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PCL470 > Cognitive enhancers > Flashcards

Cognitive enhancers Flashcards

1
Q

nootropic drugs

A

enhance cognition in healthy brains

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2
Q

Can drugs increase IQ?

A

No, but they can improve attention

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3
Q

What NTs are involved in the arousal system, i.e. promoting activity of which NTs promotes wakefulness?

A

Acetylcholine, histamine, NE, 5 HT, orexin
HANSO

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4
Q

reticular formation

A

arousal system

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5
Q

which NT promotes sleep

A

adenosine
- accumulates when brain is awake (from ATP use) and clears during sleep

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6
Q

What does the viPOA (slow-wave-sleep-on) region inhibit?

A

viPOA inhibits:
- the arousal system (and vice versa the arousal system inhibits the viPOA)
- orexinergic neurons in the LH

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7
Q

What signals modulate the LH orexinergic neurons?

A

biological clock (time of day, light) - activates
hunger signals - activate
satiety signals - inhibit

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8
Q

orexin

A

Regulates arousal and hunger

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9
Q

Psychostimulants

A

drugs that promote wakefulness and attention
- often increase motor activity as well (undesired)

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10
Q

what kind of drug is caffeine

A

psychostimulant

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11
Q

how does caffeine work

A
  • blocks adenosine receptor which stops adenosine from signalling that you’re sleepy
  • also inhibits phosphodiesterase which indirectly increases NE and E
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12
Q

Phosphodiesterase

A

enzyme that breaks down cAMP
- inhibited by caffeine

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13
Q

Why are NE and E signalling levels increased with caffeine intake

A

NE and E act through Galpha-s protein which increases cAMP (when they bind to their receptors, cAMP is increased)
- preventing breakdown of cAMP by inhibiting phosphodiesterase works in same direction as NE and E (more cAMP) so their signal is amplified

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14
Q

dependence vs addiction

A

dependence: body performs best with the drug, would prefer to have it

addiction: compulsion to take drug despite adverse consequences

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15
Q

caffeine adverse effects

A

dry mouth, heart burn, agitation, nausea, diarrhea, insomnia, racing heart

  • a lot of these similar to adrenaline because cAMP (dry mouth, rapid HR)

fatal doses rare but have happened (cardiac arrest)

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16
Q

What happens during slow wave sleep

A

brain increases pumping of fluid - metabolites washed away

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17
Q

Most psychostimulants are…

A

DAT and NET blockers
- ex. cocaine, methamphetamine, amphetamine, and methylphenidate

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18
Q

adderall vs ritalin

A

adderall = amphetamine
ritalin = methylphenidate

19
Q

are psychostimulants addictive?

A

they can be:
cocaine is a psychostimulant and so is meth, but something like ritalin (methylphenidate) isn’t.
Depends on the route of admin and dose (also is individual variation though)

20
Q

Effects of psychostimulants

A

wakefulness, euphoria, suppressed appetite, insomnia, agitation, restlessness, dry mouth, racing heart, GI upset, constipation, grandiosity, paranoia, psychosis

21
Q

Dopamine recycling:
- normal
- on cocaine
- on amphetamine

bonus: which drugs act same way as last two on DAT?

A

normal
- VMAT (vesicular monoamine transporter) packages DA
- DAT takes up DA from synapse to be repackaged

cocaine
- DAT is plugged so DA is accumulated in synapse and activates more DRs

Amphetamine
- reverses the DAT, DA from cytosol actually goes into synapse
- amphetamine also displaces DA from the vesicles which pushes DA into cytosol (this flips the conc gradient and allows VMAT to reverse)

BONUS: methylphenidate does same as cocaine and plugs DAT, methamphetamine does same as amphet

22
Q

drugs like amphet, cocaine, methylphen act on which transporter(s)?

A

mostly act on DAT but also do the same thing to SERT and NET, just to a lesser extent

23
Q

Neuropathology of Alzheimer’s Disease (AD)

A
  • amyloid plaques and neurofibrillary tangles are clearly visible in microscopy
  • gross diffuse atrophy of brain and loss of neurons, neuronal processes, synapses
  • degeneration in temporal and parietal lobes, as well as part of frontal cortex
24
Q

Which NT reduced in AD? Elevated?

A

Acetylcholine is reduced as well as 5HT and NE

glutamate usually elevated

25
Q

Debate with beta amyloid plaques?

A

Are these biomarkers causative or correlational?
- shown that reducing beta amyloid plaques doesn’t work

26
Q

Pharmacotherapy for AD

A
  • cholinesterase inhibitors (prevent breakdown of Ach)
  • low-affinity NMDA receptor antagonists (to slightly reduce glutamate signalling)
27
Q

why are cholinesterase inhibitors prescribed for AD?

A

reduction in acetylcholine (ACh) by loss of cholinergic neurons throughout brain associated with AD:
- cholinesterase inhibitors elevate Ach levels, allows more to bind (doesn’t actually fix prob which is loss of cholinergic neurons)

28
Q

Types of cholinergic receptors

A

`muscarinic receptors - are GPCRs
nicotinic receptors - are sodium channels

29
Q

Unique characteristic of acetylcholine

A

only NT whose actions are terminated by enzyme degradation in the synaptic cleft
- acetylcholinesterase in synapse rapidly metabolizes Ach to choline which is retaken up and used to produce more

30
Q

Acetylcholine signalling (major systems)

A
  • ACh is the NT at the neuromuscular junction
  • ACh is NT of the parasympathetic NS
    (ACh is also used by sympathetic NS at the sympathetic ganglia but then secondary neurons use NE and E)
31
Q

Reversible vs irreversible cholinesterase inhibitors

A
  • reversible ones are cholinesterase drugs prescribed that increase cortical Ach
  • irreversible inhibitors are POISONS (sarin gas, organophosphate insecticides)
32
Q

Examples of cholinesterase inhibitors

A
  • donepezil
  • galantamine
  • rivastigmine
33
Q

How is efficacy of cholinesterase inhibitors tested

A

objective/subjective measures

activities of daily living: bathing, dressing, eating, moving from car to bed, voluntary urinary and fecal discharge, using toilet, walking

looks at disturbances in memory, language, and attention

34
Q

Adverse effects of cholinesterase inhibs

A

nausea, GI cramping, vomiting, diarrhea, bradycardia, anorexia, vivid dreams

35
Q

Do cholinesterase inhibitors help healthy people?

A

no - they help memory recall in AD patients but not healthy brains

36
Q

Five receptor types for glutamate

A
  • AMPARs (Na channels) MAJOR ONE
  • Kainate Rs (Na channels)
  • NMDARs (Na and Ca channels)
  • mGluRs (GPCRs)
  • delta receptors (Na channels)
37
Q

Learning = forming a memory = _____

A

strengthening the connections between those neurons that together make the memory

38
Q

NMDARs are required for…

A

LTP
- calcium influx triggers cascades that lead to increased AMPA receptors at synapse (more sensitive)

39
Q

What’s special about NMDARs

A
  • they let in sodium - to depolarize the neuron -
    and calcium - allows for intracellular changes
  • requires glutamate AND coagonist glycine to open
  • has a magnesium ion in its pore which has to be expelled by prior depolarization of membrane
40
Q

competitive antagonists for NMDARs bind at____ and non-competitive antagonists are ___

A
  • the glutamate binding site
  • NMDAR channel blockers
41
Q

Memantine

A
  • low-affinity, non-competitive NMDAR antagonist (so blocks the pore)
  • binds at the PCP site
  • has VERY fast on and off which is how it doesn’t impair cognition but still reduces glutamate signalling slightly
  • Memantine has been associated with reduced rate of deterioration on global, cognitive, and functional measures (also behavioural improvements)
  • safe for use with AChIs
42
Q

How does memantine reduce cognitive decline?

A

Might seem counterintuitive because NMDARs needed for learning and memory, HOWEVER excessive activation leads to excitotoxicity

  • neurons trigger glutamate as they die
  • surrounding neurons overexcite and die

memantine has neuroprotective effects - blocks enough NMDA to prevent excitotoxicity but leaves enough for learning and mem

43
Q

adverse effects of memantine

A

(recall this is a drug for AD - NMDAR antagonist at PCP site)

  • headache, body ache, fatigue, dizziness

PCL470 (14 decks)

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