lecture 2 - noradrenaline, acetylcholine and alertness Flashcards

1
Q

the brain stem
the thalamus
what are these important in

A

-these two areas are really important in alertness and arousal

  • Basic behavioural functions: sleep/wake cycle, reflexive responses to sensory input

-areas present in much less evolved creatures

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2
Q

what is the ascending reticular activating system (ARAS)

-how does this system work
-which neurotransmitters are involved
-what does it result in

A

-ascending comes from parts of the brain that are old and lower down (in the brain)-go upwards
-reticular - type of cells

Axons of ARAS project from
brain stem to higher cortical
regions (incl. via thalamus)
-cell bodies in brainstem projecting their axons elsewhere and making synapses

  • Source of major excitatory
    neurotransmitters:
    noradrenaline (NA) &
    acetylcholine (ACh)- cause new action potentials where they arrive
  • Regulates general levels of
    cortical arousal, alertness &
    consciousness
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3
Q

what is the link between ARAS and extraversion

A

Eysenck (1967) suggested a link between ARAS & extraversion:
extraverts have low ‘resting’ ARAS activity (so they seek out more
stimulation); introverts have high ‘resting’ ARAS activity (so they avoid
overstimulation)

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4
Q

difference between noradrenline and acetylcholine systems and the gaba and glutamate systems

A

cells that produce glutamate and gaba can be found all over the brain and all over the cortex -main information system with excitation and inhibition
-however na and acy , their cell bodies are just down there in the brain stem - are not located / widely distributes across the brain, they have specific regions

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5
Q

what are the anterior and posterior attention systems in our cortex

A
  • Anterior (frontal) system = ‘top-down’ (cognitive), voluntary,
    controlled, task- or goal-driven attention, ‘executive functions’
  • Posterior (parietal) system = ‘bottom-up’ (sensory), involuntary,
    automatic, stimulus-driven attention, ‘orienting reflex’
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6
Q

definitions
-alertness
-attention
-arousal

A
  • Alertness: generalised readiness to process stimuli and
    respond. Measured by subjective feelings or simple
    psychomotor tasks.
  • Attention: enhanced processing of specific/selected
    stimuli. Measured by behavioural performance – e.g.,
    RT/accuracy.
  • Arousal: physiological activation in autonomic nervous
    system (e.g., skin conductance) or central nervous
    system (using EEG, fMRI, etc.); sleep/wake cycle
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7
Q

how can we measure alertness

A

1) simple detection / reaction time tasks
2) vigilance (or continuous performance) tasks

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8
Q

-simple detection / reaction time tasks
- measuring tonic and phasic alertness

A

-eg ‘press when you see X’
-means reaction time depends on average alertness during task (tonic alertness)
-eg ‘press when you see the x; the dot will warn you that its about to appear
-means the rt depends on temporary increase in alertness following warning cues (‘phasic’ alertness)

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9
Q

vigilance (or continuous performance) tasks
-what kind of attention does this require

A

show people a series of letters one at a time
Respond only to pre-specified
target stimulus/sequence (E.g.
“only respond to X”;
or “only respond
if same letter is presented twice in
succession”.)
* Targets are rare (e.g. 5% of
trials); presentation is rapid

Requires sustained attention (= vigilance) & is more cognitively
demanding than simple RT task (e.g. additional demands on working
memory & response inhibition); involves anterior system

  • Measures: average RT to targets, errors of omission (missed
    targets) & errors of commission (false alarm; responding to non-
    targets)
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10
Q

what are stimulants
-what do these drugs do

A

Drugs that increase alertness/arousal are called
stimulants – examples include caffeine, nicotine,
amphetamines & methylphenidate (Ritalin)

These drugs mimic or enhance the effects of
noradrenaline and/or acetylcholine in the brain – i.e.,
they are noradrenergic or cholinergic agonists.

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11
Q

what are sedatives

A

Drugs that reduce alertness/arousal are sedatives –
examples include GABA agonists (see previous lecture),
noradrenergic beta-blockers, & cholinergic antagonists
(e.g. scopolamine).

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12
Q

noradrenaline
-where is their main source
-what do they do, what does it allow for

A

noradrenaline comes from cells whose cell bodies are located in a particular part of the brain

Neurons in the locus coeruleus
(LC, ‘blue spot’) in the brain stem
are main source of NA. (they look blue under a microscope)

  • They project to many different
    ‘higher’ brain areas (incl. via
    thalamus)
  • These projections allow LC to
    modulate general levels of brain
    arousal & alertness

Increased activity in LC (therefore, increased release of NA) is
also associated with stress, anxiety, & panic attacks

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13
Q

drugs that increase NA- ergic activity (noradrenaline activity)
-how do these drugs do this
-what effect do these drugs have

A

Amphetamines are synthetic drugs, derived from ephedrine or pseudoephedrine (found in the
Ephedra plant)

Amphetamines increase release and block reuptake of noradrenaline (& dopamine)
imagine the synapse, having all the noradrenaline stored in the vesicles , amphetamine will cause that to be released into the synapse more than it would be otherwise. once its in the synapse they block it from being taken back up into the presynaptic cell. more of it in the synapse, and its there for longer.

These have psychostimulant (alertness-increasing)
& anxiogenic (anxiety-producing) effects

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14
Q

amphetamines - acute effects
-subjective effects
-effects on task performance at low and high doses

A

Subjective effects – feelings of alertness & energy;
increased anxiety at higher doses.

Task performance
– Low dose: improved performance in simple psychomotor & vigilance tasks

– High dose: impaired task performance; increased
distractibility

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15
Q

explain the inverted U relationship between arousal and task performance
-why does this effect occur?

A

Under-arousal (fatigue, boredom) AND over-arousal (anxiety, stress, excitement) can both impair performance

Therefore, increasing arousal with a
psychostimulant can improve
performance (if arousal low) OR impair performance (if arousal high).

  • This effect may be due to arousal
    narrowing the attentional focus, which can be too narrow for optimal
    performance (esp. with complex tasks) (you dont want to be too concentrated or focused on something complex like driving as you have to focus on quite a few things at the same time)
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16
Q

drugs that reduce NA ergic activity

A

These have sedative (alertness reducing) & anxiolytic
(anxiety reducing) effects.

  • Noradrenergic beta-blockers (e.g., propranolol; mainly used clinically for effects on blood pressure & heart) are β-receptor antagonists.
17
Q

Acetylcholine (ACh)
-what neurons release this
-where do they project from, and what do they do

A

Cholinergic neurons release
acetylcholine (ACh).

there cell bodies are in the midbrain and basal forebrain

  • Cholinergic neurons project
    from basal forebrain nuclei
    throughout entire cortex.
    Activation of these systems is
    associated with alertness,
    attention, learning &
    memory.

Cholinergic nuclei in midbrain (upper brain stem) project to
thalamus and regulate arousal & sleep/wake cycle.

18
Q

what are drugs that reduce cholinergic activity
-what do these drugs cause
-example of these drugs

A

Cholinergic receptor antagonists
block effects of ACh at receptors.
Therefore, they reduce subjective
alertness.

  • These drugs cause general
    cognitive impairment (‘delirium’)
    similar to Alzheimer’s disease. (a general confusion/disorientation)
  • An example of a cholinergic
    antagonist is scopolamine, which is
    found in various toxic plants (e.g.,
    deadly nightshade family).
19
Q

what drugs increase cholinergic activity

A

-a way to increase the activity is to stop the neurotransmitter being broken down

Cholinesterase inhibitors are used in the treatment of Alzheimer’s disease. (ACh cells in basal forebrain are lost in AD; cholinesterase inhibitors ↑ ACh availability.)

or use cholinergic receptor agonists (nictotine) mimic the effects of ach

20
Q

study which showed scopolamine reducing subjective alertness

A

-they gave scopolamine or placebo and measured how they did on various different cognitive tasks

Wesnes et al, 1988 (Human Psychopharmacology 3, 27-41).
0.6mg sub-cutaneous scopolamine (v. placebo)
- reduced subjective alertness
- increased errors & slower RTs in vigilance task
- impaired memory for word list (all
p < .001), in healthy participants

21
Q

Attention Deficit Hyperactivity Disorder (ADHD)
-affects ___ of population
-which gender is it more common/more frequently detected in
-when do adhd characteristics start to show
-what are the key characteristics

A

ADHD is estimated to affect about 5% of the population.

  • It is more common (or at least more frequently detected) in males
    than females
  • Its characteristics are first present in childhood; these persist
    significantly into adulthood in about 50% of cases.

-Key characteristics: inattention and/or hyperactivity.
* Also can include: forgetfulness; impulsivity; distractibility.

22
Q

what medications are used for ADHD
-what do they do
-what can newer drug treatments do

A

Psychostimulant drugs are often prescribed for ADHD:

– amphetamine (Adderall)
– methylphenidate (Ritalin)

  • These drugs increase levels of both noradrenaline and
    dopamine in the brain
  • Some newer drug treatments more selectively target noradrenaline levels (e.g. atomoxetine, a noradrenaline reuptake inhibitor).
23
Q

describe the study - response to methylphenidate in boys with ADHD Zeiner et all 1999
- sample,
- type of study
- results

A

36 boys diagnosed with ADHD, aged 7-11 years.
– Double-blind, placebo-controlled, crossover (within-subjects)
design. each of the boys did the drug condition and the placebo condition
– Three weeks of daily drug/placebo.

– One week ‘washout’ period in between. to get rid of it and then would start the other treatment

– Assessments were made in final (third) week in each case.

results

-found vigilance was improved, fewer errors in a task where the boys were read out a list of numbers and then got a paper with the same list-which sometimes didn’t match. rare targets that had to be found-fewer missed targets

-motor control task (metal stylus in a maze) errors reduced in that

-working memory task - boys given numbers 1 at a time and add each number to the one they were previously gave. Better accuracy in this

-teacher and parent interviews showed behaviour improved, and less hyperactivity, fewer problems

24
Q

paradoxical effects
-why would a stimulant drug reduce hyperactivity?

A

If ADHD involves abnormally low levels of intrinsic arousal (fitting
with, e.g., low vigilance scores), hyperactivity might be aimed at
increasing arousal to more optimal levels.

  • Increasing arousal with a psychostimulant drug instead could then reduce the need for hyperactivity, as well as improve cognitive functioning.

-ADHD may be extreme end of extraversion personality dimension

imagine people with adhd have a low baseline for arousal. maybe hyperactivity isnt necessarily a core feature of adhd its more of a behavioural response for having adhd- if your arousal is too low you seek for it to by higher by being hyperactive (seems more like a side effect)
may not be true but logically explains it