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Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
In the pons, the locus coeruleus projects norepinephrine toward the spinal cord as well as into the thalamus and forebrain. The forebrain projections appear to alter affective components of behavior, while the spinal projections inhibit pain transmission in the dorsal horn via α2 receptors on the dorsal horn. α2 receptor binding is both pre-synaptic on the C fibers and post-synaptic on the dorsal horn neurons. Opiates inhibit the activity of the cells of the locus coeruleus. During withdrawal from opiates, the increased activity of these cells becomes symptomatic. Clonidine has been used as an antagonist to blunt the withdrawal effect.
Changing the Paradigm from Neurochemical to Neuroelectrical Models
Published in Hanno W. Kirk, Restoring the Brain, 2020
Part of the excitement of that period in the new field of neurophysiology was the discovery and identification of the function of the growing numbers of the chemical NTs. With that came intensive research on how either over- or under-production of specific NTs, or dysfunctions at the synapse level, could negatively impact brain functioning. For example, norepinephrine (noradrenaline), an excitatory NT, is produced in the locus coeruleus in the pons of the brain. In response to arousal stimuli, the locus coeruleus distributes norepinephrine to various centers in the brain to regulate the body’s physiological arousal response via long axon connections. One of the conditions associated with overproduction of norepinephrine is post-traumatic stress disorder (PTSD), in which the limbic system is in a constant state of over-arousal due to hypervigilance. On the other hand, if too little norepinephrine reaches key cortical areas involved in cognitive processing and emotions, then attention, motivation, decision- making, learning, and memory are likely to be degraded or depressed (as in ADHD). For over-production, the pharmaceutical industry came up with anxiolytics; for under-production, the answer became stimulant medication.
Life Enrichment through Movement
Published in Lisa D. Hinz, Beyond Self-Care for Helping Professionals, 2018
Rhythmic movements of all types can help reduce tension, stress, and anxiety (Kinsbourne, 2011; Thayer, 2001). Studies show that chewing and grooming behaviors appear in rats that are under stress; engaging in these behaviors appears to help calm them. Stress activates dopamine circuitry in the limbic system of the brain, and with too much stress the basal ganglia take control of behavior over higher cortical systems, generating simple and instinctive rather than learned actions. Familiar repetitive movements moderate the dopamine effect and reduce arousal levels (Kinsbourne, 2011). Rhythmic movement also activates the cerebellum and releases norepinephrine in the locus coeruleus (LC), providing a calming effect. The LC is a brain structure located in the brainstem which plays a role in attention/arousal; people with AD/HD often use repetitive movements to increase task attention. In addition, the LC also is connected to the limbic system through the amygdala and plays a role in emotion regulation. Many people regulate tension or anxiety with repetitive or rhythmic motions such as nail biting, but because they cannot perceive that they can control these habits, they often do not feel good about them. However, a similar soothing rhythm is created when people knit, crochet, or engage in various other types of craftwork, and there is evidence that this soothing rhythm is one of the many characteristics of working with textiles that makes them so appealing and therapeutic (Collier, 2011).
Correlations with REM sleep behavior disorder severity in isolated rapid eye movement sleep behavior disorders patients
Published in International Journal of Neuroscience, 2023
Sang Jin Kim, Eun Ju Chung, Ki-Hwan Ji, Mi-Ri Kang, Jin Yong Hong, Sunseong Lee, Ji Sun Park, Jungsu S. Oh, Jae Seung Kim, Suk Yun Kang
The correlation between pain and visuospatial dysfunction with RBD severity may be associated with RBD pathophysiology. This pathophysiology is currently poorly understood, but RBD is thought to be associated with several nuclei in the pontomedullary brainstem that include the locus coeruleus, subcoeruleus/sublateral dorsal nucleus, laterodorsal tegmental nuclei, the PPN, and medullary magnocellular reticular formation [8]. These nuclei play a role in pain modulation, visuospatial attention, and cognition including visuospatial function and memory [24–26]. The locus coeruleus is a norepinephrine-producing nucleus in the dorsal pons, and projects to the brain widely and is involved in homeostasis, sensory processing, and cognitive and motor function [24,26]. The raphe nuclei are serotonin-producing nuclei in the midline from the medulla to the midbrain and are also involved in sensory processing that includes pain, heat, touch [27], and visual orientation [28]. One recent study reported increased thermal detection threshold in iRBD patients, and they assumed that peripheral small nerve fibers might be associated because they did not find a difference in laser evoked potentials and conditioned pain modulation between iRBD patients and controls. However, more studies are needed, because they did not perform skin biopsies to check nerve pathology and did not assess the presence and severity of pain in iRBD patients [29]. Besides, there was no PSG data to determine RBD severity in that study.
Optimizing sleep across the menopausal transition
Published in Climacteric, 2023
Work in animal models shows that ovarian hormones, including estradiol, regulate female sleep [70]. However, the underlying neurobiological substrates, mechanisms and pathways remain unknown [71], and further work is needed to define the neural circuits involved [72], considering circadian timing and reproductive stage, especially given some of the paradoxical effects [73] of estradiol on sleep–wake behavior in rodents versus women. Estradiol is a neuroactive steroid and there are estrogen receptors in sleep and arousal-regulating nuclei, including the preoptic area of the hypothalamus, suprachiasmatic nucleus and locus coeruleus [71]. Estradiol (and other hormones of the hypothalamic pituitary ovarian axis), therefore, may influence sleep–wake regulation directly, for example by influencing adenosinergic actions in the preoptic area (a sleep-promoting nucleus) to affect sleep homeostasis [73] or by influencing arousal systems in the lateral hypothalamus (rich in hypocretin-releasing neurons, which promote wakefulness) [71], or the locus coeruleus (primary site of norepinephrine, involved in arousal) [71]. Estradiol could also act indirectly to influence sleep via other systems, including thermosensory and thermoregulatory sites in the hypothalamus, which overlap with sleep-active sites [74].
Mental energy: plausible neurological mechanisms and emerging research on the effects of natural dietary compounds
Published in Nutritional Neuroscience, 2021
Patrick J. O’Connor, David O. Kennedy, Stephen Stahl
A clear distinction exists between low mental energy and diagnosable psychiatric/neurological conditions, but the underlying neurological processes are related. The neurotransmitter hypothesis of mental illness originally implicated imbalances in specific neurotransmitters as the underlying cause [21]; however, this theory does not account for the impact of other relevant factors [22]. The monoamine hypothesis of mood disorders postulates that dysregulation in norepinephrine, dopamine, and serotonin pathways causes the symptoms observed with these conditions [22]. This theory has evolved to shift focus from specific neurotransmitters to interactions among these systems. Noradrenergic neurons originating in the locus coeruleus are located near the midbrain raphe nucleus, where they interact with serotonergic neurons. Therefore, it has been proposed that major depression is likely associated with deficiencies in all three monoamines and that different levels of dysregulation produce the various depressive phenotypes observed clinically [22].