(Electroencephalogram) measures the EPSP and IPSPs of cerebral cortical neurons
(Electro-oculogram) measures eye movements
(Electromyogram) measures skeletal muscle activity as well as heart rate and breathing pattern.
Phases of sleep
are distinguished by Synchronized or DesynchronizedEEG
means the EPSPs and IPSPs are not summing on the EEG
when the EPSPs and IPSPs are temporally Synchronized, they sum up to a wave with greater amplitude on EEG
EEG findings memory key: BATS Drink Blood (
b waves when awake, a in stage 1, q waves during late stage 1, sleep spindles during stage 2, d waves during stage 4, b waves return during REM)
Non-Rapid Eye Movement Sleep (characterized by Synchronized EEG) "Idling brain in a movable body"
characterized by "Vagal Tone": regular HR, RR, BP, muscle tone,
ß brain O2 consumption, homeothermic, ß erections
Transitional between wakefulness and stage 2
during wakefulness and early stage 1, the EEG is desynchronized
during drowsiness, there is synchronizing of EEG that is especially apparent over occipital cortex forming
late stage 1 shows slowing in the EEG with low voltage desynchronized theta waves of moderate frequency (3-7Hz)
Light NREM sleep
EEG has "sleep spindles" (High frequency bursts-12-14Hz) and K complexes which are related to
Transitional between light and deep NREM sleep (low % d waves)
Deep NREM sleep; highest threshold for arousal – difficult to wake up
EEG has highly synchronized, high amplitude, low frequency (0.5-2Hz)
Neurophysiologic Basis of NREM Sleep
(1) Deafferntation Theory of Sleep
: loss of sensory input from brainstem Þ sleep
ascending Reticular Activating System (MRF, PRF, Med RF) is very important for wakefulness, as are LC, LDT/PPT and Raphe nuclei
lesions through the rostral brainstem cause synchronized EEG at first, due to the disconnection of above structures with cortex
eventually desynchronized waves will return after lesion is made
(2) Sleep as an active process
: argues that hypothalamic inputs cause sleep
: Ventrolateral preoptic nucleus is small, contains adenosine receptors (caffeine blocks these) and is in anterior hypothalamus
lesions of VLPO results in insomnia = permanently desynchronized EEG
(sets circadian rhythms) interacts with VLPO
Theory = VLPO has active control over the process of sleep
Tubero mammilary nucleus
(TMN) – in posterior hypothalamus; projects to and activates broad areas of cortex; stimulation causes EEG to de-synchronize
histamine is neurotransmitter, so antihistamine may cause drowsiness by interrupting this system
studies show that NREM sleep is an actively controlled process by VLPO which contains inhibitory GABA in its projections to the posterior hypothalamus, shutting off TMN as well as LC, Dorsal Raphe and LDT/PPT
Mechanism for Synchronized EEG of Sleep
: loop of cortical thalamic neurons
3-cell loop contains neurons in the reticular thalamic nucleus, thalamic cortical neurons and cortico-thalamic neurons
during wakefulness there is activation of cortical neurons by LC, Dorsal Raphe, LDT/PPT and TMN of hypothalamus
during wakefulness the thalamic cells spend most of their time depolarized
during sleep there is loss of excitatory input from reticular nuclei which allows thalamic neurons to hyperpolarize
the intrinsic pattern of cortico-neurons is slow oscillation of there membrane potential
summation results from the hyperpolarized thalamic-cortico loops expressing their intrinsic properties which gives rise to rhythmic, repetitive, synchronized, inputs to the cortex which allow recording of Synchronized EEG
so the cortex is deafferntated, but it is done actively. (nucleus solitarius can also do this but unknown how)
– Rapid Eye Movement Sleep (characterized by Desynchronized EEG) "Highly active brain in a paralyzed body"
also called Paradoxical sleep because EEG pattern is the same as awake; EEG characterized by saw tooth waves.
Ý brain O2 consumption, polkilothermic, Ý erections, etc.
: associated with eye movements and myoclonic twitches.
: period between these phasic events.
: which records EEG, EOG and EMG at the same time help distinguish REM from NREM and Wakefulness.
during wakefulness, there is tonic and phasic EMG activity vs REM in which EMG shows muscle Atonia (paralysis)
REMactivity in excitatory ACH cells of LDT/PPT project to:
(1) Thalamus and remove inhibitory currents from VLPO which results in Desynchronization on the EEG
(2) area of Magoun and Rhines located in MedR which inhibits
a motor neurons when stimulated Þ Atonia
cell groups such as LC(norepinephrine), Raphe (serotonin) and TMN (histamine), which are also active during wakeful Desynchronization are inactive during REM sleep.
Summary of Sleep Stages
Non-Rapid Eye Movement (NREM) or Synchronized Sleep
Stage 1 – transitional state between wakefulness and Stage 2 sleep
EEG: theta waves 3-7 Hz
EOG: slow, rolling eye movements (NOTE: greatest in Stage 1.)
Stage 2 – light NREM sleep
EEG: sleep spindles 12-24 Hz and K complexes
EOG: slow, rolling eye movements
Stage 3 – transitional state between light NREM sleep and deep NREM sleep
EEG: delta waves 0.5-2 Hz (<20% of 30-s epoch)
EOG: slow, rolling eye movements
Stage 4 – deep NREM sleep
EEG: delta waves 0.5-2 Hz
EOG: slow, rolling eye movements
Rapid Eye Movement (REM) or Desynchronized or Paradoxical Sleep
EEG: low-voltage (<20 :V), high frequency (>12 Hz) waves, and sawtooth waves
EOG: episodic, conjugate rapid eye movements
EMG: Atonia occasional myoclonic twitches
PGO waves: Ponto-geniculo-occipital waves (have not been recorded in humans)
NREM Sleep EEG is characterized by large amplitude, slow oscillations in the EEG.
Signature waveforms include: Sleep spindle, K Complex, Delta waves
: These waveforms result from cortical neurons discharging synchronously under the influence thalamic neurons. Corticothalamic loops in the absence of sensory and reticular inputs will become synchronous and form waveforms such as "sleep spindles," K complexes, and delta waves.
Thalamic cell hyperpolarization
– loss of excitatory input from reticular nuclei allows thalamic nuclei to hyperpolarize. This allows expresion of the intrinsic proerties of the corticothalamic loop which gives rise to the synchronized EEG (The degree of synchronization in the EEG increases as thalamic cells hyperpolarize). Represents a functional "deafferentation" of the cerebral cortex.
: A deafferentation of the thalamus – loss of thalamic input from the brainstem monoaminergic systems.
: hypothalamic nuclei (anterior hypothalamus (Ventrolateral pre-optic, VLPO) decrease activity of monoaminergic nuclei in the brainstem.
(1) Reticular formation
– desynchronization of the EEG
played a very important role in the control of the sleep-wake cycle
in the area of the Tuberomammillary Nucleus – desynchronization of the EEG (rem)
in the area of the preoptic nucleus – synchronized EEG
REM sleep is a desynchronization of the EEG but without the awareness, consciousness.
Desynchronized EEG results from cholinergicactivation of cortical activity. Achieved by cholinergic cells in the:
(1) rostral dorsolateral pons
(2) pedunculopontine tegmentum
(3) lateral dorsal tegmentum (PPT/LDT)
These neurons project to the reticular formation
which as you know has wide spread rostral projections.
Features of EMG activity
alpha motoneurons are actively inhibited during REM sleep – the inhibitory area of Magoun and Rhines in located in the caudal medullary reticular formation is the source of this inhibition (the cell are activated by a pontine cholinergic mechanism)
Difference between REM and wakefulness.
The desynchronized EEG differs from that in wakefulness in that the thalamic relay neurons are not depolarized.