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PSYC2020 > Lecture2 > Flashcards

Lecture2 Flashcards

1
Q

How do neurons differ from other cells?

A

They are excitable, conduct electrical signals & communicate with other neurons through chemical signals

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2
Q

What are the three functions of neurons?

A

Reception, conduction & transmission

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3
Q

What type of neuron is a motor neuron?; Describe the length of fibres; Location; Function

A

Multipolar, efferent neuron; short dendrites & long axon; Dendrites & cell body inside spinal cord, axon outside spinal cord; Relays messages from brain & spinal cord to muscles & organs

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4
Q

What type of neuron is a sensory neuron?; Describe the length of fibres; Location; Function

A

Unipolar, afferent neuron; long dendrites & short axon; Cell body & dendrite outside spinal cord, axon in a dorsal root ganglion; Relays messages from sensory receptors to brain or spinal cord

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5
Q

What type of neuron is an interneuron?; Where is it located? What is its function?

A

Neuron with short dendrites & a short or no axon; Entirely within the brain or spinal cord (CNS); integrates sensory neuron with appropriate motor neuron & relays messages within structures

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6
Q

What are Ribosomes?; Where are they located?

A

Internal rough cellular structures on which proteins are synthesised; On the Endoplasmic Reticulum - a system of folded membranes in the cell body (smooth portions play a role in the synthesis of fats)

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7
Q

Define Golgi Complex

A

A connected system of membranes that packages molecules in vesicles

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8
Q

What are Mitochondria?

A

Sites of aerobic (oxygen-consuming) energy release; power stations of the cell

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9
Q

What are Microtubules responsible for?

A

Tubules responsible for rapid transport of material throughout neurons down to terminal buttons

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10
Q

What are Synaptic Vesicles?

A

Spherical membrane packages that store neurotransmitter molecules ready for release near synapses

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11
Q

What is the neuron cell membrane composed of? What are the 2 types of proteins embedded in this?

A

A Lipid Bilayer (2 layers of fat molecules); Channel Proteins - allow specific molecules to pass through membrane; & Signal Proteins - indirectly transmit signals from outside layer to inside

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12
Q

Which four key ions are involved in membrane potential?

A

Na+ (Sodium), K+ (Potassium), Cl- (Chloride) & protein-

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13
Q

Describe the five factors for the resting potential & their functions

A

Random motion; concentration gradients; (both contribute to homogenise the charge; in high concentration it wants to diffuse & evenly distribute); differential permeability of the membrane (more favourable to k+ & Cl-); electrostatic pressure (ions with like charge repel one another); sodium-potassium pump (maintains balance of -70mv)

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14
Q

Describe the function of Sodium-Potassium pumps

A

They are energy consuming mechanisms in the cell membrane that pump Na+ ions out of neurons & k+ ions into neurons to maintain resting equilibrium. They continually exchange 3 Na+ ions for 2 k+ ions

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15
Q

Which types of ions have a greater concentration outside a resting neuron than inside?

A

Na+ (Sodium) & C- (Chloride)

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16
Q

How does the distribution of C- (Chloride) ions across the neural membrane maintain balance or equilibrium?

A

They move down their concentration gradient into the neuron during resting potential (-70mv) and the 70mv of electrostatic pressure drives them out

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17
Q

How much pressure from the concentration gradient is needed to push k+ ions out of a cell?; How much to push Na+ ions into the cell? What do both these effects result in?

A

k+: 90mv, resulting in leakage; Na+: 50mv, which act in the same direction as electrostatic gradient resulting in 120mv of pressure forcing them into resting ions (70mv of electrostatic for both types)

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18
Q

What occurs when an Excitatory Post Synaptic Potential (EPSP) is generated?

A

Receptive membrane depolarises, decreasing resting potential to around -65mv, membrane opens & allows Na- ions into cell (reverses polarity), increasing the likelihood that an action potential will fire

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19
Q

What occurs when an Inhibitory Post Synaptic Potential (IPSP) is generated?

A

Receptive membrane hyperpolarises, increasing resting potential to around -72mv, decreasing the likelihood that an action potential will fire

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20
Q

What happens if two simultaneous EPSPs or IPSPs are generated?

A

The sum of them will produce a greater EPSP or IPSP. If one of each occurs they will cancel each other out

21
Q

Explain Saltatory Conduction

A

It’s the transmission of action potentials in myelinated axons; the signal is conducted passively (instant & decremental), along each segment of myelin to the next node of ranvier resulting in faster conduction than non-myelinated axons

22
Q

What are the three phases of an action potential?

A

If excitation threshold is reached (-65mv) AP will fire. In Rising phase: Na+ channels open, followed by k+ channels, reaching a peak of depolarisation (+50mv); Repolarisation: Na+ channels close, decreases back towards -70, but k+ channels close slower, leading to a momentary Hyperpolarisation: it undershoots before settling back to resting potential

23
Q

What’s the difference between the absolute refractory period & the relative refractory period?

A

Absolute: brief period (1-2 ms) after initiation of an action potential where it’s impossible to elicit a second one; Relative: Follows the absolute period & now it’s possible to fire the neuron again but needs higher level of stimuation

24
Q

What are Schwann Cells?

A

Glial cells which have a similar function to Oligodendrocytes but in the PNS; they wrap around the axon like a snail & can guide axonal regeneration

25
Q

What kind of degeneration leads to multiple sclerosis?; What are some symptoms?

A

Degeneration of myelin sheath; Impairments in vision, motor skills (weak muscles, slurred speech, poor posture, tics), sensory (numbness, tingling, pain), coordination & balance & cognitive (memory)

26
Q

What are the functions of Astrocytes?

A

Also known as “star cells”, they’re the largest glial cells & provide structural support & clean up debris or dead cells.

27
Q

How are neurotransmitters released from the terminal button?

A

A cluster of protein molecules lie at the pore of the synaptic vesicle membrane, calcium enters & as the pore opens, synaptic vesicle membrane fuses with presynaptic membrane & releases neurotransmitters

28
Q

How many action potentials occur before smaller vesicles release neurotransmitters as opposed to larger vesicles?

A

One AP for smaller & multiple APs for larger vesicles

29
Q

What are the differences between Axodendritic, Axosomatic, Dentritic and Dendrodentritic Synapses? Which two are the most common?

A

Axodentritic synapses - axon terminal buttons on dendrites; Axosomatic - axon terminal buttons on somas (cell bodies); Dentritic - axon terminal buttons on spines of dendrites; Dendrodentritic - dendrite to dendrite (often bidirectional transmission); Axodentritic & Axosomatic

30
Q

Why are Axoaxonic synapses particularly important?

A

They can mediate presynaptic facilitation and inhibition of that button on postsynaptic neuron

31
Q

What is the difference between presynaptic facilitation and inhibition?; What is the advantage of these?

A

Presynaptic facilitation increases the effects of one neuron on another; Presynaptic inhibition decreases the effects of one neuron on another; They selectively influence single synapses rather than the entire neuron

32
Q

What is the difference between Directed and Non-Directed synapses?

A

Directed are synapses at which the site of the neurotransmitter release and the site of neurotransmitter reception are in close proximity; Non-Directed are synapses at which the site of release is at some distance from the site of reception

33
Q

How are neurotransmitter molecules released in a non-directed String of Beads synapse?

A

They’re released from a series of Variosities (bulges or swellings) along the axon and its branches are widely dispersed to surrounding targets; the effects are more slow and diffuse

34
Q

List three things that can occur once neurotransmitters are released.

A

They can be: Taken up by presynaptic receptors (receptors act as a feedback mechanism, regulating the amount of flow); Destroyed in the gap before they reach postsynaptic receptors (drugs facilitate this); Taken up by postsynaptic receptors (shape of receptor matches neurotransmitter)

35
Q

There are two general types of neurotransmitters. Which ones are small molecules & what do they include?; Which ones are large molecules and what do they include?

A

Small are Neurotransmitters; They include GABA, Glutamate, Acetylcholine & Norepinephrine; Large are Neuropeptides; They include Substance P and Endorphins

36
Q

Where are small-molecule transmitters synthesised?

A

In the cytoplasm of the terminal button and packaged in synaptic vesicles by the Golgi Complex

37
Q

What causes the auto-immune disease, Myasthenia Gravis?; What are some symptoms?

A

Synaptic transmission is disrupted, action potentials in nerves are normal but there’s a problem with synapses on muscles; Extreme fatigue, fluctuating muscle weakness (proximal>distal), problems chewing (dysphagia) and talking (dysarthria) & respiratory weakness

38
Q

Which receptors does Myasthenia Gravis disorder destroy?; How is this treated?

A

Acetylcholine (ACh) receptors; Immunosuppressive drugs, removal of thymus gland, or Anticholinesterase (AChE) inhibitors - enzymes which increase or prolong effects of ACh on the postsynaptic membrane

39
Q

Which amino acid neurotransmitter is the most prevalent excitatory neurotransmitter in the CNS?; Most prevalent inhibitory neurotransmitter?

A

Glutamate; GABA (but does have some excitatory effects at some synapses)

40
Q

What can neurotransmitters be referred to as when they’re released in postsynaptic neurons?; Why?

A

Ligands; Each receptor is a protein that contains binding sites for particular neurotransmitters & a Ligand includes any molecule that binds to another

41
Q

Name the two different types of receptors and what they’re asscociated with

A

Ionotropic receptors - ligand activated ion channels (fast acting, immediate effect of opening channel causes change in neural activity); Metabotropic - Signal proteins and G proteins (slower acting, protein breaks off & binds to ion channel or stimulates second messenger)

42
Q

What are two mechanisms of neurotransmitter degradation in synapses?

A

Reuptake - once released, majority of transmitters are almost immediately drawn back into presynaptic buttons by transporter mechanisms; Enzymatic degradation - proteins stimulate or inhibit biochemical reactions without being affected by them (eg. acetylcholine)

43
Q

What are the three classes of small molecule transmitters & the differences between them?

A

Amino Acids (eg. GABA & Glutamate) - molecular building blocks of proteins; Monoamines (eg. Norepinephrine) - synthesised from singular amino acid, slightly larger & more diffuse; Acetylcholine - at neuromuscular junctions at many synapses in autonomic nervous system & CNS

44
Q

What are the two different classes of Monoamines & how are they synthesised or converted?

A

Catecholamines - Tyrosine> L-Dopa> Dopamine> Norepinephrine (Noradrenalin)> Epinephrine (Adrenalin); Indolamines - Tryptophan> Seretonin

45
Q

List the 7 stages in neurotransmitter action

A
  1. Synthesis of NT molecules under enzyme influence
  2. Storage of NTs in vesicles
  3. Leaking NTs from vesicles destroyed by enzymes
  4. Action potentials cause vesicles to fuse with presynaptic membrane & release NTs
  5. Binding of NTs with auto-receptors, inhibiting subsequent NT release
  6. NTs bind to postsynaptic receptors
  7. Released NTs deactivated by reuptake or degradation
46
Q

What’s the difference between Agonists & Antagonists?

A

Agonists - drugs which increase or facilitate neurotransmitter activity; Antagonists - drugs which decrease or inhibit activity

47
Q

How may a drug alter neurotransmitter activity: while still in the presynaptic neuron?; At the synapse junction?

A

In neuron - by reducing production & inhibiting release; At junction - by promoting destruction, blocking uptake (antagonist) or blocking re-uptake (agonist)

48
Q

Name two examples of Agonists & how they work

A

Cocaine (catecholamine agonist) - blocks re-uptake, preventing activity of NT from being turned off; Benzodiazephines (GABA agonists) - binds to & increases GABA molecule binding; muscle relaxants & anticonvulsants

49
Q

Name two examples of Antagonists & how they work

A

Atropine (ACh antagonist) - binds & blocks muscarinic receptors (metabotropic receptors in the brain); high doses disrupt memory. Curare (ACh antagonist) - binds & blocks nicotine receptors (ionotropic receptors at neuromuscular junction); causes paralysis; also used for schizophrenia

PSYC2020 (11 decks)

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