Sleep I & II

effects of a poor nights sleep

Reduced activity in the fronto-parietal network (Prefrontal cortex and bilateral Parietal lobe)

Insula, and right Parahippocampal cortex

Attention, working memory, long-term memory

Sleep deprivation (SD) amplifies amygdala reactivity (red) in response to negative emotional stimuli and decreases associated amygdala–medial prefrontal cortex (mPFC) connectivity.

Emotional reactivity; reduced emotional control

Mouse study

• Lose weight even though eat more

• Decrease in body temperature

• “debilitated appearance”, lesions on paws and tails

• Increase plasma norepinephrine

• Eventually die

what happens to a hamster in constant dim light

still rythm, slightly moved back each day (evidence that circadian rythms are endogenous)

are circadian rythms endogenous or exogenous?

1. Circadian rhythms are endogenous

2. But circadian rhythms are regulated by external environment!

When timing of light shifted, hamster shows phase shift of activity. What does this tell us?

biological clock entrains to light

-synchronizes to environmental stimulus

Zeitgeber

A stimulus that entrains circadian rhythm

ex: light-dark cycle, other examples?

Suprachiasmatic nucleus (SCN)

in hypothalamus, near LGN

Lesions to SCN interfere with circadian rhythms

SCN transplant changes period of the clock (tau mutant hamster)

SCN is core pacemaker, source of biological clock

SCN Neuron

Genes in SCN provide a molecular clock: Rhythmic gene expression, 24hr cycle

transcription-translation negative feedback loop

Per

Patterns of expression of gene called period

Transcription-translation negative feedback loop

1. Cells in SCN make 2 proteins: Clock & Cycle (Cycle → Bmal-1 in mammals)

2. Promote transcription of per & cry genes

3. Per and Cry proteins bind together →inhibit Clock/Cycle

4. Slows transcription of per & cry genes

5. Slows production of Per and Cry proteins

8. Per / Cry eventually degrade with time, allowing Clock/Cycle to again promote per & cry transcription

How does light entrainment work?

Signals from Retinohypothalamic Tract:

External light-dark signals →specialized retinal ganglion cells →hypothalamus ( SCN )

Retinohypothalamic Tract:

External light-dark signals →specialized retinal ganglion cells →hypothalamus ( SCN )

• ”Entrainment Pathway” = non-image forming pathway

• Don’t go to rods and cones and bipolar, straight to ganglion

Intrinsically photosensitive retinal ganglion cells (ipRGC)

• Respond directly to light….Do not receive input from rods or cones!

• Contain photopigment melanopsin (most sensitive to blue light)

• Release glutamate in SCN

Glutamate release…

• Glutamate drives light-evoked change in gene expression (e.g., rapid transcription of per)

• Resets molecular feedback loop

• Synchronizing SCN clock to light-dark signals

• In other words, glutamate release “sets” molecular clock in SCN by influencing SCN genes

Electrical SCN activity

Each individual SCN neuron displays a circadian rhythm of electrical activity

Groups of SCN neurons synchronize activity through electrical synapses

Sends rhythmic signal to body/brain

SCN signals to Pineal Gland influences sleep-wake cycle

 Pineal glad produces melatonin = sleep signal

 Can be influenced by (blue) light →inhibit melatonin secretion →Awake

Wake

Desynchronized (mixture of high/low freq: Beta rhythms)

Stage 1

Alpha rhythms (8-12Hz)

Stage 2

Sleep spindles / k-complex (10Hz)

Stage 3/4

Slow delta rhythms (3-4 Hz) Slow Wave Sleep, Low Frequency (slow) Waves High Amplitude

REM: Rapid Eye Movement

EEG resembles wake even loss of muscle tone (brainstem inhibits spinal motor neurons) - Paradoxical Sleep, Mixed frequency waves, Low amplitude, Less synchronized, like wake

Dreams

Longer REMs as the night goes on