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NE2 > Arousal Systems > Flashcards

Arousal Systems Flashcards

1
Q

NTs for Coma to Arousal/Wakefulness

A

EAA/ACh

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2
Q

NTs for Arousal/wakefullness to awareness

A

Norepi/5HT

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3
Q

NTs for Awareness to Alertness

A

Dopamine

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4
Q

What do disruptions of consciousness often arise from>

A

Smaller lesions in brainstem, midbrain or hypothalamus

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5
Q

Why can’t those in PVS “wake up”?

A

Their cortical neurons are up to 30mV below threshold (hyperpolarized), so nothing is strong enough to activate the neuron.

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6
Q

Why doesn’t the cortex have intrinsic mechanism for activation

A

Bc they are too hyperpolarized and must rely on ascending influences.

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7
Q

Describe a coma

A

Not awake or aware
No sleep/wake cycles
Absent brain wave changes

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8
Q

Describe PVS

A 
EEG shows sleep/wake cycles
No awareness
reflexive motor response
Cannot elicit volitional response
Hyperpolarized neurons
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9
Q

Describe minimally conscious state

A

EEG shows sleep/wake

Responds to simple commands inconsistently and w/ varying correctness due to neural plasticity

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10
Q

Damage to which areas can lead to coma or PVS

A

Lower brain (pons, midbrain & hypothalamus, diencephalon (especially thalamus))

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11
Q

Where is EAA arousal system

A

Occupies mid-ventral portion of medulla and midbrain.

Arises from parabrachial nuclei in rostral pons

Parabrachial nuclei (medial, intermediate, and lateral) crucial for arousal/activation

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12
Q

Where is cholinergic arousal system

A

Associated w/ 2 pontine nuclei (Pedunculopontine tegmental and laterodorsal; PPT/LDT)

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13
Q

Where is noradrenergic arousal system

A

Locus ceruleus

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14
Q

Where is serotonergic arousal system

A

Midline raphe nuclei

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15
Q

Where is dopaminergic arousal system

A

Ventral tegmental area (VTA), substantia nigra pars compactica (SNPC) and medullary periventricular system

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16
Q

Inputs of RAS

A

All modalities of ascending sensory tracts
Trigeminal tracts
Auditory and visual

17
Q

How does RAS respond equally well to multiple sensory modalities?

A

The brain just knows something happened because of CONVERGENCE or loss of modal specificity.

18
Q

Describe dorsal pathway

A

Axons go to thalamus, synapse at nonspecific nuclei including the intralaminal nucleus of thalamus, release glutamate at thalamus, axons from thalamocortical neurons release EAA

19
Q

Describe ventral pathway. Which nuclei output only travel ventrally?

A

Bypasses thalamus, via basal forebrain and hypothalamus, diffuse from here to all higher levels

Parabrahcial nuclei output travel only w/ ventral pathway

20
Q

What is the main NT utilized by both parabrachial and RAS neurons?

A

EAA/Glutamate, regardless of dorsal or ventral pathway to brain.

Substantial # of interneurons releasing GABA in RAS, RAS also has a neuronal population releasing ACh

21
Q

Inputs and outputs to Cholinergic (PPT/LDT) system

A

I: Afferents sending collateral w/ convergence resulting in loss of modal specificity.

O: Dorsal and ventral pathway w/ ACh being major NT

22
Q

What happens if PPT and/or LDT are injured

A

Results in slow cortical processing resulting in memory loss because making new memories requires repetitive memory circuit activation and this baseline wake/arouse is lost

Often injured in Alzheimers pts.

23
Q

Inputs to noradrenergic locus ceruleus

A
  • Brainstem nuclei (paragigantocellularis in rostral medulla which receives input from all ascending sensory tracts)
  • Perifascicular area of nucleus prepositus (PrH)
  • Periaqueductal grey for pain (PAG)
  • Hypothalamus, amygdala, cortex
24
Q

Outputs from LC

A

Consciousness inputs join dorsal and ventral
Dorsal adrenergic bundle to all areas of higher brain except striatum
unrelated outputs to spinal cord

25
Q

When is locus ceruleus active and absent?

A

Active in stress and excitement, decreased when drowsy, absent in REM sleep

26
Q

Inputs and outputs for raphe nuclei

A

I: Sensory from spinal cord (fine proprioception), CN V, PAG

O: Stronger pathway w/ ventral pathway, dorsal pathway

27
Q

Functions of serotonergic activating system. How do certain drugs affect 5HT?

A 
Quiet awareness
Pain
Circadian
Food intake
Mood & Affect (Antidepressants increase 5HT, LSD is 5HT agonist, ecstasy induces lots of 5HT release leading to hallucination and euphoria)
28
Q

Describe VTA, SNPC, and Medullary areas involved in the dopaminergic system

A

VTA: 50-70% neurons here make dopamine, fire in response to novel stimuli

SNPC: Motor and emotion, damage = parkinsons

Medullary: Scattered along walls of 3rd and 4th ventricle, diffuse system

29
Q

Inputs into dopaminergic

A

Sensory input from all higher levels

30
Q

Outputs out of dopaminergic (there are 3, all Ms)

A

Mesencephalic: sends inputs to dorsal and ventral

Mesostriatal: motor control

Mesolimbic: emotion and pleasure

31
Q

Are thalamocortical neurons excitatory or inhibitory?

A

Excitatory. From thalamus, the thalamocortical neurons release EAA as their NT.

32
Q

How do we get the waves on an EEG?

A

Since EAA and GABA do respective excitation and inhibition, that gives us the up and down waves.

33
Q

In PVS, which regions of the brain show neuronal loss exceeding that of the cortex?

A

Rostral regions of pons, midbrain, and thalamus (thalamus is the worst)

34
Q

What happens to thalamocortical neurons when we sleep?

A

They are hyperpolarized and show occasional short bursts of AP. Hyperpolarization cuts the cortex off from excitatory influence during deepest levels of sleep.

35
Q

What arousal system is damaged in a coma, PVS, cognitive impairment and Alzheimers?

A

Coma: All RAS levels
PVS: Noradrenergic, 5HT
Cognitive impairment and Alzheimers: Cholinergic

NE2 (12 decks)

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