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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
Alzheimer's Disease | - Cause
Degeneration of cholinergic neurones in the basal forebrain
26
Sleep Definition | - Behavioural
Sleep is the normal suspension of consciousness
27
Sleep Definition | - Electrophysiological
Sleep is the emergency of specific brain wave activity
28
Sleep-Wakefulness Rhythm Origin
Suprachiasmatic nucleus (SCN) of the hypothalamus
29
Affect of Removing Light/Dark Sleep Cues
Sleep-wake rhythm remains bu lengthens or shortens by half an hour
30
Stages of Sleep | - Awake EEG
``` 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 ```
31
Stages of Sleep | - Number of Stages of Non-REM Sleep
4
32
Stages of Sleep | - Stage 1 Non-REM Sleep EEG
Drowsy period Theta waves - Decreasing frequency 4-8Hz - Increasing amplitude
33
Stages of Sleep | - Stage 2 Non-REM Sleep EEG
- 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
Stages of Sleep | - Stage 3 Non-REM Sleep EEG
Moderate to deep sleep - Delta rhythms
35
Stages of Sleep | - Stage 4 Non-REM Sleep EEG
Deepest sleep - More pronounced delta rhythms with lowest frequency and highest amplitude
36
Stages of Sleep | - REM Sleep EEG
The electroencephalogram is very similar to the awake state, containing β rhythms
37
Stages of Sleep | - Physiological Characteristics of Non-REM Sleep
Decreases in: - Muscle tone - Heart rate - Breathing - Blood pressure - Metabolic rate
38
Stages of Sleep | - Physiological Characteristics of REM Sleep
``` 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
Stages of Sleep | - Brain Activity in REM Sleep vs Awake State
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
Stages of Sleep | - Brain Activity in REM sleep vs Non-REM Sleep
Primary visual cortex is less active during REM sleep Extra-striate cortex is more active during REM sleep
41
Functions of Sleep
- Restoration of bodily and mental functions including removal of toxins produced by neurones during the day - Brain development in children - Memory consolidation
42
Importance of Sleep
Prolonged sleep deprivation causes death
43
Neural Mechanisms of Sleep | - Important Brain Areas
- Brainstem modulatory neurotransmitter systems in the reticular formation - Thalamus
44
Neural Mechanisms of Sleep | - Stimulating the Thalamus
Low frequency pulses in awake animals produced slow wave sleep
45
Neural Mechanisms of Sleep | - Key to Sleep-Wakefulness
Whether the thalamus and cortex are synchronised or not - Intrinsic burst firing mode or intrinsic oscillatory state - Tonically active state
46
Neural Mechanisms of Sleep | - Thalamo-Cortico Synchronicity
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
Neural Mechanisms of Sleep | - Altering Thalamo-Cortico Synchronicity
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
Neural Mechanisms of Sleep | - Reticular Formation
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
FLIP-FLOP Model of Sleep-Wakefulness | - Important Brain Area
Ventrolateral pre-optic area of the hypothalamus (VLPOA) | - Contains sleep inducing neurones
50
FLIP-FLOP Model of Sleep-Wakefulness | - VLPOA Lesions
Total insomnia and death due to sleep deprivation
51
FLIP-FLOP Model of Sleep-Wakefulness | - VLPOA Stimulation
Drownsiness
52
FLIP-FLOP Model of Sleep-Wakefulness | - Mechanism
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
FLIP-FLOP Model of Sleep-Wakefulness | - Balance
What tips the balance between the VLPOA and brainstem and forebrain arousal systems is unclear.
54
FLIP-FLOP Model of Sleep-Wakefulness | - Hypothalamic Inputs
Hypothalamic systems feed into this model: - Orexin is excitatory - Melanin concentrating hormone (MCH) is inhibitory
55
Insomnia | - 2 Types
- Short term insomnia | - Long term insomnia
56
Insomnia | - Causes of Short Term Insomnia
- Stress - Jet lag - Caffeine consumption
57
Insomnia | - Causes of Long Term Insomnia
- Psychiatric disorders, which upset the balance of neuromodulatory transmitter systems - Fatal familial insomnia
58
Insomnia | - fatal Familial Insomnia
Rare genetic disorder which is a prion disease that causes gradual onset of insomnia that leads to death
59
Narcolepsy | - Description
Frequent REM sleep attacks during the day and cataplexy, which is temporary loss of motor control
60
Narcolepsy | - Cause
In dogs an orexin receptor 2 mutation has been identified In humans, loss of orexin neurones causes narcolepsy
61
Orexin Neurones | - Location
Found exclusively in the tuberal regions of the lateral hypothalamus
62
Orexin Neurones | - Activity
Most active during wakefulness, particularly during locomotion
63
Orexin Neurones | - Projections
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
Orexin Neurones | - Loss of Orexin Receptors
Weakens the switch between states, so switching becomes more frequent
65
Orexin Neurones | - Activation
Activated by hunger signals from the NPY neurones in the arcuate nucleus and stimulate eating
66
Orexin Neurones | - Actions
Stimulate feeding Activate brainstem and forebrain arousal systems so that animals are awake to eat
67
MCH Neurones | - Action
Inhibit the brainstem and forebrain arousal systems giving motivation to sleep
68
Circadian Rhythmicity | - Physiological parameters
- Alterness - Temperature - Growth hormone secretion - Cortisol secretion - Plasma [K+]
69
Circadian Rhythmicity | - Removal of External Cues
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
Circadian Rhythmicity | - Important Brain Structure
- Retina | - Suprachiasmatic nucleus (SCN)
71
Circadian Rhythmicity | - SCN Location
Anterior hypothalamus, above the optic chasm on each side of the 3rd ventricle
72
Circadian Rhythmicity | - SCN Input
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
Circadian Rhythmicity | - Retina
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
Circadian Rhythmicity | - Lesioning the SCN
Destroys biological rhythms, both physiological and behavioural
75
Circadian Rhythmicity | - SCN Neurones
Circadian oscillatorio coupled to make a pacemaker to synchronise peripheral clocks
76
Circadian Rhythmicity | - SCN Connections
- 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
Circadian Rhythmicity | - SCN Control of Sleep-Wake Cycle
Regulation of VLPOA of the hypothalamus via the dorsomedial nucleus

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