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Brain PD > week 4 part 2 > Flashcards

week 4 part 2 Flashcards

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1
Q

What are cannabinoids?

A

terpenophenolic constituents of the hemp plant (cannabis sativa)

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2
Q

What has cannabinoids been used for?

A

over 4000 years as a recreational drug due to its mind-altering effects

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3
Q

What is the primary psychoactive constituents of cannabis?

A

Δ8-tetrahydrocannabinol (Δ8-THC)

Δ9-THC

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4
Q

What has cannabinoids been shown to produce?

A

a unique syndrome of effects on the behaviour of humans and animas that include:

  1. disruption of short-term memory
  2. cognitive impairments
  3. a sense of time dilation
  4. mood alterations
  5. enhanced body awareness
  6. reduced ability to focus attention
  7. filter out irrelevant information
  8. dicoordination
  9. sleepiness
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5
Q

What did Queen Victoria use cannabinoids for?

A

Analgesics effect

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6
Q

What was cannbinoids used to treat?

A

seizures

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7
Q

How many compounds does cannabis have?

A

30 compounds

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8
Q

What are some examples of effects cannabis has on humans?

A
  1. Euphoria
  2. Heightened sensory perception
  3. Distorted sense of time and space
  4. Hallucinations
  5. Drowsiness, sleep
  6. Impairment of memory
  7. Increased motor activity followed by inertia and ataxia
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9
Q

What did animal research show?

A

potential for cannabinoid dependence exists

cannabinoid withdrawal symptoms can be observed

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10
Q

What does injection of THC into mice cause

A
  1. Inhibition of spontaneous locomotor activity
  2. Antinociception (analgesia)
  3. Hypothermia
  4. Immobility
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11
Q

Where are endocannabinoids produced?

A

In the body when needed, under stress, or in response to synaptic activity

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12
Q

What are the most studied endocannabinoids?

A
  1. Anandamide (AEA)

2. 2-AG

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13
Q

what are endocannabinoid?

A

considered to be dominant

agonist for CB1 and CB2 receptors, with higher affinity to CB1 binding

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14
Q

What did Allyn Howlett demonstate?

A

Cannabinoids cause inhibition of adenylyl cyclase in neuroblastoma cells

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15
Q

What did this suggest?

A

Cannabinoids may exert their effect by binding to a GPCR

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16
Q

What is CP 55,940?

A

Cannabinoid in which mimics the effects of naturally occuring THC

A full agonist at both CB1 and CB2 receptors

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17
Q

What was [3H] CP 55,940 used for?

A

It is a radiolabelled synthetic cannabinoid which is 10-100 times more potent in vivo than delta 9-tetrahydrocannabinol and used to characterise and localise a specific cannabinoid receptor in brain sections

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18
Q

What did autoradiography show?

A

in all species very dense binding was found in the

  1. Globus pallidus
  2. Substantia nigra
  3. Pars reticulata
  4. Molecular layers of the cerebellum and hippocampal dentate gyrus
  5. stratium
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19
Q

For autoradiography where did very low and homogenous binding characterise?

A
  1. Thalamus

2. most of the brain stem

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20
Q

Where are CB1 receptors abundant in?

A

Putamen part of the relay system within basal ganglia that regulates body movement

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21
Q

What is the function of cerebellum?

A

Coordinates body movement

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22
Q

What is the function of hippocampus?

A

Involved in learning, memory and response to stress

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23
Q

What is the function of cerebral cortex?

A

Concerned with the integration of higher cognitive functions

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24
Q

Where is CB2 receptors located?

A

cells of the immune system

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25
Q

Where are both CB1 and CB2 found?

A

Alpha clade of the rhodopsin group of GPCRs

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26
Q

What can immunocytochemical methods be used to localise?

A

CB1 proteins in the brain

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27
Q

What does immunoctyochemical studies using different antibodies reveal?

A

Generally consistent pattern of staining that corresponded with the distriubtion of cannabinoid binding sites

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28
Q

What did these studies provide?

A

Important evidence that CB1 is likely to be mediated the effects of cannabinoids in the brain

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29
Q

What did determination of the neuroanatomical distribution of CB1 receptor in the brain provide?

A

A framework for interpreting the behavioural effects of cannabinoids

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30
Q

Wjat was CB1 knock out mice been generated independently shown to be?

A

unresponsiveness to cannabinoids in a standard set of behavioural assays

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31
Q

Where is the highest concentration of cannabinoid binding sites?

A
  1. Basal ganglia and cerebrellum

2. Regions of the brain that are involved in the inititation and coordination of movement

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32
Q

Where is low level or no binding present?

A
  1. Brainstem (medulla and pons)

consistent with the lack of cannabinoid activity on vital respiratory and cardiovascular function

33
Q

Where is CB1 receptor targeted?

A

To axons and terminals of neurons, not only in the basal ganglia but probably in all neurons that express the CB1 gene in the brain

34
Q

What is the function of fatty acid amide hydrolase (FAAH)

A

Catalyse hydrolysis of two putative fatty acid amide signalling molecules, oleamide and anandamide

catalyses hydrolysis of 2-AG

participate in inactivation of both anandamide and 2-AG

35
Q

What did measurement of FAAH enzyme activity in eight regions of rat brain reveal?

A

highest concentration: Hippocampus and cortex

Lowest concentration: brainstem and hypothalamus

with intermediate concentration in cerebellum, olfactory bulb, stratium and thalamus

36
Q

Comparisons of the distribution of FAAH in rat brain regions based on enzyme assays and western blotting data revealed a significant overlap with expression of CB1

A

High concentration of FAAH and CB1 are found in both hippocampus and neocortex whilst lower concentration of FAAH and CB1 are found in the brainstem and hypothalamus

37
Q

What 3 brain regions are enriched with both FAAH and CB1?

A
  1. Cerebellum
  2. Hippocampus
  3. Neocortex
38
Q

in cannabunoid signalling where is CB1 located?

A

presynaptically

39
Q

in a model of cannabinoid signalling what does anandamide function as?

A

Retrograde signalling

40
Q

What does retrograde signalling molecule do?

A

modulates (inhibits) the release of ‘classical’ anterograde transmitters by presynaptic terminals

41
Q

What step 1 of retrograde signalling?

A

Anandamide is synthesises and released by the postsynaptic cell

42
Q

What is step 2 of retrograde signalling?

A

Diffuses into the synaptic cleft where it binds to and activates presynaptic CB1-type cannabinoid receptors

43
Q

What is step 3 of retrograde signalling?

A

Activated CB1 receptors cause inhibition of neurotransmitter release from presynaptoc terminals via G-protein-mediated mechanisms involving activations of K+ channels or inhibitions of Ca2+ channels

44
Q

What is step 4 of retrograde signalling?

A

Anandamide dissociates from CB1 receptors and then following uptake into the postsynaptic cell

45
Q

What is step 5 of retrograde signalling?

A

Hydrolysed intracellularly by FAAH

46
Q

Where was CB1-immunoreactivity observed?

A

somata of GABAergic interneurons in the hippocmapus

47
Q

Where is CB2 (and CB1) receptors expressed?

A

Perivascular macrophages and microglia

48
Q

Where is CB2 expression enhanced?

A

Following CNS injury and in neuritic plaques in Alzheimer’s disease

49
Q

What does microglia cells use cannabinoids as?

A

signalling molecule

50
Q

What is anandamide?

A

'’Bliss molecule’’

A substance produced by our body to bind to cannabinoid receptots

51
Q

What is key to making anandamide?

A

NAPE-PLD

52
Q

What is one way of making anandamide?

A

from phosphatidylethanolamine FA within membrane and forming PLD

53
Q

How is anandamide synthesised?

A

upon demand from phospholipid precursors in cell membranes in response to rise in intracellular calcium levels

54
Q

Where are enzymes metabolising 2-AG located?

A

Both post-synaptically and pre-synaptically

55
Q

How is 2-AG synthesised?

A

arachidonic acid containing diacylglycerol (DAG) which is derived from the increase of inositol phospholipid metabolism by the action of diacylgylcerol lipase

56
Q

What does CB1 receptor using GPCR reduce?

A

CAMP

decrease ca2+ permeability and inhibit neurotransmitter release

57
Q

What does endocannabinoid cause?

A

depolarisation-induced suppression of excitation

58
Q

What are two related forms of short-term synaptic plasticity of GABAergic and glutamatergic transmission?

A

Depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE)

59
Q

What are DSI/DSE?

A

DSI/DSE are two closely related forms of short-term plasticity, which share the same modes of induction, the same type of retrograde messengers (i.e. endocannabinoids) and similar mechanisms of expression.

60
Q

How does DSI work?

A

classically produced in a brain slice experiment
where a single neuron is “depolarized”
for a period of 1 to 10 secondsAfter the depolarization, inhibitory GABA mediated neurotransmission is reduced.

61
Q

What did experimental evidence suggest?

A

rather large increases in intracellular [Ca2+] are required for the induction of DSI and DSE via the release of endocannabinoids

62
Q

what does PLCbeta 1 serve as?

A

coincidence detector through its ca2+ dependency for endocannabinoid release in hippocampal neurons

63
Q

What occurs in the cerebellum?

A

bursts of parallel fiber (PF) activity evoke endocannabinoid release from Purkinje cell dendrites that results in retrograde synaptic inhibition lasting seconds

64
Q

What do endocannabinoid mediate?

A

transient associative synaptic plasticity

65
Q

What are endocannabinoids?

A

key activity-dependent signals regulating synaptic transmission throughout the central nervous system

66
Q

What are endocannabinoids involved in?

A

Neural functions ranging from feeding homesostasis to cognition

67
Q

What is DSI?

A

a transient suppression of inhibitory neurotransmitter release onto a neuron following depolarization of that neuron

68
Q

What is the working model for DSI?

A

Depolarisation of the post-synaptic cell increases dendritic calcium levels which stimulates the production of an endocannabinoid

φ This endocannabinoid is believed to travel retrogradely, from the dendrite, across the synaptic cleft to activate CB1 receptors on the presynaptic terminal and preterminal axon segment. The activated CB1 receptors inhibit calcium channels (and may also stimulate potassium channels or have direct effects on the synaptic vesicle release machinery) thus decreasing neurotransmitter release

69
Q

What is the efficacy of anandamide as a TRPV1 agonist influenced by

A

succession of factors:

  1. Receptor reserve
  2. Phosphorylation
  3. Metabolism and uptake
  4. CB1 receptor activation
  5. voltage
  6. Temperature
  7. PH
  8. bovine serum albumin
70
Q

What does this indicate?

A

endocannabinoid system may play a role in the modulation of TRPV1 receptor activation

71
Q

what does the activation of TRPV1 receptors by anandamide has potential implications in ?

A

treatment of inflammatory, respiratory and cardiovascular disorders

72
Q

What is Retrograde short term depression mediated by?

A

dendritic L-type Ca2+ 2-AG synthesis and presynaptic CB1 actions

73
Q

What is LTD mediated by?

A

mGLUR5 and AEA production - acting on postsynaptic TRPV1

74
Q

Why does the levels of endocannabinoid and/or the expression of cannabinoid receptors in tissue vary?

A

to increases in intracellular calcium concentration, changes in metabolic enzyme expression and availability of phospholipid precursors

75
Q

What does endocannabinoid directly target?

A

hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice

76
Q

What is necessary and sufficient to provide substantial endogenous protection against kainic acid (KA)- Induced seizures?

A

CB1 receptors in glutamatergic hippocampal neurons

77
Q

What does CB1 antagonists given during febrile seizures do?

A
  1. Blocked persistent DSI potentiation
  2. Abolished CB1 upregulation
  3. Prevented long-term limbic hyperexcitability
78
Q

What are CB1 antagonist?

A

Acutely proconvulsant

Brain PD (15 decks)

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