Ch. 8 Sleep And Biological Rhythm

Front 1

What 4 measures do we take when studying sleep?

Back 1

EMG for muscle tone

EOG for eye movement

EEG for brainwave activity

Blood flow to genitals

Front 2

Under what conditions would we expect to see alpha or beta waves on an EEG respectively. Describe the waveforms.

Back 2

Alpha: Eyes closed, synchronized high amp low frequency waves

Beta: Awake and active, desynchronous low amp high frequency waves

Front 3

Define paradoxical sleep

Back 3

When EEG waveforms show wakeful patterns but is instead asleep. This is characterized by REM

Front 4

Order the frequency of brainwaves from highest (most awake) to lowest (deepest sleep)

Back 4

Beta > Sleep spindles > Alpha > Theta > Delta

Front 5

What EEG features let us know that an individual is entering sleep stage 2

Back 5

K complexes and Sleep spindles

Front 6

In what stage of sleep would we expect to see delta and theta waves? Describe the waveforms

Back 6

Delta: Stage 4 synchronous

Theta: Stage 3 synchronous

Front 7

How does REM differ from SWS?

Back 7

REM shows desynchronous waveforms whereas SWS slows synchronous waveforms

REM has lack of muscle tonus whereas SWS shows moderate muscle tonus

REM = Rapid eye movement, SWS = slow or absent eye movement

REM = erections and secretions, SWS = no genital activity

REM = Vivid emotional dreams, SWS = Logical/rational dreams

Front 8

How do sleep terror and nightmares differ?

Back 8

Sleep terrors occur in SWS stage 3 and 4

Nightmares during REM

Front 9

What is the effect of exercise on sleep?

Back 9

Increased SWS activity, increased body temperature, but no effect on REM

Front 10

What are the physiological consequences of sleep deprivation on rats?

Back 10

Increased eating and activity, eventually become ill and die, and autopsies show ulcers

Front 11

When do humans experience the most amount of REM? What does this tell us about the function of REM?

Back 11

40 weeks into life. This may facilitate brain development

Front 12

What 2 lines of evidence do we have that sleep is most likely not regulated by a blood born chemical?

Back 12

1) Siamese twins with a conjoined circulatory system sleep at separate time

2) Some animals can sleep independently in each hemisphere

Front 13

What is the consequence of glycogen mobilization by astrocytes?

Back 13

Accumulation of adenosine increases SWS related EEG activity

Front 14

Electrical stimulation of what brain structure stimulates arousal?

Back 14

brain stem

Front 15

What are the 2 arousal pathways?

Back 15

Dorsal: RF --> Medial thalamus --> Cortex

Ventral: RF --> Lateral hypothalamus, basal ganglia, and forebrain

Front 16

What are the 5 arousal NT's

Back 16

1) ACh

2) NE

3) 5-HT

4) Histamine

5) Hypocretin aka orexin

Front 17

How do concentrations of hypocretin change throughout the day?

Back 17

Cycle between highly active during exploration but silenced during REM

Front 18

Where do we find ACh neurons? What are the EEG consequences of ACh? What are the consequences of ACh agonists and antogonists respectively?

Back 18

ACh neurons are in the pons and basal forebrain. ACh induces desynchrony. Agonist increases arousal whereas antagonists decrease

Front 19

When would we expect to find peak ACh concentration in the hippocampus and cortex?

Back 19

Peak ACh concentration in the hippcampus during REM

Peak ACh concentration in the cortex during active wakefulness

Front 20

Where do we find NE neurons in rats? When would we find high, low, and No NE activity respectively? What may be the role of these neurons?

Back 20

Locus Coeruleus

High Activity: Wakefulness

Low Activity: Sleep

No activity: REM

These neurons play a role in sustaining vigilance

Front 21

5-HT stimulation increases ____, whereas antagonism ______ cortical arousal. Thus, what is the relationship between 5-HT concentrations and sleep stages?

Back 21

arousal, decreases. The deeper the sleep, the lower the serotonergic neural activity, but spikes during REM

Front 22

What stimulatory NT cell bodies are found in the tuberomammilary nucleus of the hypothalamus? Where do the axons of these cell bodies project to?

Back 22

Histamine. The neurons project to the cerebral cortex, thalamus, hypothalamus, basal ganglia, and basal forebrain.

Front 23

Why do antihistamines make you drowsy?

Back 23

The histamine neuron projections are directly related to cortical activation, and through indirect projections from the basal forebrain to the cortex, histamines stimulate ACh-ergic neurons

Front 24

What structure regulates SWS and where is it found? What happens if we lesion this area?

Back 24

Ventrolateral preoptic area rostral to the optic chiasm. Lesions lead to total insomnia and death

Front 25

Stimulation of ______ induces signs of drowsiness, because this structure contains _____ergic neurons that project to what 3 structures in order to inhibit what NT's?

Back 25

vlPOA, gaba-ergic neurons, and projects to the tuberomammilary nucleus (Histamine), raphe nucleus (5-HT), and locus coeruleus (NE)

Front 26

_______found in the lateral hypothalamus is excitatory and promotes wakefulness. The neurons project to the _____ nucleus, ____ neurons in dorsal pons, basal forebrain, and cortex. Loss of these neurons leads to _______

Back 26

Orexin aka hypocretin, tuberomamillary nucleus, and ACh neurons. Loss of these neurons leads to narcolepsy.

Front 27

The _______ helps stabilize the on/off flip/flop which is controlled by the ________ ______ area

Back 27

orexinergic, ventrolateral preoptic area

Front 28

What is the consequence of adenosine build up on the sleep/wake system? How do we prevent adenosine's effect on the on/off sleepwake system?

Back 28

Adenosine stimulates the vlPOA, inhibiting the waking-on system and also inhibiting the LH orexinergic neurons. Biological clock and hunger signals both stimulate the arousal system, consequently inhibiting the vlPOA.

Front 29

What is the function of orexin in the on/off sleep/wake system and realted NT's.

Back 29

Orexin stimulates the wakeful/arousal system, thus inhibiting the sleep promoting vlPOA. This stimulates ACh, NE, 5-HT, and histamine

Front 30

What is the effect of biological clocks, hunger signals, and satiety signals respectively on REM sleep flip-flop? What structures are involved in the REM flip-flop. Where are the REM-OFF and REM-ON neurons?

Back 30

Biological clock and hunger signals both stimulate the LH orexinergic neurons, whereas satiety signals inhibit them. Stimulation of LH orexinergic neurons stimulate the ventrolateral periaqueductal gray (vlPAG) (REM-OFF), inhibiting the sublaterodorsal nucleus (SLD) within the dorsolateral pons which contains REM-ON neurons

Front 31

When the sleep/waking flip-flip switches into sleep, SWS begins. At this point, the activity of the excitatory orexinergic, noradrenergic, and serotonergic inputs to the REM-OFF region begins to _____. As a consequence, the excitatory input to the REM-OFF region is _____, and we can enter REM sleep.

Back 31

Decrease, removed

Front 32

Why does the degeneration of orexinergic neurons cause nacolepsy?

Back 32

With the loss of orexinergic neurons, Emotional stimuli activates the amygdala which stimulates the sublaterodorsal nucleus of the dorsolateral pons which contains the REM-ON neurons and conversely inhibits the REM-OFF neurons in the vlPAG resulting in cataplexy

Front 33

What are the 2 structures responsible for the REM sleep Flip-Flop?

Back 33

ventrolateral periaqueductal gray and the sublaterodorsal nucleus of the dorsolateral pons

Front 34

How does the vlPOA interact with vlPAG and LH orexinergic neurons? What is the consequence of this on REM and the Arousal system?

Back 34

vlPOA inhibits the LH orexinergic neurons and vlPAG which allows for the REM-ON neurons of the sublaterodorsal nucleus of the pons to activate. Inhibition of the LH orexinergic neurons inhibits the arousal system.

Front 35

How does activation of the sublaterodorsal nucleus of the pons stimulate genital activity?

Back 35

SLD stimulates ACh neurons in pons which stimulates the lateral preoptic area stimulating genital activity

Front 36

How do we promote paralysis during REM?

Back 36

REM-ON neurons of the sublaterodorsal nucleus (SLD) within the dorsolateral pons stimulates inhibitory interneurons inhibiting motor neurons and preventing movements

Front 37

What structure and molecule regulates circadian rhythms?

Back 37

The melanopsin molecule interacts with the suprachiasmatic nucleus (SCN) to regulate circadian rhythms.

Front 38

What NT concentrations are elevated during REM and which are low?

Back 38

High during REM: ACh, 5-HT

Low during REM: NE, Histamine, Orexin

Front 39

What NT concentrations are elevated during SWS and which are low?

Back 39

High: NE

Low: ACh, 5-HT, Histamine, Orexin

Front 40

Although NE concentrations are _____ during SWS than REM, the concentrations are still _____ relative to being awake

Back 40

higher, lower

Front 41

What is a zeigeber?

Back 41

A stimuli that synchronizes an endogenous rhythm. In this situation, it's light.

Front 42

The suprachiasmatic nucleus recieves input from _____ and _____ cells in the retina which may account for the ability of light to act as a zeitgeber

Back 42

Amacrine and ganglion cells

Front 43

What structure mediates the ability of other environmental stimuli to reset circadian rhythms?

Back 43

The intergenicular leaflet of the lateral geniculate nucleus

Front 44

The SCN stimulates the _____ zone which stimulates the ______ hypothalamus. This hypothalamic region has opposite effects on the ____ and ____ neurons, which has a common effect on the arousal system which is to _______

Back 44

Spuraventricular zone (SPZ), dorsomedia hypothalamus, vlPOA and LH orexinergic neurons. The common effect is stimulation of the arousal system by inhibiting the vlPOA while stimulating LH orexinergic neurons

Front 45

SCN glucose metabolism is higher during the day than during the night. We investigate this metabolism with the use of what radioisotope?

Back 45

2-deoxyglucose

Front 46

The PER and TIM genes are suspected to encode an essential proteins that regulates circadian rhythm. The TIM gene encodes the ____ protein which is in a negative feedback loop with itself. The PER gene encodes the ____ protein which is in a negative feedback loop with itself. Thus, high levels of PER/TIM products ____ expression of the PER/TIM gene.

Back 46

tim, per, inhibits

Front 47

What are the genetic factors that make someone susceptible to advanced and delayed sleep phase syndromes respectively? What are the consequences of these disorders?

Back 47

Advanced results in a 4-hour advance of sleep and temp. rhythms caused by a mutation in the per2 gene.

Delayed results in a 4-hour lag of sleep and temp. rhythms caused by a mutation in the per3 gene.

Front 48

What gland attached to the dorsal tectum produces a molecule involved in the regulation of of circadian seasonal rhythms? How does a male hamsters season testosterone rhythm change? How can we prevent these seasonal changes?

Back 48

pineal gland! Testosterone secretion in male hamsters increases as length of days increases. We can abolish this by lesioning the SCN

Front 49

How is the SCN connected to the pineal gland?

Back 49

SCN --> Paraventricular nucleus --> Pineal gland

Front 50

What is a melanopsin?

Back 50

Photopigment found in the retina that regulates circadian rhythms

Front 51

What are the 3 symptoms of nacolepsy?

Back 51

Cataplexy

Sleep paralysis

Hypnagogic hallucination