We decided that we would all research elements on sleep, and share our findings. My research is based on the chemicals associated with sleep, and the brain mechanisms. My results were mostly found in Psychological Science, Second Canadian Edition by Gazzaniga, Heatherton, Heine and McIntyre (chapter 4). Following are my findings:
The circadian rhythm theory of sleep states that sleep has evolved to keep animals quiet and inactive during times of the day when there is greatest danger (foremost dark time for humans since lack of light puts us in possible danger). Therefore, some physiological (body temperature, hormone levels) and brain processes are regulated around these circadian rhythms. According to this theory, animals need a specific amount of time to accomplish the tasks associated with survival, the remaining time is spent being inactive (hidden away). Therefore, sleep duration is a function of the time required for the animal to seek food, how easily it can hide, and how vulnerable it is to attack.
I included a "roadmap" to better identify the different areas involved in the discussion.
As previously stated, multiple neural mechanisms are involved in maintaining these circadian rhythms. The biological clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Light-sensitive photoreceptors in the eye send signals to the SCN. Individual neurons in the SCN work as our biological clock. The SCN also signals the pineal gland to secrete melatonin: a hormone that travels through the bloodstream and affects various receptors in the body and the brain. Darkness triggers melatonin releases, and bright light suppresses its production.
Sleep involves alterations in brain mechanisms associated with the production of aroused states. In 1949, Moruzzi and Magoun identified the reticular formation in the brainstem as being responsible for the cerebral cortex arousal. Low levels of activity in the reticular formation produce sleep, and high levels awakening. More recent research concluded that multiple regions within the reticular formation take action in the control of these sleep-wake cycles. In particular, one specific region sends the neurotransmitter norepinephrine which increases the cortical arousal.
Non-REM sleep (non dreaming phases) is triggered by a small area of the forebrain. REM sleep (dreaming phases) is triggered by acetylcholine neurons in the pons (brainstem region - see the first chart). In the minute before REM episodes, these neurons become increasingly active. Signals from this region are transmitted to the thalamus and the occipital lobes. Brain-imaging studies show activation of limbic structures (amygdale), and certain regions of prefrontal cortex (middle region behind the eyes). Areas involved in rational thought and decisions making (other prefrontal cortex) have their activity lessened. Visual association areas are activated (triggering the vivid imagery in dreaming). The phase is associated by the activation of various neural processes: some lead to paralysis of motor systems, others lead to the activation of mental circuits related to motivational states. Neurons in the pons send signals to the spinal cord that block movement during REM sleep. Hence, surgical lesioning of the pons causes animals to become very active while in REM sleep! Dreaming associated with REM is a result of the activation of brain structures involved in motivation, emotion, and reward, along with the visual associations areas.
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