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Neuropharmacology Flashcards

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1
Q

how many neurons in the brain?

A

100 billion

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2
Q

how many synapses in the cortex?

A

0.15 quadrillion

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3
Q

what are the two types of receptors?

A

ion channels and g protein coupled receptor

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4
Q

how do ion channels function? and what do they allow?

A

NT attaches to receptor which then opens the gate of the ion channel, and only allows selective ions to flow through, eg, calcium channel only allows calcium ions to flow through

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5
Q

how do g protein coupled receptors work?

A

NT binds to this receptor that activates second messenger system that can open a channel or cause other changes to take place in the cell, (eg, dna being transcribed and new proteins being made)

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6
Q

what is the main difference between a NT and neuromodulator

A

serving the function of being released at a anatomically specialised location to have localised and specific effect, while NM are sort of a bit more all over the place

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7
Q

can the same molecule act as both a NT and NM?

A

yes

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8
Q

in regards to NT and NM, what is the currency, and what is the gov/police?

A

NT’s are currency (excitatory or inhibitory)

NMs are more the police (serotonin, dopamine, noradrenaline etc)

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9
Q

which is excitatory, which is inhibitory out of glutmate and gaba?

A 
glutamate = excitatory 
gaba = inhibitory
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10
Q

NMs alter what at the pre-synapse? they alter what at the post synapse?

A

pre: NT release
post: NT action (excitability/firing pattern)

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11
Q

for drugs to have an effect, what do they HAVE to do?

A

dock onto a receptor

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12
Q

how do drugs have an effect on receptors?

A

they mimick natural NTs or NMs

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13
Q

drugs acting as agonists do what?

A

activate the receptor like the natural compound does

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14
Q

drugs acting as antagonists do what?

A

block the receptor and prevent the natural compound from activating the receptor

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15
Q

is the process from synthesis to NT action slow or fast ?

A

the synthesis is thought to be slow, but the NT action is very fast as it is sitting, waiting for release

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16
Q

what are the most common NTs in the CNS?

A

Glutamate and GABA

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17
Q

what makes ‘true’ NT?

A

directly affecting the likelihood of the post synaptic Neuron firing

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18
Q

what is released by ALL excitatory neurons?

A

Glutamate

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19
Q

estimated that over half of all brain synapses release what?

A

glutamate

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20
Q

what actually is glutamate?

A

glutamic acid

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21
Q

is glutamate used as a NT in its raw form?

A

yes

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22
Q

is glutamate an amino acid?

A

yes

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23
Q

why does glutamate as an amino acid still need to be synthesised in the brain despite it already being a NT?

A

because this amino acid cannot pass through the blood barrier

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24
Q

what is glutamate synthesised from?

A

glutamine

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25
Q

T or false, excitatory connections are not point to point.

A

false

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26
Q

how many glutamate receptors are there? what are they all called?
specify which are ion channels (ionotropic) and which are g protein coupled (metabotropic)

A 
4
ion channels 
NMDA receptor
AMPA receptor 
Kainate Receptor

g protein coupled
metabotropic glutamate

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27
Q

how many different binding sites are on the NMDA receptor?

A

6.

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28
Q

what is glycine?

A

an amino acid

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29
Q

if the NMDA receptor is open, what channel does it open, allowing what to flow through it?

A

calcium channel

Ca2+

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30
Q

the NMDA receptor only works if what molecule is attached?

and if what is not bound to the inside?

A

glycine

magnesium cannot be bound to the inside

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31
Q

alcohol is what an an NMDA receptor? resulting in?

A

antagonist, resulting in the NMDA receptor being blocked

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32
Q

reduction on glutamate as a result of alcohol is believed to contribute to what?

A

general sedative effects and memory effects

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33
Q

while alcohol is an NMDA antagonist, what is it also?

what does this lead to?

A

it is also an agonist for GABA

further brain inhibition

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34
Q

which two drugs in addition to alcohol affect NMDA receptors? are they antagonists or agonists?

A

Phencyclidine (PCP) and ketamine

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35
Q

both ketamine and PCP cause what?

A

dissociative hallucinations

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36
Q

what are dissociative hallucinations?

A

people feel disconnected, but do not have “sensory overload” like other hallucinogens do

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37
Q

can ketamine kill someone?

A

no, it does not harm the actual body, but there is a risk of suicidal behaviour

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38
Q

what is psychosis? what are the symptoms of it?

A

not a diagnosis, but a cluster of symptoms

  • delusions
  • hallucinations
  • depression
  • anxiety
  • suicidal thoughts or actions
  • disorganised speech
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39
Q

what is the percentage of population experiencing psychosis?

A

around 3%

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40
Q

is there a link between glutamate and psychosis?

A

some have suggested a link but there is much more to it

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41
Q

what does NMDA-R encephalitis involve?

A

inflammation of the brain caused by autoimmune response to NMDA receptors

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42
Q

NMDA receptor is crucial for what?

A

learning, memory, perception and synaptic plasticity in general

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43
Q

what have large schizophrenia studies identified?

A

likely that the NMDA receptor gene is likely relevant to dev of schizophrenia

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44
Q

what is the primary inhibitory NT?

A

GABA

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45
Q

what does gaba stand for?

A

gamma - amino - butyric - acid

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46
Q

what does GABA do?

A

decreases likelihood of post synaptic neuron firing

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47
Q

what is the importance of GABA and inhibitory NTs

A

keeps the brain under wraps, otherwise there would be constant firing which is bad (seizures)

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48
Q

How does gaba help neurons fire?

A

it plays important role in the selectivity of neurons firing

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49
Q

what is GABA produced from

A

glutamic acid

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50
Q

how many types of gaba receptors are there? what are they called and what type of receptor are they?

A

2
GABA a receptor (ion channels)
GABA b receptor (g protein coupled)

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51
Q

how many people in Aus experience seizure disorders?

A

400,000

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52
Q

what is a generalised seizure?

A

a seizure that is widespread and involves most of the brain

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53
Q

what is a partial seizure?

A

seizure that is restricted to small part of the brain

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54
Q

what is a complex seizure?

A

a seizure where the individual loses consciousness

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55
Q

what is a simple seizure?

A

a seizure where changes in consciousness can happen, but no loss in consciousness takes place

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56
Q

the majority of genes that have been found to be involved in seizures are linked to what?

A

ion channels, thus influencing the level of positive or negative charge in the brain that drive action potentials

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57
Q

what are the two main nuclei responsible for the synthesis and release of dopamine?

A 
substantia nigra (SN)
ventral tegmental area (VTA)
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58
Q

T or F?

the substantia nigra and the ventral tegemental area can release both dopamine and another NT?

A

false

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59
Q

what is tryrosine? where is it found? what is it/what does it do?

A

amino acid
found in food
it is the building block of dopamine

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60
Q

what is tryrosine hydroxylase?

A

it is a synthesis enzyme for tryrosine

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61
Q

what does Tryrosine Hydroxylase turn tryrosine in to?

A

DOPA

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62
Q

what synthesis enzyme turns DOPE into dopamine?

A

Amino acid decarboxylase

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63
Q

if dopamine is synthesised by dopamine beta-hydroxylase, what does it become?

A

noradrenaline

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64
Q

what are the three variations of elements in the dopamine synthesis?

A

Tryrosine
DOPA
dopamine

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65
Q

What is L-DOPA ? what does it do?

A

a synthetic version of DOPA that can be synthesised to Dopeamine

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66
Q

what is the cause of parkinson’s?

A

death of dopamine cells in substantia nigra

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67
Q

what are symptoms of parkinson’s?

A

motor tremor, cog impairments, dementia and overall reduced exec. function

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68
Q

what are some potential side effects of receiving treatment for parkinson’s?

A

impulsively, gambling, hyper-sexuality

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69
Q

what is the use of reward prediction error

A

provides us with explanation of how dopamine works

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70
Q

what does dopamine actually code?

A

not the reward itself, but rather the expectation or unexpectedness of the reward

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71
Q

what are “real” rewards

A

food and sex

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72
Q

what are “symbolic” rewards?

A

money

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73
Q

what are “virtual” rewards?

A

points in a game

74
Q

in gambling, what adds to the boost of dopamine?

A

the unpredictability of it

75
Q

how is drug addiction defined?

A

a chronic relapsing disorder which consists of compulsive pattern of drug seeking and drug taking behaviour

76
Q

what are two key things that make an “addiction”

A
  • takes place at expense of other activities

- persists despite adverse consequences

77
Q

what does cocaine do to dopamine release? what is the result?

A

blocks the re-uptake of dopamine transmitters after they have been released from the pre synaptic neuron, thus increasing the dopamine signal as more dopamine NTs are left in the synapse

78
Q

what are the two main dopamine drugs

A

cocaine and amphetamine

79
Q

what are the two types of amphetamine drugs? which is more pure

A

ice and speed

ice is most pure and speed is less pure

80
Q

what do amphetamines do to dopamine release, what is the result?

A

they reverse the re-uptake of dopamine NTs, resulting in even more dopamine being released into the synapse compared to simply blocking the re-uptake

81
Q

how do addictive drugs “hijack” the reward response?

A

because the drug releases dopamine, these drugs are coded by the brain as even better than expected

82
Q

what influences how addictive dopamine drugs are ?

A

the faster the DA release, the more addictive

83
Q

in dopamine drugs, what influences the greatness of the high experienced?

A

the amount of DA released

84
Q

what are the 2 “problems” of how addiction takes place?

what is the result?

A
  1. drugs initiate “wanting”
  2. cognitive (top down) processing is reduced by impaired function of the prefrontal cortex, which is caused by excessive dopamine
    loss of top down control contributes to loss of control over urge to take drugs
85
Q

what is the more common name for methylphenidate?

A

Ritalin

86
Q

what does Ritalin do in the brain? what is it used to treat?

A

it inhibits the re-uptake of dopamine and noradrenaline and is a treatment for ADHD

87
Q

what is the base amino acid for noradrenaline?

A

Tryrosine

88
Q

what does the enzyme monoamine oxidase do?

A

breaks noradrenaline down to an inactive metabolite, thus ending the stream of the dopamine and noradrenaline

89
Q

if noradrenaline undergoes one more synthesis step in the adrenal glands what is released?

A

the hormone adrenaline is produced

90
Q

noradrenaline is generated from… ?

A

the locus coeruleus

91
Q

how many neurons does the locus coeruleus contain?

A

around 30,000

92
Q

what is norepinephrine ?

A

exact same thing as noradrenaline

93
Q

when do neurons in the LC fire?

when are they practically ‘silent’?

A

during highly aroused situations, eg transient noxious event or extremely positive stimulus
- during REM sleep

94
Q

what are the 4 f’s?

A

Fight, flight freeze fornicate

95
Q

what can sustained LC/NA activity lead to?

A

stress

anxiety

96
Q

what can inappropriate spikes in LC/NA lead to?

A

panic attacks

97
Q

how long do symptoms have to show for for anxiety to be diagnosed?

A

6 months

98
Q

at moderate levels of LC activity, what does noradrenaline do ?

A

acts to consolidate decisions

99
Q

what is the overall theory that aims to describe noradrenaline’s existence? how does it do this?

A

buys the brain a few seconds to actually act on the decisions that are made. it essentially shuts down the competing alternatives, so decisions are not changed immediately

100
Q

what seems to happen with noradrenaline in the LC after every decision? what does this allow?

A

neurons fire after every decision, when a behavioural response is selected and executed
this is followed by a period where those neurons are inhibited
this allows the selected behaviour to be exploited

101
Q

what influences how big a noradrenaline burst is?

A

how salient the stimulus is

102
Q

what happens in the absence of a burst of firing of noradrenaline?

A

the baseline levels of firing of NA increase, and there is a gradual build up of NA throughout the brain

103
Q

pupil dilation reflects what?

A

activity in the LC

104
Q

pupil constriction is driven by..

A

ACh

105
Q

t or F… there is a pupil dilation at the time of the switch during perceptual rivalries

A

True

106
Q

is noradrenaline involved only in motor decisions? or cognitive/internal decisions as well? what study showed this?

A

both

rock paper scissors dilation study

107
Q

what is locked in syndrome?

A

a stroke in deeper regions of the brain where the person is completely paralysed, but have relatively normal brain functioning

108
Q

T or F? NA and the LC play different roles in perceptual/cognitive decisions, and behaviour like optimising a balance between exploitation and stability?

A

False

109
Q

what is 5-hydroxytryptamine (5-HT)?

A

serotonin

110
Q

is serotonin (5-HT) a neuro modulator or NT ?

A

NM

111
Q

reduction in serotonin can lead to?

A

sadness, depressed states

112
Q

neurons that release and synthesise serotonin are located in the….

A

raphe nucleus

113
Q

what does “raphe” mean

A

midline

114
Q

True or false, serotonin has many receptor subtypes

A

true

115
Q

how does the one compound (serotonin) affect various things like temperature function, appetite regulation etc

A

because of all the different types of receptor subtypes

116
Q

true or false, drugs often activate lots of receptor subtypes

A

false, they are often more selective

117
Q

what is tryptophan? where is it found?

A

an amino acid found in cheese, chicken and chocolate

118
Q

what is the amino acid required for serotonin?

A

tryptophan

119
Q

what is the name of the enzyme that synthesises tryptophan to form serotonin?

A

tryptophan hydroxylase (TPH)

120
Q

monoamine oxidase breaks down what compounds?

A

serotonin, dopamine and noradrenaline

121
Q

what are the requirements according to DSM-V to diagnose depression

A

5 of the 9 symptoms
persisting over 2 week period
at least one of the symptoms is depressed mood or loss of interest/pleasure?

122
Q

what was removed in DSM-5 as a symptom of depression?

A

grief/bereavement

123
Q

what are the percentages of men and women who will experience depression?

A

women; 10-25%

men: 5-12%

124
Q

how much is depression estimated to cost aus in health care a year?

A

over 15 billion

125
Q

when does 1st onset of depression often occur?

A

around 15 to 18 years old

126
Q

PET studies show what?

A

receptor bindings

127
Q

what have PET studies showed regarding depression

A

serotonin receptors are relatively reduced in depressed patients

128
Q

a gene involved in transportation of serotonin is linked to what?

A

increased risk of developing depression

129
Q

how are serotonin and stress related?

A

serotonin function is important in managing the feedback control of the brain’s stress response

130
Q

how much more likely is depression after a stressful event?

A

5-6x

131
Q

what are some serotonin anti depressant drugs?

A

citalopram, fluoxetine, paroxetine, sertraline

132
Q

what are SSRI’s?

A

selective serotonin re-uptake inhibitors (serotonin antidepressants)

133
Q

how do SSRI’s work?

A

they selectively block the re-uptake of serotonin, meaning that there are more serotonin NM’s in the synapse, allowing for more NM’s to attach to receptors

134
Q

how long does it take for SSRIs to cause therapeutic effects? how long does it take for these to reach the brain if they are taken orally?

A

often takes weeks, but reaches the brain after approx. 1 hour

135
Q

what does long latency onset describe?

A

it describes why it takes SSRIs a relatively long amount of time to take effect

136
Q

True or false, SSRIs can promote new brain cell growth

A

true

137
Q

despite SSRIs promoting new brain cell growth, they do not offer any neuro protective benefits, t or f?

A

false

138
Q

in healthy people, what has prozac been seen to do?

A

increase empathy and prosocial behaviour

139
Q

what do monoamine oxidase inhibitors do? what is the result?

A

blocks the breakdown of serotonin.

there is more serotonin in the persons system

140
Q

what does cheese syndrome involve

A

potential cause of death due to eating foods with high tryptophan amounts, leading to lethal levels of serotonin

141
Q

what are the 4 non traditional NTs?

A

peptides, nucleoids, lipids and gases

142
Q

what do peptides consist of?

A

2 or more amino acids

143
Q

how are peptides “synthesised”?

A

they are not traditionally synthesised, as they are actually broken down from larger compounds (poly - peptides)

144
Q

are peptides NMs, or hormones acting as NTs?

A

they can be both in different circumstances

145
Q

what is the most commonly known family of peptide NTs

A

endogenous opioids

146
Q

areas where the highest density of opiate receptors are located are associated with what?

A

pain reception

147
Q

what does endogenous opioid mean?

A

something occurring internally in the brain that is like opium

148
Q

what does opiate mean?

A

artificial sources of opium including morphine, heroin, and opium

149
Q

how can heroin affect health/cause death?

A

through respritory failure, but is not neurotoxic

150
Q

how does heroin act in the brain? what is the result?

A

it is a full agonist, therefore attaching to receptors the same way as a natural compound would

151
Q

what are 3 heroin dependency treatment drugs

A

Buprenorphine , naloxone, methadone

152
Q

how does Buprenorphine treat heroine dependence?

A

it is a partial agonist. it has the same affect as heroin but nowhere near as much, thus, it blocks the affect of heroin on the receptors and blunts the impact of the drug

153
Q

how does naloxone treat heroine dependence?

A

is a full antagonist, thus rapidly blocking heroin receptors

154
Q

how does methadone treat heroine dependence?

A

it is also a full agonist, but has a much smaller time course than heroin, as such has a more controlled/stable effect

155
Q

what are lipids?

A

naturally occurring molecules like fats and waxes

156
Q

lipds are hydrophobic, what does this mean?

A

they fear water

157
Q

what are the main biological function of lipids?

A

energy storage and structural components of cell membranes

158
Q

what are the best known lipid NTs?

A

endocannabinoids

159
Q

what are the 2 known cannabinoid receptors?

A

CB1 and CB2

160
Q

where do CB1 receptors sit?

A

on the pre-synaptic neuron

161
Q

activation of the CB1 receptor does what ? what is the effect?

A

it shortens the duration of the action potentials in the pre-synaptic neuron, decreasing amount of released NTs

162
Q

regulating CB1 receptors serve to…

A

modulate the modulators

163
Q

what is the active compound in marijuana?

A

THC (tetrahydrocannabinol)

164
Q

what are some effects from consuming THC/marijuana

A

changes in appetite, time perception, “underachievement”

165
Q

therapeutically, what does THS/marijuana offer?

A

reduce nausea, relieves asthma attacks, decreases pressure in the eyes in glucoma

166
Q

what are nucleic acids?

A

the hereditary controlling parts of all living cells eg dna and rna

167
Q

what are nucelosides? how are they obtained?

A

a subunit of nucleic acids

by chemical/enzymatic breakdown

168
Q

true or false, nucleosides are also modulators to the modulators?

A

true

169
Q

what is an example of nucleoside?

A

adenosine

170
Q

is adenosine an inhibitory or excitatory NT?

A

inhibitory

171
Q

adenosine forms from the breakdown of what?

A

adenosine triphosphate (ATP)?

172
Q

ATP is responsible for what?

A

is primary energy source in cells for transport systems and enzymes

173
Q

high postsynaptic firing rate where adenosine is the primary NT leads to what ?

A

increased sleepiness and supreses arousal throughout the day

174
Q

drugs that are relevant to countering adenosine is…

A

caffeine

175
Q

how does caffeine work to counter adenosine?

A

it acts as a receptor antagonist, blocking adenosine receptors

176
Q

what is a soluble gas ?

A

gases that dissolve in fluid

177
Q

which two gases are used as NTs in the brain?

A

nitric oxide, and carbon monoxide

178
Q

what is nitric oxide in the cardiovascular system? that can do what?

A

a signalling molecule

it dilates blood vessels, which can increase blood flow to various areas of the brain

179
Q

what amino acid is nitric oxide produced from? by how many neurons?

A

arginine

subpopulation of 1-2% of neurons in the cortex

180
Q

how is nitric oxide very different to traditional NTs

list 3 reasons

A
  • not synthesised and stored in vesicles
  • NO is produced all throughout the cell and simply defuses out of the cell
  • it does not activate receptors on the next cell, but simply enters it
181
Q

how do NMs actually modulate?

A

they modulate the function or sensitivity of pre and post synaptic in slower and more global signals

Bio Psych (5 decks)

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