- EEG patterns and what they represent about cortical activity during wakefulness and the stages of sleep and REM sleep.
A little luck often goes a long way regarding scientific discovery. In chapter two, we learned about Otto Loewi, who discovered the role of acetylcholine because of a dream he had. He even stated that if he wasn’t in a rush to perform the experiment in the middle of the night before he forgot it (as he had once before) he probably would have discounted it. The measurement of sleep stages using an EEG (Electroencephalograph) was also a happy accident. Before measuring brain activity during sleep, scientists didn’t even suspect stages of sleep. An EEG records an average of the electrical potentials of the cells/fibers in the brain areas nearest to each electrode on the scalp. Data from an EEG can be combined with that of a polysomnograph to better understand the stages of sleep. Alpha waves are present at a certain frequency during relaxation while awake. Stage 1 sleep brain activity as measured by EEG is lower than it is in a state of relaxation but higher voltage than other sleep stages. During stage 2, recordings indicate bursts of 12-14 Hz waves, called sleep spindles, which are accompanied by temporary inhibition of neuronal firing, called K-complex synchrony (Cash et al., 2009; Eschenko et al., 2016; Mednick., et al., 2013; Hennies et al., 2016, as cited in, Kalat, 2019, p. 269). Sleep spindles are associated with consolidation of memories. Slow Wave sleep is marked by inhibition of input from the cerebral cortex and neuronal synchrony. What most of us know as REM sleep, was once referred to as Paradoxical sleep; the terminology is still used in reference to some animals that don’t have rapid eye movements during their sleep cycles (Jouvet, 2019, as cited in, Kalat, 2019, p. 269). During REM sleep there are high levels of brain activity. EEG readings indicate low-voltage and fast waves. Essentially, sleep does depend partially on decreased activity in the cerebral cortex, but this is not the same as halting activity. GABA is our brains major inhibitory neurotransmitter, and axons that release GABA become very active while we sleep (Massamini et al., 2005, as cited in, Kalat, 2019, p. 273). Basically, neurons have a steady firing rate, and this does not stop; what does stop is sharing of information throughout the brain which is accomplished by release of this inhibitory neurotransmitter.
2. What brain structures are involved in REM sleep including structures that inhibit motor movement, activate the thalamus, and visual areas of the cortex?
The Pons and Medulla send inhibitory messages during REM, interfering with the body’s ability to use its large muscles. Increased activity is present in the pons, medulla, and the limbic system. REM is marked by waves of neural activity from the pons, lateral geniculate (a part of the thalamus) and then the occipital cortex; these waves are referred to as PGO waves. The activity increase in the pons is what signals REM sleep; interestingly, the initiation is due to inhibitory messages that inhibit other inhibitory neurotransmitters.
- The suprachiasmatic nucleus. Where is it located? What are its functions? Which brain areas does it activate or inhibit? What excites it to set its time?
The suprachiasmatic nucleus, also referred to as SCN is a part of the hypothalamus. Damage to the SCN results in disrupted circadian rhythm. The SCN is essential to the generation of circadian rhythms; though it isn’t the only generator of these evolutionary rhythms it plays a predominate role. Research has shown that the SCN keeps its rhythm, independently of the body in which they exist; this was shown by cells from the SCN of a hamster being transplanted into another hamster. The donor cells retained their rhythm instead of modifying to that of the recipients. The SCN is right above the optic chiasm. A path from the optic nerve to the SCN, the retinohypothalamic path, heavily influenced by optic signals which is associated with the influence of light signals and circadian rhythm. Genes that synthesize proteins, such as PER, help set out circadian rhythms; mutations in these genes can have a great effect on sleep schedules. For instance, one mutation causes a person to get tired extremely early in the evening or later in the afternoon; moreover they often get tired earlier and earlier each night, keeping an extremely odd schedule. The pineal gland, which is part of the endocrine system releases a hormone called melatonin, that also contributes to our sleep schedule. Melatonin is released in the evening and in humans, increases sleepiness. In other animals the release of melatonin can signal wakefulness. A tumor on the pineal gland could potentially cause a person to stay awake for days on end.
4. Why is it unlikely that one could act out their dreams unless they had REM behavior disorder?
REM sleep is also called paradoxical sleep because during REM, while neuronal activity is high, the major postural muscles are completely relaxed. People who have REM behavior disorder do no relax in the same way and are able to move around during REM cycles. The role of GABA and inhibitory neurotransmission associated with vigorous and similar movements in mice, indicates that REM behavior disorder may be caused by inadequate inhibitory signals. Dream content during NREM sleeps is less prevalent and usually very simplistic. Sleep walking doesn’t occur doing REM sleep and isn’t generally paired with dreaming so it isn’t likely that one would act out a dream while sleep walking.
5. Describe the roles of each of the following neurotransmitters on both sleep and arousal. Discuss neural pathways involved:
Norepinephrine:
The Locus Coeruleus is a small spot in the pons that spends much of its time in hibernation with small bursts of activity, particularly when emotionally aroused. This is associated with the fact that we are more likely to remember certain things if they are accompanied by strong emotion. Norepinephrine is released by axons in the locus coeruleus, increasing strong connections, essentially increasing activity in highly active areas and decreasing activity in less active areas; this concept is referred to as “gain”. This promotes attention to important information and enhances memory. Norepinephrine interrupts REM sleep.
Serotonin:
The primary serotonergic neurons are found in the Raphe Nucleus. The role serotonin plays in the wake/sleep cycle is complicated. Serotonergic neurons fire most while we’re awake, decrease during NREM, and essentially stop during REM. Serotonin interrupts REM sleep; therefore, many people who take SSRI’s get less REM sleep than average. It was once theorized that REM was important for memory consolidation but the fact that SSRI’s that affect REM don’t often impair memory contradicts that theory; to the contrary sometimes anti-depressants improve memory.
Acetylcholine:
Acetylcholine is associated with both REM, and wakefulness. The ponstometencephalon is part of the reticular formation that is important for wakefulness. Axons release acetylcholine to arouse the hypothalamus, thalamus and basal forebrain; partly by regulating the levels of K+. A drug called carbachol can be injected to stimulate acetylcholine synapses and initiate REM sleep faster. Not only does acetylcholine promote onset of REM but is also essential to the motor inhibition. Otto Loewi’s Nobel prize winning experiment found acetylcholine; which is known to dilate blood vessels, increases bodily secretions, and slows heart rate. Without acetylcholine we don’t dream!
Why antihistamines produce drowsiness; The neural structure and its effects on brainstem arousal centers
The hypothalamus has neurons that produce sleep and that produce wakefulness alike. Under the hypothalamus in the tuberomammillary nucleus, is where you will find the axonal pathway that releases a neuromodulator, histamine. Histamines are potent and enhance arousal throughout the brain. Histamines dilate blood vessels, which in-tern lowers blood pressure. This extra permeability also allows white blood cells to attack pathogens. Antihistamines that cross the blood-brain-barrier counteract this transmitter and make us tired, as it doesn’t differentiate between good and bad histamine.
References:
Kalat, J. W. (2019). Biological psychology (13th ed). Boston, MA: Cengage.
Antihistamines (2020. Retrieved from: https://www.nhs.uk/conditions/antihistamines/ (Links to an external site.)
Also Brain & Behavior YouTube videos from Wendy Suzuki (If I post the web address it will post the video preview as well).
My Aria 
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