Rem and Dreaming
|The proper APA Style reference for this manuscript is:|
GIBBS, E. (2001). Rem and Dreaming. National Undergraduate Research Clearinghouse, 4. Available online at http://www.webclearinghouse.net/volume/. Retrieved July 15, 2018
INDIANA UNIVERSITY EAST DEPARTMENT OF PSYCHOLOGY
Sponsored by: SUSAN SHAPIRO (email@example.com)
|There are four stages of sleep; slow, delta, spindle and REM. REM sleep has been linked to dreaming by observation on human subjects and chemical manipulation in animal studies. Hobson’s reciprocal-interaction model gives a biological explanation to the chemical transaction that take place during REM. REM is generated in the pontine reticular formation and REM is turned on by cholinergic neurotransmitters. Serotonergic and noradrenergic neurotransmitters inhibit the cholinergic neurotransmitters turning REM off. The function of REM has not been definitely determined. One theory is an evolutionary, adaptive function. Another function may be a restorative process for some types of memory during REM sleep.|
Dreamin,g everyone does it, though not everyone remembers his or her dreams. (Hobson 1988) In a life span of seventy years an individual will spend 50,000 hours that is 2,000 days or six full years dreaming. Over the centuries and in current times dreams have been of interest. Speculation of sleep observations and scientific research began as early as the nineteenth century by such scientist as Wilhelm Wundt and psychoanalyst Sigmund Freud. Although Freud’s theory over shadowed many ground breaking neurological studies on dreaming. The result has been, over the years dreams have been believed to have a mysterious meaning of an individuals unconscious desires and past experiences. Current studies prove dreams derive from biological processes in the brain. It is unlikely that dreams have psychoanalytical meaning the way Freud proposed. With so much time being spent dreaming some biological function must derive from dreaming. Let us start at where sleep and dreaming begin. Sleep begins with NREM (SWS) and progress to REM sleep. There are three major slow oscillatory rhythms present during NREM and a fast oscillating rhythm during waking and REM.( Mahowald 1997) The first NREM cycle, happening after the initial preparing for sleep alpha waves, stage one (slow rhythm) consist of frequencies of with a <1 Hz. Stage two (delta rhythm) consist of frequencies of 1 to 4 Hz. The cortex generates the stages one and two. Stage three (spindle rhythm) has a frequency of 7 to 14 Hz. The spindle rhythm is generated by the reticular nucleus of the thalamus. It is the spindle stage that blocks transmittion of the outside environment to the cortex. . Though neither the cortex nor the thalamus require the other for function during these stages they do interact. Hobson now believes that there is abundant evidence that rest activity rhythms, and NREM sleep are controlled by peptide hormones. Peptide hormones are responsible for controlling states of mood over a 24 hour to week period. The fourth stage is REM with fast oscillating gamma rhythms of 20 to 40 Hz, though Hobson (Hobson et al., 1998) reported 30 to 70 Hz. It is well documented now that REM is when dreaming occurs. The discovery occurred when waking human subjects after observation of rapid- eye-movement. Observers then questioned subjects to report what was currently on their minds. The most vivid and bizarre dreams occur during REM sleep. These dreams are also the dreams most likely to be remembered upon waking up. It is now believed that dreaming happens during all stages of sleep NREM and REM. The stages of sleep one to four happen in about 90 to 100 minutes depending on the individual. (Hobson 1988) It is thought that the length of the REM sleep cycle may be correlated to brain size. Though it has not been proven, it has been positively correlated by testing the length of time that protein can be transported down axons in cats. It takes 30 minutes for protein to move across half the brain stem in cats. This is the same time frame of a REM sleep cycle in cats. It has been established that REM is where dreaming occurs in the sleep cycle. Let us now explain the four features of dreams, bizarreness, motor hallucination, emotion and memory deficit. (Hobson et al., 1998) Bizarreness is described as being: the incongruence of plot, the instability of time, people and places. Bizarreness consists of many aspects of activation and deactivation within the brain. The deactivation of the fusiform gyrus, responsible for face recognition. The deactivation of the parietal operculum, responsible for special imagery. The dorsolateral prefrontal areas and precuneus both associated with the encoding and retrieving episodic memory. The prefrontal area and the parietal lobules associated with working memory. Motor hallucinations, visual and motor, are active behaviors such as running, flying etc… Emotions are perceived as an increased intensified fear, anxiety and anger. Memory deficits make recall during consciousness difficult. The causes of these features are the activation of, or deactivation of certain structures within the brain and brainstem. Motor hallucinations may be caused by the activation of the basal ganglia, visual cortex, lateral geniculation nucleus motor cortex and auditory cortex. Emotions are the activation of the medial limbic structures and the paralimbic, which shapes the plot of the dreams through the emotions not vise versa. Memory deficits are thought to be the absence of noradrenaline and serotonin, crucial to learning and memory.. Where does the activation and deactivation of these structures originate? (Been 1997) Hobson and McCarley activation-synthesis hypothesis of dreaming states that dreams are internally generated in the brain stem and is independent of the external world or internal somatic drives for its origin. Specifically REM begins in the pontine reticular formation located in the pons. The pontine reticular formation, locus coeruleus and raphe nuclei are the major structures that play a role in REM-on and REM-off. During REM-on the brain sends signals upward via the thalamus and down ward to the spinal cord. First consider the downward signal to the spinal cord. During this activation the bulbar reticular formation, located with in the medullary reticular formation nuclei, send toxic hyperpolarizing signals to motor neurons in the spinal cord resulting in muscle atonia. This inhibition is thought to prevent self-injury, in forms of acting out dreams, during REM sleep. Such would be the case during the motor hallucination. The pontine reticular formation also sends some signals downward to the spinal cord generating twitching of the extremities. (Hobson 1988) An Italian scientist Santa de Sanctis observed the first observations of twitching in 1899. His observations of sleeping dogs led him to believe animals like humans also dream. Lucia Fontana, in the seventeenth century associated the movement of the eyes with dreaming. The movement of the eyes, now known to be generated by the pontine reticular formation. The pontine reticular formation transmits signals to the oculomotor neurons causing a twitching action. This is not to say that the muscles around the eye are moving. Like the other muscle in the body the eye muscles are inactive. What is it about the pontine reticular formation that activates REM? It produces a cholinergic excitory neurotransmitter, acetylcholine. Two inhibitory neurotransmitters seen during sleep are serotonine and norepinephrine, both responsible for REM-off states. Norepenephrine is manufactured in the locus coeruleus, located within the anterior dorsal portion of the pontine reticular formation. The raphe nuclei, located medially along the pontine reticular formation extending into the midbrain reticular formation and medullary reticular formation, manufactures serotonin. The discovery of the three interconnecting systems within the brain stem led to the reciprocal-interaction hypothesis (figure 1). The reciprocal-interaction hypothesis begins; an excitatory response within the pontine reticular formation activates the cholinergic REM-on cells, acetylcholine. This activation sends signals: in a circular pattern exciting itself for the period of REM sleep. It also sends signals to the aminergic REM-off cells. The later signals are inhibited until an excitatory response triggers the release of the inhibitory noradrenoline and serotonin aspect of REM-off cells. It also maintains its state reciprocally while inhibiting REM-on cells. This interaction is the 90-100 minute sleep cycle throughout the evening. (Hobson 1988) states, “ The brain stem is the mighty battle ground of warring neuronal function, and REM sleep and dreaming are the result of temporary domination of one neuronal population over the other.” Most of the studies use cats or rats as subjects. Cats are a favored choice because of their sleep patterns, fourteen hours of sleep per day, their independent personalities, and a brain structure very similar to humans. (Hobson 1988) To test the theory of reciprocal-interaction hypothesis two techniques were used. A cholinergic agonist, such as charbacol and bethenchol were injected to increase acetylcholine. Charbachol activates at least two kinds of acetylcholine receptors: one acetylcholine receptor is turned on by nicotine the other by muscarine. Muscarinic receptors are part of the parasympathetic nervous system, specifically smooth muscle. Activation of the muscarinic receptors enhances REM sleep. (Hobson et al., 1998) The study in Neuroreport, concluded carbochol indeed induced REM sleep, and may be responsible for the generation of REM. Cholinergic LTD (lateral dorsal tagmental) evokes excitatory post synaptic potentials (EPSP’s) in the pontine reticular formation neurons. These cholinergic LTD nuclei are located in the midbrain reticular formation. It is in this location that electrical signals are sent rostrally via the thalamus to cortical areas during REM. The EPSP’s can be blocked by scopolamine. Scopolamine and atropine are muscarinic blockers. The second technique used to enhance acetylcholine action is to produce acetylcholinesterase inhibitors. Acetylcholinestrase is responsible for braking down acetylcholine. The association of the acetylcholine and REM sleep was confirmed by observation in the Neuroreport. (Hobson et al., 1998) Microdialysis studies show enhanced acetylcholine release in the medial pontine reticular formation during natural and carbochol induced REM sleep. Thalamic acetylcholine originating from the mesopontine is higher in both wake and REM than in NREM. During this study an acetylcholine increase was also observed in the lateral geniculate body. But for there to be an cholinergic REM-on state NREM serotonine and noradrenaline has to be inhibited. During cat studies levels of serotonine are higher in NREM than in REM and are higher in waking than NREM, in the raphe nuclei and medial pontine reticular formation. (Hobson et al., 1998) The reduction of serotonine in REM sleep has been recently discovered in the human amygdala, hippocampus, orbitofrontal cortex and cingulated cortex. PET images revealed discrepant activation in these areas. (Hobson et al., 1998) “It can be inferred that the human limbic system is turned on but demodulated during dreaming.” In another study using PET and statistical parametric mapping, (Maquet et al., 1996) They reported findings of REM sleep, operationally defined as human subjects who maintained REM sleep while scanning and recalled dreams upon wakening. The results show a positive correlation between REM and increase cerebral blood flow in the pontine tagmentum, left thalamus, both amygdaloid complexes, anterior cingulated cortex and right parietal cortex (supramarginal gyrus), precuneus and posterior cingulated cortex. It is reported that cortical activation during REM is not uniform. Several regions are more or less activated than others. We now have an idea of what causes REM sleep and where it is generated. But why dream? What significance and function can dreaming provide? There are two main theories to provide an explanation: an adaptive evolutionary function, and a restorative memory function. Whether we sleep to forget or to remember is argued between the psychoanalyst and neurobiologist. (Been 1997) Psychoanalyst Berger, Kramer and Rotor suggest the purpose of REM sleep is to “regulate and stabilize affect-related information” into a format that has already proven successful. Disturbances in REM sleep resulting in irritability and emotional outburst night terrors and narcolepsy are support for the affect-regulation theory according to Berger, Kramer and Rotor. Research on patients with posttraumatic stress disorder observed an increased REM latency and decreased REM time. The conclusion then is that these patients were not allowing “traumatic affect-related material” to become included into the dream. Therefore, not allowing the trauma to become part of the long-term memory. Evolutionary perspectives give an opinion on REM sleep and the difficulty of psychoanalysis. (Ramachandran 1996) Ramachandran suggest that dreaming sets the stage for incorporation of memory. He states, “the brain, during dreaming, brings out repressed memories for an improve rehearsal” to see if they can be incorporated into long-term memory without harm to the ego. If the dream doesn`t "make sense” it is repressed again. Ramachandra believes that psychoanalysis tries to uncover during wakefulness what nature does naturally during dreaming making psychoanalysis difficult. Hobson looks at a biological perspective on REM as memory function. (Hobson et al., 1998) It is believed that the bizarreness and nonsense of dreams is just that and any function must be looked at as the attention and the enhancement of learning processes such as memory consolidation. Dreams begin at the end of a 90 to 100 minute cycle, in REM sleep. The reciprocal-interaction model gives a functional model of the chemical and electrical processes exchanged during REM. Current research suggest a more involved chemical exchange in the reciprocal-interaction model than was once thought. Though dreams may not have meaning as Freud suggested. Dreams still seem to reflect an individual’s stored memory and emotion brought about by chemical exchanges in the brain and brainstem.
REFERENCES Been, Harold. (1997). Dreams: The Convergence of Neurobiologic And Psychoanalytic Perspectives. Journal of The American Acadamy of Psychoanalysis. 25 (4). 647-651. Hartmann, Ernest. (1998). Nightmare After Trauma as Paradigm for All Dreams: A New Approach to the Nature and Functions of Dreaming. Psychiatry. 61. 235,236. Hobson, Allan J., Stickgold, Robert and Pace-Schott, Edward F. (1998). The Neuropsychology of REM sleep dreaming. NueroReport. 9. R1-R14. Hobson, Allan J., Pace-Schott, Edward f., Stickgold, Robert and Kahn, David. (1998). To dream or not to dream? Relevant data from new neuroimaging and electrophysiological studies. Current Opinion in Neurobiology. 8. 239-244. Hobson, Allan J. (1988). The Dreaming Brain. New York. Basic Books , Inc., Publishers. Mahowald, Mark W., M.D. (1997). Synchrony, sleep, dreams and consciousness: Clues from K-complexes. Neurology. 49.909-911. Maquet, Pierre, Peters, Jean-Marie, Aerts, Joel, Delfiore, Guy, Degueldre, Christian, Luxen, Andre & Franck, Georges. (1996). Functional neuroanatomy of human rapid-eye-movement sleep and dreaming. Nature. 383. 163-165. Ramachandran, V.S. (1996). The Evolutionary Biology of Self Deception, Laughter, Dreaming and Depression: Some clues from Anosognosia. Medical Hypotheses. 47. 356-357.
APPENDIX Figure 1. Chemical interaction between REM-on, cholinergic and REM-off, serontonergic and noradrenergic reciprocal-interaction model.
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