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Sleep Deprivation

 

           Antidepressant Effects, Dopamine

           Eye-Blink Rate, Dopamine

           Effect on the Frontal Lobes

           Adrenaline

           Related Topics

 

Antidepressant Effects, Dopamine

"So why is sleep deprivation making a comeback now? Because use of newer antidepressant drugs together with sleep deprivation treatment is proving effective for helping to prevent return of depressive symptoms after sleep deprivation and for improving depressed patients' response to their medication."

WebMD: Doctors Waking Up to Benefits of Sleep Deprivation Treatment for Depression

 

"The hypothesis has been put forward that the antidepressant effect of sleep deprivation (SD) is mediated by an enhanced dopamine release resulting in an amphetamine like action of SD."

Neuropsychopharmacology: Eye-blink rates and depression. Is the antidepressant effect of sleep deprivation mediated by the dopamine system?

 

          The Brain: Dopamine

 

Eye-Blink Rate, Dopamine

"A series of studies demonstrated a possible correlation between eye-blink rate and central dopamine activity."

Neuropsychopharmacology: Eye-blink rates and depression. Is the antidepressant effect of sleep deprivation mediated by the dopamine system?

 

"Therefore, the blink rates of

          12 drug-naive [not previously exposed to therapy or treatment] patients with major depression and

          12 healthy controls

were compared

          before and after SD [sleep deprivation] and

          before and after 2.5 mg bromocriptine [a medication that mimics the activity of dopamine] as a dopaminergic [dopamine producing] challenge [a chemical substance that is administered to a patient to see whether a normal response occurs].

The main result of the study was that

          The depressed patients had a significantly higher increase of blinking after SD [sleep deprivation] both with and without a dopaminergic challenge.

          Basal eye-blink rate was not different in nonretarded major depression patients [individual is not lethargic and not slow to initiate action] compared to controls.

          Sleep deprivation

  • Increased blink rate in depression patients but not in controls, and
  • The increase was proportional to improvements in depressive state after sleep deprivation.

          Bromocriptine did not increase blink rate 1 hour after application.

This result is consistent with the hypothesis that antidepressant SD [sleep deprivation] acts through dopamine release, although it is not conclusive, because other neurotransmitters like acetylcholine may be involved in the regulation of blinking."

Neuropsychopharmacology: Eye-blink rates and depression. Is the antidepressant effect of sleep deprivation mediated by the dopamine system?

 

           The Brain: Dopamine

 

Effect on the Frontal Lobes

"Lack of a night's sleep is paid for the next day in impaired function of the frontal cortex, as measured by electroencephalograph (EEG) potentials."

SFN: Losing Sleep Impairs Frontal Cortex Function

 

"'When you are sleep-deprived, you are recruiting more parietal resources [because the frontal lobes are impaired],' said Dr. Godbout. 'The parietal lobe counterbalances for lack of frontal function,' Dr. Godbout stated. The frontal cortex is thought to govern so-called executive function, such as decision making, which matures only at the end of adolescence."

SFN: Losing Sleep Impairs Frontal Cortex Function

 

Adrenaline

"Six studies on sleep/wake patterns and circadian rhythms were carried out. In summary:

(1)   Adrenaline excretion, self-rated activation, and body temperature rhythms

         Persisted during sleep deprivation,

         Resisted adjustment to rotating shift work, but

         Adjusted rather well to permanent night work.

Noradrenaline

         Adjusted to most schedules and lost its rhythm during sleep deprivation.

         When night sleep was reintroduced the noradrenaline rhythm reappeared while the existing adrenaline rhythm was accentuated.

(2)   Exposure to a performance stressor at the trough raised adrenaline to daytime levels. An equally large response was seen at the peak.

(3)   Interindividual [occurring between two and four individuals] day-to-day consistency of 3 and 24 hour levels was high for both catecholamines [neurotransmitters that activate--examples are dopamine, epinephrine and norepinephrine]. Intraindividual [being or occurring within the individual] consistency of the 24-hour pattern was high for adrenaline but low for noradrenaline. Cosine estimates of adrenaline phase showed a considerable intraindividual consistency while interindividual consistency was poor. Noradrenaline had poor cosine fit.

(4)   Sleep deprivation did not change catecholamine excretion either during the vigil or during recovery sleep.

(5)   It was concluded that adrenaline excretion, rated alertness, and body temperature exhibited self-sustained circadian rhythms which made adjustment to new sleep/wake patterns very difficult, and that the noradrenaline excretion rhythm depended on exogenous [outside the body] factors."

Acta Physiol Scand Suppl.: Altered sleep/wake patterns and circadian rhythms. Laboratory and field studies of sympathoadrenomedullary and related variables.

 

          Wikipedia: Noradrenaline

          Stedman's Online Medical Dictionary, 27th Edition: Noradrenaline

 

Related Topics

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