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READING Flashcards

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The Brain flashcards
1
Q

what is the difference between a neurotransmitter and a hormone?

A
  • neurotransmitters are released in the brain
  • hormones are released by the pituitary and travel in the bloodstream
  • often structurally similar, the main difference between the two is the distance they have to travel
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2
Q

what is the difference between the electrical information flow in the nervous system and the flow of electricity in a wire?

A
  • the electrical information flow in the nervous system is much much slower than the flow of information through a wire
  • this is because in the nervous system it is the passage of charged ions that carry the current and not the passage of electrons
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3
Q

at resting potential, what side of the membrane has what charge?

A

the extracellular side of the membrane has a charge of -70mV relative to the intracellular charge of the membrane

the intracellular charge isnt actually 0 but we consider it 0 as when we look at potential differences we look at the extracellular charge relative to the intracellular charge

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4
Q

What is the difference between proteins made on the RER and proteins made from free floating ribosomes?

A
  • proteins designed to be inserted into the cell membrane are made on the RER. This is because as the protein is being assembled it is threaded back and fourth through the membrane of the RER where it is trapped.
  • neurons have a lot of RER because they have a lot of membrane proteins
  • proteins destined to reside in the cytosol of the neuron is made in free floating ribosomes
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5
Q

what protein do microtubules consist of?

A

tubulin

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6
Q

what protein are microfilaments made of?

A

actin

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7
Q

what 3 structures make up the cytoskeleton in order of increasing size?

A

microfilaments
neurofilaments
microtubules

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8
Q

what distinguishes the axon from the soma?

A

there are no RER in the axon and very few free ribosomes

The protein composition of the membrane is very different in the axon

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9
Q

what is the name of axon branches?

A

axon collaterals

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10
Q

what are neurites?

A

axons and dendrites

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11
Q

How are dendritic spines correlated with intellectual disability

A
  • intellectually disabled infacts have fewer dendritic spines and the ones they do have are abnormally long and thin
  • the extent of the spine difference was well correlated with the degree of intellectual disability
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12
Q

what is the difference between unipolar, bipolar and multipolar cells?

A

unipolar- neuron has a single neurite
bipolar- two neurites
multipolar- multiple neurites

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13
Q

what is the difference between the pyramidal cells and the stellate cells in the cerebral cortex?

A

stellate cells are star shaped and are local circuit neurons

pyramidal cells are pyramid shaped and are projection neurons

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14
Q

what are the 3 main types of neurons in terms of what connections are made?

A

primary sensory neurons
interneurons
motor neurons

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15
Q

what is the difference between golgi type 1 neurons and golgi type 2 neurons?

A

golgi type 1

  • otherwise known as projection neurons
  • these have long axons that extend from one part of the brain to the other

golgi type 2

  • otherwise known as local circuit neurons
  • these have short axons that do not extend beyond the vicinity of the cell body
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16
Q

whats the function of ependymal cells

A
  • they line fluid filled ventricles within the brain

- they play a role in directing cell migration during brain development

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17
Q

what is the equilibrium potential in relation to the membrane potential?

A

The equilibrium potential is the membrane potential that would balance out the ions concentration gradient so that no net ionic current would flow if the membrane were permeable to that ion

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18
Q

are k+ ca2+ and na+ more concentrated inside or outside the membrane

A

k+ is more concentrated inside the membrane

ca2+ and na+ are more concentrated outside the membrane?

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19
Q

which ways does the sodium pottasium pump transport ions across the membrane?

A

pumps na+ outside the membrane and k+ inside

uses atp as this is against the concentration gradients

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20
Q

which way does the calcium pump transport calcium?

A

outside the membrane

uses atp as against concentration gradient

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21
Q

what is the blood brain barrier?

A

a specialisation in the walls of the brain cappilleries that limits the movement of pottasium and other substances into the extracellular fluid of the brain

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22
Q

do electrical synapses exist

A

yes

23
Q

where do electrical synapses occur?

A

gap junctions

gap junction often connect a neuron with a non neuronal cell, but they can connect two neurons in an electrical synapse

24
Q

what are connexins and connexons

A

the proteins present in electrical synapses, they combine to form connexon channels. two connexon channels can then combine to form gap junction channels that allow ions to directly transfer from one cell to another

25
Q

are electrical synapses directional or bidirectional?

A

they are bidirectional as gap junction channels allow ions either way

26
Q

what is a neuromuscular junction?

A

a chemical synapse between motor neurons in the spinal chord and skeletal muscle

27
Q

what is the post synaptic membrane of a neuromuscular junction called?

A

the motor end plate

28
Q

what are the 3 major categories of neurotransmitters?

A

amino acids
amines
peptides

29
Q

what is the difference between AMPA and NMDA receptors

A

AMPA are permeable Na+ and K+
NMDA are permeable to NA+ K+ AND Ca2+
NMDA-gated channels are voltage dependent
this is because at normal resting potential the NMDA channel is clogged by Mg2+ ions. Mg2+ is only unclogged when the membrane depoarizes. This usually follows the activation of AMPA channels at the same synapse

30
Q

what two neurotranmitters mediate most inhibition in the CNS

A

GABA mediates most inhibtion

Glycine mediates most of the rest

31
Q

what ion do GABA and Glycine channels allow in

A

Cl- ions

32
Q

how do barbituates and benzodiazepines influence the GABAa receptors?

A

When GABA is present, benzodiazepines increase the frequency of channel openings and barbituates increase the duration of channel openings
- this results in more CNS inhibition

33
Q

why does ethanol enhance inhibition in some brain areas and not others?

A

specific a,b and y subunits are nessercary for contructing an ethanol sensitive GABA

34
Q

what 4 main protein subtypes do drugs bind to?

A

receptors
enzymes
carriers
ion channels

35
Q

what is the difference between agonists and antagonists?

A

agonists activate the receptors and antagonists block the receptors

36
Q

What is the difference between on target and off target side effects?

A
  • on-target effects are unwanted side effects mediated through the same receptor as the clinically desired effects
  • Off-target effects are unwanted side effects arising from the action of a different receptor
37
Q

what is the difference between affinity and efficacy?

A

affinity is the tendency of a drug to bind to its receptors

efficacy is the tendency of it, once bound, to activate the receptors

38
Q

what happens to the agonist log concentration-effect curve in the prescence of a competitive antagonist?

A

It shifts to the right, without a change of slope or maximum

39
Q

what is a dose ratio?

A

the ratio by which the agonist concentration has to be increased in the presence of the antagonist in order to restore a different level of response

40
Q

what is the relationship between the dose ratio and antagonist concentration?

A

there is a linear relationship between the dose ratio and the antagonist concentration

41
Q

What are 3 features of reversible competitive antagonism?

A
  • shift of the agonist log concentration–effect curve to the right, without change of slope or maximum (i.e. antagonism can be overcome by increasing the concentration of the agonist)
  • linear relationship between agonist dose ratio and antagonist concentration
  • evidence of competition from binding studies
42
Q

what is irreversible competitive antagonism?

A
  • Irreversible competitive (or non-equilibrium ) antagonism occurs when the antagonist binds to the same site on the receptor as the agonist but dissociates very slowly, or not at all, from the receptors, with the result that no change in the antagonist occupancy takes place when the agonist is applied
  • with irreversible competitve antagonism the antagonist reduces the maximum response, however this may be hard to detect if there are a lot of spare receptors
43
Q

whats stephensons formulation of efficacy?

A
  • the reciprocal of the occupancy need to produce a 50% maximum response
  • e.g e= 25 implies that 50% of the maximal response occurs at 4% occupancy
44
Q

what is a full agonist?

A

a drug whose efficacy is sufficient that it produces a maximum response when less than 100% of receptors are occupied

45
Q

what happens to the dose response curve of a full agonist in the presence of a partial agonist

A
  • it shifts the dose curve to the right

- so in effect the partial agonist can act as a competitive antagonist to the full agonist

46
Q

what is constitutive activation and what are inverse agonists

A

activation of a receptor when no ligand is present

sometimes a drug can reduce the amount of constituent activation and they are known as inverse agonists

47
Q

why do agonists activate receptors and antagonists dont?

A

receptors have two states: Resting (R) and Active (R*)

Agonists have a higher affinity for R* so cause a shift of the equilibrium to R*

Antagonists have a neutral affinity for either R or R*

Inverse agonists have a higher affinity for R

48
Q

What is biased agonism?

A
  • some receptors can induce multiple different intracellular responses
  • Biased agonists are more likely to induce one particular intracellular response from the same receptor
49
Q

what is positive and negative affinity modulation?

A

positive modulation increases the affiity for the agonist, negative affinity modulation decreases it

50
Q

what are 6 different mechanisms that give rise to tolerance and desensitisation?

A
  • change in receptors
  • translocation of receptors
  • exhaustion of mediators
  • increased metabolic degradation of the drug
  • physiological adaptation
  • active extrusion of drug from cells
51
Q

How can change in receptors lead to tolerance or desensitisation?

A

receptors can change so that:

  • agonists binding dont open the ion channel
  • receptors are desensitised by phosphorylation
  • phosphorylation causes the agonist to be less likely to induce a g-protein response
52
Q

how does translocation of receptors lead to desensitisation

A

prolonged exposure to agonists can lead to a decrease in the number of receptors, due to receptors being taken into the cell via endocytosis

53
Q

how does exuastion of mediators work

A

depletion of an essential substance

e.g amphetamines cause the release of amines from the nerve terminals however the amine store can become depleted

54
Q

how does altered drug metabolism work

A

desensitisation can occur because increased metabolic degradation can lower the drug plasma concentration

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