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Principles of Animal Physiology > The Brain > Flashcards

The Brain Flashcards

1
Q

What is neuroscience?

A

The study of the nervous system, including cellular and molecular processes, behaviour, affective and cognitive abilities, systems or circuitry & disease.

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2
Q

What year was Descartes dualism theory of the mind & body published?

A

1649

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3
Q

Briefly describe Golgi stains

A

Invented in 1873
Chemicals include Potassium dichromate & Silver nitrate
Neurons stain dark brown/black
Vital for establishing connectivity between neurons

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4
Q

Electrochemical properties of neurons were discovered by which two scientists?

A

Hodgkin & Huxley

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5
Q

Briefly describe Nissl stains

A

Invented in 1885
Dyes RNA in the Endoplasmic Reticulum blue
Dye either thionine or cresyl violet
Stains ALL cells
Excellent for studies that examine the number of neurons

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6
Q

What is the function of dendrites?

A

To transmit information from sensory receptors to other neurons

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7
Q

What is the function of the cell body?

A

To integrate information

Contain the cell’s nucleus

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8
Q

What is the function of the axon?

A

Signal output

Passes information to subsequent neurons

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9
Q

Why did neuron structure evolve and vary?

A

To better suit their individual functions

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10
Q

What is a neuron circuit?

A

Sensation - Perception - Motor control

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11
Q

What is the neuron doctrine?

Briefly explain each stage

A
  1. Neural unit - Brain is made up of individual neurons with specific characters (i.e. dendrites, cell body, axon)
  2. Neuron specialisation - units differ in size, shape and structure according to location and function
  3. Neuronal fibers - Outgrowths of neurons
  4. Neuronal contacts - Neurons connected by sites of contact NOT cytoplasmic continuity
  5. Dale’s Law - Each neuron has specialised chemicals (neurotransmitters) - INCORRECT
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12
Q

True or False:

Particles move from low concentration to high concentration

A

FALSE

Particles move from high concentration to low concentration

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13
Q

Neuron cell body has a lower voltage than what?

A

Neuron cell body has a lower voltage than extracellular fluid

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14
Q

The membrane acts as a capacitor. What does this mean?

A

The membrane maintains voltage difference to allow resting potential

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15
Q

Resting potential is the product of what?

A

Resting potential is the product of the electrical difference between intracellular and extracellular solutions

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16
Q

What chemicals are important for maintaining the electrochemical gradient? What are their charges?

A

Sodium (Na+)
Potassium (K+)
Chlorine (Cl-)
Calcium (Ca2+)

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17
Q

Which chemical can move freely through channels in a 1:1 ratio?

Which chemical is tightly regulated?

A

K+ can move freely through channels

Na+ is tightly regulated

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18
Q

Summation of graded potentials can lead to what?

A

Action potentials

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19
Q

The initial rising phase of the action potential is caused by an influx of what chemical?

A

The initial rising phase of the action potential is caused by an influx of Na+

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20
Q

What is the “falling” phase of the action potential caused by?

A

The “falling” phase is caused by the outward movement of Na+ and K+.

21
Q

Briefly describe the electrochemical phases of the action potential.

A

Resting potential:
Open K+ channels

SOME Na+ channels open to depolarise

Threshold:
Sufficient depolarisation of axon results in action potential

At threshold, additional voltage-gated Na+ channels open, rapidly changing polarity

Positive polarisation:
Na+ channels deactivated

Gated K+ channels open re-polarising and hyper-polarising cell

After potential:
All gated channels closed

Cell returns to resting potential

Delayed K+ release into extracellular space leads to hyper-polarisation (the refractory period)

22
Q

What does the refractory period prevent?

A

Refractory period prevents bi-directional propagation current

23
Q

What does the relative refractory period permit?

A

Relative refractory period permits a semi-action potential

24
Q

What does the refractory period allows for?

A

The refractory period allows for the gradual reestablishment of the resting potential

25
Q

What does EPSP stand for?

What is it?

A

EPSP = Excitory Presynaptic Potential

Presynaptic neuron stimulates mild depolarisation, graded increase in voltage.

26
Q

What does IPSP stand for?

What is it?

A

IPSP = Inhibitory Presynaptic Potential

Presynaptic neuron stimulates hyperpolarisation, graded decline in voltage.

27
Q

Sensory neurons can exhibit different action potential activity depending on stimuli. What are the two types of response?

A

Phase response & tonic response

28
Q

In 1771, Galvani used dead frogs to prove what?

A

He put electrical impulses to dead frogs and showed stimulation of muscle contractions - Proved cells pass information using voltage currents.

29
Q

Electrochemical propagation down the axon. The signal originates where and transmits to where?

A

The signal originates in cells and transmits to the synapse

30
Q

Myelin sheath is composed of what?

A

Layered glial cell membrane

31
Q

Oligodendrocytes send out projections & wrap around axons. Nodes of Ranvier increase speed of voltage down the axon. How?

A

At the Node of Ranvier, Na+ channels are open, generating an action potential

Myelin prevents K+ leakage out, channeling the depolarisation down the axon interior

Depolarisation spreads within axon very rapidly

Action potential triggered at new Node of Ranvier.

32
Q

Multiple Sclerosis (MS) is a result of myelin degradation. Briefly describe.

A

MS is an autoimmune disease that disrupts the transfer of nerve signals leading to a loss of vision, ataxia, and fatigue.

Affects 2.5million people worldwide. More prevalent the further north you travel. Women are twice as likely as men to get MS.

33
Q

Action potentials reaching the synapse stimulate chemical communication. Voltage-gated calcium channels located in the presynaptic terminal stimulate the release of transmitters from extracellular vesicles. Briefly explain.

A

a) Terminal at rest
b) Action potential arrives, vesicles fuse with terminal membrane, producing exocytosis of transmitter
c) Transmitter binds to postsynaptic receptor proteins, ion channels open
d) Transmitter is removed from cleft, fused membrane is recycled.

34
Q

Termination of chemical communication involves enzymes, autoreceptors and transporters. Briefly describe.

A
  • Enzymes & precursors for the synthesis of transmitter and vesicle wall are continuously transported to axon terminals*
    1) An action potential is propagated over the presynaptic membrane
    2) Depolarisation of the presynaptic terminal leads to an influx of Ca2+
    3) Ca2+ causes vesicles to fuse with the presynaptic membrane & release transmitter to the synaptic cleft
    4) Binding of the transmitter to receptor molecules in postsynaptic membrane opens channels, permitting ion flow & initiating EPSP or IPSP
    5) EPSP or IPSP spread passively over dendrites and the cell body to the axon hillock
    6a) Enzyme present in the extracellular space breaks down the excess transmitter
    6b) Re-uptake of transmitter slows synaptic action & recycles transmitter to the subsequent transmission
    7) Transmitter binds to autoreceptors in the presynaptic membrane
35
Q

Chemical communication across the synapse can involve two distinct processes: Slow vs fast mechanisms. What are the differences?

A

There are minor presynaptic differences (e.g. vesicle size and transmitter abundance)

The key difference is attributable to the post-synaptic receptor: either IONOTROPIC (fast) or METABOTROPIC (slow)

Metabotropic (slow) (Beta-receptor):

  • G Protein-coupled receptor
    1. Neurotransmitter binds G protein-coupled receptor
    2a. G protein activated
    2b. Activated G protein subunit moves to adjacent ion channel (causes brief delay)
    3. Channel flows open - ions flow across the membrane for a longer period of time (than in ionotropic)

Ionotropic (fast) (alpha-receptor):

  • Ligand-gated ion channel
    1. Neurotransmitter binds directly to the channel protein
    2. Channel opens immediately
    3. Ion flows across the membrane for a brief time
36
Q

What does GABA stand for?

What is its job?

What drugs is the GABA site a major target for?

A

GABA = Y-Aminobutyric acid

GABA = Predominant inhibitory neurotransmitter in the central nervous system. GABA reduces voltage by causing an influx of Cl-

1) Barbiturates (depressants); anxiolytics, hypnotics, and anticonvulsants
2) Benzodiazepines; psychoactive drugs - valium

37
Q

Summarise the different classes of neurotransmitters

A

Amino Acids:

  • Glutamate
  • Aspartate
  • Glycine
  • GABA

Monamines:

  • Catecholamines
    i) Norepinephrine
    i) Dopamine
    i) Epinephrine
  • Indolamines
    i) Serotonin

Soluble gases:

  • Nitric oxide
  • Carbon monoxide

Acetylcholine

Neuropeptides:

  • Endorphins
    i) Dynorphin
    i) Opioids
  • Oxytocin
  • Prolactin
  • Gonadotrophin Releasing Hormone (GnRH)
38
Q

What is an agonist? Briefly describe

A

Agonist = Endogenous ligand

Naturally occurring, binds to receptor. Usually activates cognate receptor.

39
Q

What is a receptor agonist? Briefly describe

A

Receptor agonist = Exogenous ligand

Resembles endogenous ligand but is a drug/toxin. Can bind & activate receptor.

40
Q

Briefly describe a competitive antagonist

A

Some substances bind to receptors but do not activate them. They block agonists.

41
Q

Briefly describe non-competitive agonists/antagonists

A

Some substances bind to receptors at a different site.

42
Q

Functional connectivity between neurons can also develop via gap junctions. Briefly describe gap junctions

A

Gap Junctions consist of connexons.

They permit the exchange of Na+, K+, cAMP, sucrose & small peptides

43
Q

Drugs can act on the presynaptic terminal to regulate signal transduction. Briefly explain

A
  1. Synthesis of transmitters:
    - Para-chloropenylalanine inhibits tryptophan hydroxylase, preventing synthesis of serotonin from its metabolic precursor
  2. Conduction of action potentials
    - Tetrodotoxin, found in pufferfish, blocks voltage-gated Na+ channels and prevents nerve conduction
  3. Axonal transport
    - Colchicine impairs the maintenance of microtubules and blocks axonal transport
  4. The release of synaptic transmitters
    - Ca2+ channel blockers (e.g. verapamil) inhibit release of transmitters. Amphetamine stimulates the release of catecholamine transmitters. Black widow spider venom causes over-release and thus depletion of ACh.
  5. Storage of transmitters into vesicles
    - Reserpine causes synaptic vesicles to become “leaky” allowing transmitter molecules to escape and/or be exposed to the breakdown of enzymes
  6. Modulation of transmitters release by presynaptic receptors
    - Caffeine competes with adenosine for presynaptic receptors, thus preventing its inhibitory effects
  7. Inactivation of transmitter reuptake
    - Cocaine and amphetamines inhibit reuptake mechanism thus prolonging synaptic activity. Certain antidepressants inhibit serotonin reuptake.
  8. Blockade of transmitter metabolism
    - Monamine oxidase inhibitors (MAOIs) inhibit enzymes that normally inactivate transmitters, consequently, transmitter remains in the synapse longer and has greater effects.
44
Q

What is LTP?

A

Long-Term Potentiation

45
Q

What is LTD?

A

Long-Term Depression

46
Q

Highly repeated rapid electrical activity onto a postsynaptic neuron leads to what?

A

A lasting increase in synaptic function, due to greater postsynaptic receptors. Also increased transmitter release.

47
Q

There is a strong association between LTP in the hippocampus and what?

A

Learning

48
Q

Mechanisms underlying LTP and LTD recruit metabotropic receptors, showing a displacement of what?

A

Mg2+

49
Q

Formation is synapse specific. What does this mean?

A

It does NOT occur at other neuron synapses.

Principles of Animal Physiology (6 decks)

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