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NAB > 8b. Arousal, Sleep and Biological Rhythms > Flashcards

8b. Arousal, Sleep and Biological Rhythms Flashcards

1
Q

Electroencephalogram

- Action Potential Summation

A

Action potentials are too brief to sum together, except in epileptic seizures

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2
Q

Electroencephalogram

- Electrical Activity Measured

A

Slow membrane potentials

  • EPSPs
  • IPSPs
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3
Q

Reticular Formation

- Structure

A

Loosely aggregated cells of different types and sizes intermingled with fibres of differing orientations

This gives a net-like appearance

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4
Q

Reticular Formation

- Location

A

Diffuse brain system located medially in the brainstem

Continuous with:

  • Lateral hypothalamus and sub thalamic regions rostrally
  • Intermediate grey caudally
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5
Q

Reticular Formation

- Roles

A
  • Integration of basic, stereotyped patterns of responding

- Regulation of the level of arousal

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6
Q

Reticular Formation

- Integration of Basic Stereotyped Patterns of Responding

A
  1. Pattern generation to produce:
    - Posture
    - Locomotion
    - Swallowing
    - Chewing
    - Vomiting
    - Sneezing
    - Eye movements
  2. Regulation of the respiratory cycle and cardiovascular control
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7
Q

Reticular Formation

- Regulation of Arousal

A

Ascending activating system

Important for optimising the processing of sensory stimuli in the cerebral cortex, which is a form of attention function

Arousal is important in drive and motivation

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8
Q

Reticular Formation

- Electrical Stimulation

A

Widespread cortical activation, shown by desynchronisation of the electroencephalogram.

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9
Q

Reticular Formation Role in Arousal

- Inputs

A

Collateral inputs from:

  • Brain sensory pathways
  • Brain motor pathways
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10
Q

Reticular Formation Role in Arousal

- Outputs

A

Outputs to the cerebral cortex, which can be:

  • Direct via the medial forebrain bundle that runs through the lateral hypothalamus
  • Indirect via the intralaminar nuclei of the thalamus which projects to the cerebral cortex and striatum
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11
Q

Reticular Formation Role in Arousal

- Outputs

A

Outputs to the cerebral cortex, which can be:

  • Direct via the medial forebrain bundle that runs through the lateral hypothalamus
  • Indirect via the intralaminar nuclei of the thalamus which projects to the cerebral cortex and striatum
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12
Q

Reticular Formation Role in Arousal

- Components

A

The reticular formation can be fractionated into discrete chemically defined components, which are defined by populations of neurones secreting:

  • Dopamine
  • Noradrenaline
  • Serotonin
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13
Q

Reticular Formation Role in Arousal

- Isodendritic Core

A

Composed of monoaminergic systems:

  • Reticular formation neurones (dopaminergic, noradrenergic and serotonergic)
  • Cholinergic neurones of the basal forebrain
  • Histaminergic neurones of the posterior hypothalamus

All of these neurones have similar morphological features, with large cell bodies and an overlapping dendritic fields

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14
Q

Reticular Formation Role in Arousal

- Dopaminergic Neurones Location

A

Substantia nigra

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15
Q

Reticular Formation Role in Arousal

- Noradrenergic Neurones Location

A

Locus coeruleus

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16
Q

Reticular Formation Role in Arousal

- Serotonergic Neurones Location

A

Raphe nuclei

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17
Q

Reticular Formation Role in Arousal

- Dopaminergic Neurones Function

A

Activate consummatory behaviours

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18
Q

Reticular Formation Role in Arousal

- Noradrenergic Neurones Function

A

Play a major role in attention and orientating

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19
Q

Reticular Formation Role in Arousal

- Noradrenergic Neurones Activation

A

Activation of the locus coeruleus during sensory stimulation causes an increase in the signal:noise ratio, by:

  • Enhancing the inhibitory effect of meaningless tone on the hippocampal neurones
  • Enhancing the excitatory effect of a meaningful tone on hippocampal neurones

Maximally activated during stress

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20
Q

Reticular Formation Role in Arousal

- Serotonergic Neurones Function

A

Behavioural inhibition, particularly in aversive situations

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21
Q

Reticular Formation Role in Arousal

- Serotonergic Neurones Damage

A

Impulsive and obsessive- compulsive behaviours have been lined to reduced serotonin in the forebrain

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22
Q

Reticular Formation Role in Arousal

- Drugs Increasing Serotonin in the Brain

A

Prozac

Used to treat:

  • Impulsive behaviour
  • Obsessive compulsive behaviour
  • Anxiety
  • Depressive states
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23
Q

Cholinergic Neurones

- Location

A

Basal forebrain, above the amygdala

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24
Q

Cholinergic Neurones

- Function

A

Learning and memory

Particularly responsive to conditioned stimuli in the environment associated with a. food reward

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25
Q

Alzheimer’s Disease

- Cause

A

Degeneration of cholinergic neurones in the basal forebrain

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26
Q

Sleep Definition

- Behavioural

A

Sleep is the normal suspension of consciousness

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27
Q

Sleep Definition

- Electrophysiological

A

Sleep is the emergency of specific brain wave activity

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28
Q

Sleep-Wakefulness Rhythm Origin

A

Suprachiasmatic nucleus (SCN) of the hypothalamus

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29
Q

Affect of Removing Light/Dark Sleep Cues

A

Sleep-wake rhythm remains bu lengthens or shortens by half an hour

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30
Q

Stages of Sleep

- Awake EEG

A 
2 electroencephalogram patterns:
- β activity
Occurs when the eyes are open and signals an active cortex 
    - High frequency 15-60Hz
    - Low amplitude
- α activity
Quiet waking states
    - Low frequency 8-13Hz
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31
Q

Stages of Sleep

- Number of Stages of Non-REM Sleep

A

4

32
Q

Stages of Sleep

- Stage 1 Non-REM Sleep EEG

A

Drowsy period

Theta waves

  • Decreasing frequency 4-8Hz
  • Increasing amplitude
33
Q

Stages of Sleep

- Stage 2 Non-REM Sleep EEG

A
  • Further decrease in frequency
  • Further increase in amplitude

2 distinct features:

  • Spindles, which are intermittent high frequency spike clusters
  • K complexes, which is a large up-down deflection fo the electroencephalogram
34
Q

Stages of Sleep

- Stage 3 Non-REM Sleep EEG

A

Moderate to deep sleep

  • Delta rhythms
35
Q

Stages of Sleep

- Stage 4 Non-REM Sleep EEG

A

Deepest sleep

  • More pronounced delta rhythms with lowest frequency and highest amplitude
36
Q

Stages of Sleep

- REM Sleep EEG

A

The electroencephalogram is very similar to the awake state, containing β rhythms

37
Q

Stages of Sleep

- Physiological Characteristics of Non-REM Sleep

A

Decreases in:

  • Muscle tone
  • Heart rate
  • Breathing
  • Blood pressure
  • Metabolic rate
38
Q

Stages of Sleep

- Physiological Characteristics of REM Sleep

A 
Increases in:
- Blood pressure
- Heart rate
- Metabolic rate 
These parameters increases almost as high as in awake state

Paralysis of large muscles

Rapid eye movements

39
Q

Stages of Sleep

- Brain Activity in REM Sleep vs Awake State

A

Similar cortical activity in awake state and REM sleep

Other areas were more active during REM sleep:

  • Extra-striate cortex
  • Certain limbic structures

Pre-frontal cortex is less active during REM sleep

40
Q

Stages of Sleep

- Brain Activity in REM sleep vs Non-REM Sleep

A

Primary visual cortex is less active during REM sleep

Extra-striate cortex is more active during REM sleep

41
Q

Functions of Sleep

A
  • Restoration of bodily and mental functions including removal of toxins produced by neurones during the day
  • Brain development in children
  • Memory consolidation
42
Q

Importance of Sleep

A

Prolonged sleep deprivation causes death

43
Q

Neural Mechanisms of Sleep

- Important Brain Areas

A
  • Brainstem modulatory neurotransmitter systems in the reticular formation
  • Thalamus
44
Q

Neural Mechanisms of Sleep

- Stimulating the Thalamus

A

Low frequency pulses in awake animals produced slow wave sleep

45
Q

Neural Mechanisms of Sleep

- Key to Sleep-Wakefulness

A

Whether the thalamus and cortex are synchronised or not

  • Intrinsic burst firing mode or intrinsic oscillatory state
  • Tonically active state
46
Q

Neural Mechanisms of Sleep

- Thalamo-Cortico Synchronicity

A

Intrinsic burst firing or intrinsic oscillatory state:

  • Thalamus and cortex are synchronised, disconnecting the cortex from the outside world
  • Cortical disconnection is maximal during delta sleep

Tonically active state:
- Thalamo-cortico neurones transmit information to the cortex

47
Q

Neural Mechanisms of Sleep

- Altering Thalamo-Cortico Synchronicity

A

Acetylcholine and noradrenaline shift cells in the cortex and thalamus from intrinsic burst firing mode to single spiking tonically active modes.

May underlie transition from non-REM sleep to waking state

48
Q

Neural Mechanisms of Sleep

- Reticular Formation

A

During awake state cholinergic, noradrenergic and serotonergic neurones are active

During non-REM sleep cholinergic, noradrenergic and serotonergic neurone activity is decreased

During REM sleep:

  • Cholinergic neurones are active, creating PGO waves
  • Serotonergic and noradrenergic neurones decrease their activity further

Before REM offset, the serotoninergic and noradrenergic neurones increase firing

49
Q

FLIP-FLOP Model of Sleep-Wakefulness

- Important Brain Area

A

Ventrolateral pre-optic area of the hypothalamus (VLPOA)

- Contains sleep inducing neurones

50
Q

FLIP-FLOP Model of Sleep-Wakefulness

- VLPOA Lesions

A

Total insomnia and death due to sleep deprivation

51
Q

FLIP-FLOP Model of Sleep-Wakefulness

- VLPOA Stimulation

A

Drownsiness

52
Q

FLIP-FLOP Model of Sleep-Wakefulness

- Mechanism

A

GABAergic inhibitory outputs to arousal inducing areas in the brainstem and forebrain:

  • Raphe nucleus
  • Locus coeruleus
  • Histaminergic neurones

These neuromodulatory areas send inhibitory connections back to the VLPOA.

Mutual inhibition of VLPOA and brain stem and forebrain arousal systems governs the sleep-wake cycle

53
Q

FLIP-FLOP Model of Sleep-Wakefulness

- Balance

A

What tips the balance between the VLPOA and brainstem and forebrain arousal systems is unclear.

54
Q

FLIP-FLOP Model of Sleep-Wakefulness

- Hypothalamic Inputs

A

Hypothalamic systems feed into this model:

  • Orexin is excitatory
  • Melanin concentrating hormone (MCH) is inhibitory
55
Q

Insomnia

- 2 Types

A
  • Short term insomnia

- Long term insomnia

56
Q

Insomnia

- Causes of Short Term Insomnia

A
  • Stress
  • Jet lag
  • Caffeine consumption
57
Q

Insomnia

- Causes of Long Term Insomnia

A
  • Psychiatric disorders, which upset the balance of neuromodulatory transmitter systems
  • Fatal familial insomnia
58
Q

Insomnia

- fatal Familial Insomnia

A

Rare genetic disorder which is a prion disease that causes gradual onset of insomnia that leads to death

59
Q

Narcolepsy

- Description

A

Frequent REM sleep attacks during the day and cataplexy, which is temporary loss of motor control

60
Q

Narcolepsy

- Cause

A

In dogs an orexin receptor 2 mutation has been identified

In humans, loss of orexin neurones causes narcolepsy

61
Q

Orexin Neurones

- Location

A

Found exclusively in the tuberal regions of the lateral hypothalamus

62
Q

Orexin Neurones

- Activity

A

Most active during wakefulness, particularly during locomotion

63
Q

Orexin Neurones

- Projections

A

Excitatory projections to the reticular modulatory systems to increase activity in arousal pathways, tipping the balance of the FLIP-FLOP pathway to favour waking state

64
Q

Orexin Neurones

- Loss of Orexin Receptors

A

Weakens the switch between states, so switching becomes more frequent

65
Q

Orexin Neurones

- Activation

A

Activated by hunger signals from the NPY neurones in the arcuate nucleus and stimulate eating

66
Q

Orexin Neurones

- Actions

A

Stimulate feeding

Activate brainstem and forebrain arousal systems so that animals are awake to eat

67
Q

MCH Neurones

- Action

A

Inhibit the brainstem and forebrain arousal systems giving motivation to sleep

68
Q

Circadian Rhythmicity

- Physiological parameters

A
  • Alterness
  • Temperature
  • Growth hormone secretion
  • Cortisol secretion
  • Plasma [K+]
69
Q

Circadian Rhythmicity

- Removal of External Cues

A

SCN will free run with a period of 24 hours plus or minus 30 minutes, so circadian rhythmicity will remain almost normal.

Shown by:

  • Recording cellular activity in SCN neurones
  • Studies in cave explorers
  • Temporal isolation studies
70
Q

Circadian Rhythmicity

- Important Brain Structure

A
  • Retina

- Suprachiasmatic nucleus (SCN)

71
Q

Circadian Rhythmicity

- SCN Location

A

Anterior hypothalamus, above the optic chasm on each side of the 3rd ventricle

72
Q

Circadian Rhythmicity

- SCN Input

A

Receives light-dark information from the retina via the retina-hypothalamic tract, resulting in entrainment of the clock to the 24-hour light-dark cycle

73
Q

Circadian Rhythmicity

- Retina

A

Retina contains light-sensitive ganglion cells which contain light sensitive melanopsin, which is sensitive to blue wavelength light

Sends axons to the suprachiasmatic nucleus (SCN_

74
Q

Circadian Rhythmicity

- Lesioning the SCN

A

Destroys biological rhythms, both physiological and behavioural

75
Q

Circadian Rhythmicity

- SCN Neurones

A

Circadian oscillatorio coupled to make a pacemaker to synchronise peripheral clocks

76
Q

Circadian Rhythmicity

- SCN Connections

A
  • Pineal gland
  • Pituitary gland
  • Hypothalamic nuclear groups
    • Dorsomedial nucleus
    • Ventromedial prophetic area (VLPOA)
  • Midline thalamus
  • Nucleus of the stria terminals

SCN can control physiological and psychological function trhrough endocrine and autonomic output

77
Q

Circadian Rhythmicity

- SCN Control of Sleep-Wake Cycle

A

Regulation of VLPOA of the hypothalamus via the dorsomedial nucleus

NAB (37 decks)

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