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Block 1 - Week 6 > Overview of the Nervous System > Flashcards

Overview of the Nervous System Flashcards

1
Q

Current (I)

A
  • Electrical charge flowing through the neuronal membrane per unit time (units: amperes or A)
  • Water analogy: how much water (charge) is flowing through the pipe per second
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2
Q

Potential/Voltage (E or V)

A
  • The relative “pressure” on a charge across the membrane (units: volts or V)
  • Water analogy: how much pressure is being exerted on the water throughout the pipe?
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3
Q

Conductance (g)

A
  • The ease with which charge flows across the membrane (units: siemens or S)
  • Water anology: how wide is the pipe?
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4
Q

What influences conductance (g)?

A
  • The number of open ion channels for a given ion
  • E.g. during the rising phase of an action potential, there are many sodium channels open –> gNA is high at this point
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5
Q

Is the intracellular surface of a cell more negative or positive than its extracellular surface?

A
  • The intracellular surface is more negative than the extracellular surface. This is the resting membrane potential of the cell
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6
Q

Resting membrane potential

A
  • A steady-state potential of the cell (when there are no changes occuring)
  • The potential across the membrane tends to remain at the resting membrane potential
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7
Q

What charge do many macromolecules in cells have?

A

Many macromolecules in cells (e.g. nucleic acids, proteins, etc.) have a negative charge

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8
Q

“leak” ion channels

A
  • Open (no gating mechanisms)
  • Allow for the free flow of ions
  • K+ has the most leak channels, then Cl-, then Na+
    • Thus K+ plays the biggest role in creating the resting membrane potential
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9
Q

Sodium-Potassium ATPase

A
  • Uses ATP to counteract the effects of the leak ion channels
  • Pumps Na+ and K+ against their electrochemical gradients
    • Pumps 3 Na+ ions out for every 2 K+ in
    • Helps maintain the resting membrane potential
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10
Q

What is the approximate resting membrane potential in mV?

A

-65mV

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11
Q

Can neurons excite or inhibit other neurons?

A

Neurons can both excite or inhibit other neurons

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12
Q

Depolarization

A
  • Making the membrane potential more positive
  • Excitation signals depolarize the cell
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13
Q

Hyperpolarization

A
  • Making the membrane potential more negative
  • Inhibitory signals hyperpolarize the cell
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14
Q

Repolarization

A
  • Return towards resting membrane potential after depolarization or hyperpolarization
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15
Q

Threshold potential

A
  • Membrane potential at which it is possible for an action potential to occur
  • Generally occurs around -55 mV (about 10mV more positive than the resting membrane potential)
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16
Q

General phases of the Action Potential

A
  • Threshold potential met: action potential becomes inevitable (all-or-nothing principle of action potentials)
  • Rising/depolarization phase: rapid depolarization of the membrane
  • Falling/repolarization phase: slower repolarization of the membrane back towards resting membrane potential (RMP)
  • Undershoot phase: After hyperpolarization membrane potential dips under RMP
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17
Q

Voltage-gated ion channels

A
  • Become permeable and impermeable within specific membrane potential ranges. Important examples:
    • Voltage-gated Na+ channels
    • Voltage-gated K+ channels
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18
Q

Biophysic stages of the action potential

A
  1. Voltage-gated Na+ channels open –> Depolarization
  2. Voltage-gated K+ channels open –> Hyperpolarization
  3. Voltage-gated Na+ channels close –> K+ channels close slower
  4. Overshoot phase –> then repolarization
19
Q

Where are action potentials typically initiated?

What do they propagate down?

A

Axon Hillock

Axon

20
Q

Saltatory Conduction

A
  • Action potential jumping from node to node (nodes of Ranvier) for faster signaling
  • Nodes of Ranvier have much higher voltage-gated Na+ channel density
21
Q

How does myelination conserve energy?

A
  • Sodium Potasium ATPase only has to work at nodes of Ranvier
  • Fewer axonal ion channels and ATPases needed
22
Q

General result of demyelinating disorders

A
  • Action potential velocity reduced
  • Greater amount of action potentials fail
  • Sensory/motor and sometimes autonomic/cognitive symptoms
23
Q

What is a common demyelinating disorder of the CNS?

A

Multiple Sclerosis

24
Q

What is a common demyelinating disorder of the PNS?

A

Guillain-Barre syndrome

25
Q

Chemical Synapses

A
  • Presynaptic neuron secretes neurotransmitters into synaptic cleft which bind to postsynaptic neuron
  • Can amplify signal (one neuron can synapse on many neurons)
  • Are highly plastic (modifiable)
26
Q

Electrical Synapses

A
  • Direct exchange of ions/molecules at physical junctions between two neurons
  • Rapid precise communication
  • Useful for large-scale synchronization of neurons
  • Can be bidrectional
27
Q

Neurotransmitters

A

Molecules synthesized within neurons that mediate signaling at chemical synapses

28
Q

What are the three main classes of neurotransmitters?

A
  • Amino Acids
  • Monoamines
  • Neuropeptides
29
Q

What are three important amino acid neuro transmitters?

A
  • Glutamate (Glu) –> excitatory
  • y-amino butyric acid (GABA) –> inhibitory
  • Glycine (Gly) –> inhibitory
30
Q

What are some of the main monoamine neurotransmitters?

A
  • Serotonin (5-HT)
  • Epinephrine (Epi)
  • Norepinephrine (NE)
  • Dopamine (DA)

Note: DA, NE, and Epi are also catecholamines

31
Q

What classes of neurotransmitters are small-molecule NTs?

A
  • Amino Acid NTs
  • Monoamine NTs
32
Q

Small-molecule neurotransmitters synthesis

A
  • Synthetic enzymes are synthesized on the soma and transported down axon via microtubules
  • NT precursors transported into axon terminal
  • NTs synthesized by synthetic enzymes and packaged in synaptic vesicles
33
Q

Neuropeptide neurotransmitter synthesis

A
  • NT precursors and synthetic enzymes are synthesized in the soma and packaged into synaptic vesicles
  • These synaptic vesicles are then transported down the axon via microtubules
  • Synthetic enzymes cleave precursors into NTs prior to release
34
Q

Chemical Synapse (Synthesis, Release, and Binding)

A
  • NTs synthesized at presynaptic axon terminal and stored in synaptic vesicles
  • Action potential (AP) reaches axon terminal to activate voltage-gated Ca2+ channels –> influx of Ca2+
  • Increased [Ca2+] –> promotes vesicle exocytosis via interactions between synaptotagmin and SNARE complexes
35
Q

What determines the neurotransmitter’s effect(s)?

A

The NT receptor determiens the NT’s effect(s)

Note: Multiple receptors are associated with most NTs

36
Q

Ionotropic Receptors

A
  • Have two domains:
    • Extracellular: ligand-binding site
    • Transmembrane: ion channel
  • Can gate specific/nonspecific cation (NA+, K+, CA2+) or anion (Cl-) channels that induce postsynaptic potentials
  • Rapid and transient with specific responses in membrane potential
37
Q

Metabotropic Receptors

A
  • Most are G protein-coupled receptors
  • Slow and sustained with many potential responses
  • Different types:
    • Indirect gating of ion channels
    • Activation of 2nd-messenger pathways which can:
      • Gating of ion channels
      • Induce other changes postsynaptic membrane
      • Regulate gene transcription
38
Q

Excitatory Postsynaptic Potentials (EPSPs)

A

Depolarize the neuron and make it more likely for an AP to occur

39
Q

Inhibitory Postsynaptic Potentials (IPSPs)

A

Hyperpolarize the neuron and make it less likely for an AP to occur (with some exceptions)

40
Q

Postsynaptic Potentials (PSPs)

A
  • Are graded potentials: their amplitudes (sizes in mV) scale with the sizes of the input(s) that generate them (the number of NT-receptor binding events)
    • PSPs can sum together!
41
Q

Temporal Summation

A
  • Type of graded potential (PSPs)
  • Rapid PSPs from the same source within a short period of time accumulate
42
Q

Spatial Summation

A
  • Type of graded potential (PSPs)
  • PSPs from different sources arrive in close succession to sum at the same location
43
Q

What stops the continued generation of PSPs after presynaptic action potential due to continued neurotransmitter-receptor binding events?

A
  • Neurotransmitters are removed from the synaptic cleft through two mechanisms:
    • Reuptake: presynaptic neuron reuptakes NTs via transporters
    • Catabolsim: Enzymes degrade NTs
44
Q

What do reuptake inhibitors do?

What are some common examples?

A
  • Cause NT binding to occur over a greater period of time
  • Common examples:
    • SSRI
    • Psychostimulants (Cocaine)
    • Anticonvulsants

Block 1 - Week 6 (6 decks)

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