds of the muscle cell membrane. They surround myofibrils and interact with the SR

27
Q

Muscle contraction filaments (6)

A

Occurs due to sliding filaments: actin, myosin, Z-disc, nebulin, tropomodulin, and titin. Nebulin stabilizes actin, tropomodulin stabilizes actin, titin acts as a molecular spring

28
Q

Sarcomere

A

One unit of thick and thin filaments. Actin and myosin are the major filaments that slide across one another, causing muscle contraction.

29
Q

Z disc

A

caps actin at + ends, prevents depolymerization

30
Q

Nebulin

A

wraps around actin filaments, regulates size (35 aa)

31
Q

Tropomodulin

A

caps/stabilizes the negative ends of actin

32
Q

Titin

A

molecular spring, positions myosin midway b/w Z-discs

33
Q

Troponin and tropomyosin

A

Both proteins surround the actin filaments and lock them in place to prevent them from sliding. It consists of 3 proteins (I, C, and T). Troponin I-T pulls tropomyosin to a position where it blocks myosin binding. If myosin can’t bind to actin, the filaments will never slide over each other and muscle contraction can’t occur. Therefore, there is a rise in intracellular calcium. Calcium to binds troponin C, which causes troponin I-T to release their hold on actin. Troponin and tropomyosin drop off, and myosin can now bind

34
Q

Myosin 2 mechanism (5)

A
  1. When there is no nucleotide bound, the myosin head is bound to the actin
  2. Once ATP binds to the myosin, it releases its hold on the actin
  3. ATP is hydrolyzed, causing a conformational change in the myosin lever arm, moving it to the “cocked” position
  4. The head is still bound by ADP, and the ADP-bound head binds actin. Inorganic phosphate is released
  5. When the ADP is released, another conformational change occurs in the myosin. A power stroke occurs, sliding the actin filaments. As the actin filaments slide over one another, they cause muscle contraction
35
Q

Neuromuscular junction

A

When the pre-synaptic cell is a neuron and the post-synaptic cell is a skeletal muscle cell. Acetylcholine (Ach) is the neurotransmitter released from the neuron into the synapse. Ach travels across the synapse to bind to Ach-gated channels. This allows for the influx of sodium into the muscle cell. Now there is an action potential, which will eventually reach a voltage gated calcium channel in the sarcoplasmic reticulum. This allows for the increase in cytoplasmic calcium. Most of this process is taking place in the T-tubules (membrane invaginations)

36
Q

What happens in a muscle cell once Ach binds?

A

After Ach binds to the muscle cell, sodium channels open and create an action potential. The action potential reaches voltage gated calcium channels in a T-tubule membrane. T-tubules can extend so far into the cell that they are in contact with the sarcoplasmic reticulum membrane, so some calcium can come from the lumen of the T-tubule bind to a calcium gated channel in the SR. The channel opens, allowing for a robust increase in cytoplasmic calcium. Once calcium is abundant, it binds to troponin C, making the whole troponin-tropomyosin complex fall apart, and releasing its hold on actin. Now myosin can bind and undergo conformational changes to lead to muscle contraction