8b. Arousal, Sleep and Biological Rhythms Flashcards
Electroencephalogram
- Action Potential Summation
Action potentials are too brief to sum together, except in epileptic seizures
Electroencephalogram
- Electrical Activity Measured
Slow membrane potentials
- EPSPs
- IPSPs
Reticular Formation
- Structure
Loosely aggregated cells of different types and sizes intermingled with fibres of differing orientations
This gives a net-like appearance
Reticular Formation
- Location
Diffuse brain system located medially in the brainstem
Continuous with:
- Lateral hypothalamus and sub thalamic regions rostrally
- Intermediate grey caudally
Reticular Formation
- Roles
- Integration of basic, stereotyped patterns of responding
- Regulation of the level of arousal
Reticular Formation
- Integration of Basic Stereotyped Patterns of Responding
- Pattern generation to produce:
- Posture
- Locomotion
- Swallowing
- Chewing
- Vomiting
- Sneezing
- Eye movements - Regulation of the respiratory cycle and cardiovascular control
Reticular Formation
- Regulation of Arousal
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
Reticular Formation
- Electrical Stimulation
Widespread cortical activation, shown by desynchronisation of the electroencephalogram.
Reticular Formation Role in Arousal
- Inputs
Collateral inputs from:
- Brain sensory pathways
- Brain motor pathways
Reticular Formation Role in Arousal
- Outputs
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
Reticular Formation Role in Arousal
- Outputs
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
Reticular Formation Role in Arousal
- Components
The reticular formation can be fractionated into discrete chemically defined components, which are defined by populations of neurones secreting:
- Dopamine
- Noradrenaline
- Serotonin
Reticular Formation Role in Arousal
- Isodendritic Core
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
Reticular Formation Role in Arousal
- Dopaminergic Neurones Location
Substantia nigra
Reticular Formation Role in Arousal
- Noradrenergic Neurones Location
Locus coeruleus
Reticular Formation Role in Arousal
- Serotonergic Neurones Location
Raphe nuclei
Reticular Formation Role in Arousal
- Dopaminergic Neurones Function
Activate consummatory behaviours
Reticular Formation Role in Arousal
- Noradrenergic Neurones Function
Play a major role in attention and orientating
Reticular Formation Role in Arousal
- Noradrenergic Neurones Activation
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
Reticular Formation Role in Arousal
- Serotonergic Neurones Function
Behavioural inhibition, particularly in aversive situations
Reticular Formation Role in Arousal
- Serotonergic Neurones Damage
Impulsive and obsessive- compulsive behaviours have been lined to reduced serotonin in the forebrain
Reticular Formation Role in Arousal
- Drugs Increasing Serotonin in the Brain
Prozac
Used to treat:
- Impulsive behaviour
- Obsessive compulsive behaviour
- Anxiety
- Depressive states
Cholinergic Neurones
- Location
Basal forebrain, above the amygdala
Cholinergic Neurones
- Function
Learning and memory
Particularly responsive to conditioned stimuli in the environment associated with a. food reward
Alzheimer’s Disease
- Cause
Degeneration of cholinergic neurones in the basal forebrain
Sleep Definition
- Behavioural
Sleep is the normal suspension of consciousness
Sleep Definition
- Electrophysiological
Sleep is the emergency of specific brain wave activity
Sleep-Wakefulness Rhythm Origin
Suprachiasmatic nucleus (SCN) of the hypothalamus
Affect of Removing Light/Dark Sleep Cues
Sleep-wake rhythm remains bu lengthens or shortens by half an hour
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 8-13HzStages of Sleep
- Number of Stages of Non-REM Sleep
4
Stages of Sleep
- Stage 1 Non-REM Sleep EEG
Drowsy period
Theta waves
- Decreasing frequency 4-8Hz
- Increasing amplitude
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
Stages of Sleep
- Stage 3 Non-REM Sleep EEG
Moderate to deep sleep
- Delta rhythms
Stages of Sleep
- Stage 4 Non-REM Sleep EEG
Deepest sleep
- More pronounced delta rhythms with lowest frequency and highest amplitude
Stages of Sleep
- REM Sleep EEG
The electroencephalogram is very similar to the awake state, containing β rhythms
Stages of Sleep
- Physiological Characteristics of Non-REM Sleep
Decreases in:
- Muscle tone
- Heart rate
- Breathing
- Blood pressure
- Metabolic rate
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
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
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
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
Importance of Sleep
Prolonged sleep deprivation causes death
Neural Mechanisms of Sleep
- Important Brain Areas
- Brainstem modulatory neurotransmitter systems in the reticular formation
- Thalamus
Neural Mechanisms of Sleep
- Stimulating the Thalamus
Low frequency pulses in awake animals produced slow wave sleep
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
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
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
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
FLIP-FLOP Model of Sleep-Wakefulness
- Important Brain Area
Ventrolateral pre-optic area of the hypothalamus (VLPOA)
- Contains sleep inducing neurones
FLIP-FLOP Model of Sleep-Wakefulness
- VLPOA Lesions
Total insomnia and death due to sleep deprivation
FLIP-FLOP Model of Sleep-Wakefulness
- VLPOA Stimulation
Drownsiness
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
FLIP-FLOP Model of Sleep-Wakefulness
- Balance
What tips the balance between the VLPOA and brainstem and forebrain arousal systems is unclear.
FLIP-FLOP Model of Sleep-Wakefulness
- Hypothalamic Inputs
Hypothalamic systems feed into this model:
- Orexin is excitatory
- Melanin concentrating hormone (MCH) is inhibitory
Insomnia
- 2 Types
- Short term insomnia
- Long term insomnia
Insomnia
- Causes of Short Term Insomnia
- Stress
- Jet lag
- Caffeine consumption
Insomnia
- Causes of Long Term Insomnia
- Psychiatric disorders, which upset the balance of neuromodulatory transmitter systems
- Fatal familial insomnia
Insomnia
- fatal Familial Insomnia
Rare genetic disorder which is a prion disease that causes gradual onset of insomnia that leads to death
Narcolepsy
- Description
Frequent REM sleep attacks during the day and cataplexy, which is temporary loss of motor control
Narcolepsy
- Cause
In dogs an orexin receptor 2 mutation has been identified
In humans, loss of orexin neurones causes narcolepsy
Orexin Neurones
- Location
Found exclusively in the tuberal regions of the lateral hypothalamus
Orexin Neurones
- Activity
Most active during wakefulness, particularly during locomotion
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
Orexin Neurones
- Loss of Orexin Receptors
Weakens the switch between states, so switching becomes more frequent
Orexin Neurones
- Activation
Activated by hunger signals from the NPY neurones in the arcuate nucleus and stimulate eating
Orexin Neurones
- Actions
Stimulate feeding
Activate brainstem and forebrain arousal systems so that animals are awake to eat
MCH Neurones
- Action
Inhibit the brainstem and forebrain arousal systems giving motivation to sleep
Circadian Rhythmicity
- Physiological parameters
- Alterness
- Temperature
- Growth hormone secretion
- Cortisol secretion
- Plasma [K+]
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
Circadian Rhythmicity
- Important Brain Structure
- Retina
- Suprachiasmatic nucleus (SCN)
Circadian Rhythmicity
- SCN Location
Anterior hypothalamus, above the optic chasm on each side of the 3rd ventricle
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
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_
Circadian Rhythmicity
- Lesioning the SCN
Destroys biological rhythms, both physiological and behavioural
Circadian Rhythmicity
- SCN Neurones
Circadian oscillatorio coupled to make a pacemaker to synchronise peripheral clocks
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
Circadian Rhythmicity
- SCN Control of Sleep-Wake Cycle
Regulation of VLPOA of the hypothalamus via the dorsomedial nucleus
