Noradrenaline and our Presumptions of Reality (regulation of the Brain’s ‘Inner World’)?
Noradrenaline Plays a Critical Role in Sensory Perception
Summary: A new study reveals noradrenaline plays a vital role in the early stages of perception. Researchers report later processing of visual information occurs in the cerebral cortex and is affected by noradrenaline to determine if an image will enter our stream of consciousness.
Original Source: AFTAU.
Being aware of our surroundings is a fundamental aspect of our existence. But what in our biological makeup determines how we access and interpret the endless stream of information around us?
A new Tel Aviv University study published in Current Biology suggests that noradrenaline, a neurotransmitter responsible for arousal in the brain, plays a vital role in our early sensory perceptions of the world. “Until now, medical science believed that noradrenaline is involved in alertness, stress, attention and decision making,” says senior author Dr. Yuval Nir, of TAU’s Sackler Faculty of Medicine and Sagol School of Neuroscience. “Our study shows that, in fact, noradrenaline plays a vital role in earlier stages of perception, determining our ability to perceive events around us.” The research was jointly led by Dr. Hagar Gelbard-Sagiv and Efrat Magidov of TAU’s Sackler Faculty of Medicine and Sagol School of Neuroscience, in collaboration with Dr. Haggai Sharon and Prof. Talma Hendler of TAU and the Sagol Brain Institute at Tel Aviv Medical Center. The scientists ran a series of experiments on 30 participants at the Sagol Brain Institute at Tel Aviv Medical Center. Subjects took part in three different sessions in which they received (1) drugs that lowered noradrenaline levels; (2) drugs that increased those levels; or (3) a placebo. After taking the medication, the participants were asked to perform visual tasks such as detecting and discriminating between low-contrast images, while the researchers measured their brain activity by EEG or fMRI. The researchers hoped to determine how various levels of noradrenaline affected visual perception and the way the brain responds to images. “Many people suffer from difficulties in initiating and maintaining sleep,” Dr. Nir concludes. “We hope to follow up on these results and test whether noradrenaline also determines if sensory stimuli such as sounds wake us up from sleep. “We hope that in the future our findings will open new avenues for the development of better anesthetics and new tools for early detection of dangerous situations, such as lapses while driving or flying.” ref
Source: George Hunka – AFTAU
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is adapted from the Cell Press video.
Video Source: Video credited to Cell Press.
Original Research: Open access research for “Noradrenaline Modulates Visual Perception and Late Visually Evoked Activity” by Hagar Gelbard-Sagiv, Efrat Magidov, Haggai Sharon, Talma Hendler, and Yuval Nir in Current Biology. Published July 5 2018.
By David S Goldstein, National Institutes of Health, Bethesda, Maryland, USA
Noradrenaline and adrenaline are catecholamines that play major roles in the regulation of the ‘inner world’ of the body by the brain. Noradrenaline (synonymous with norepinephrine), the main neurotransmitter of the sympathetic nervous system, is responsible for tonic and reflexive changes in cardiovascular tone. Adrenaline is a key determinant of responses to metabolic or global challenges to homeostasis, such as glucoprivation, and of manifestations of emotional distress. In contrast with the view that the sympathetic nervous and adrenomedullary hormonal systems function as a unit (the ‘sympathoadrenal system’) to maintain homeostasis in emergencies, across a variety of situations adrenaline responses are more closely linked to responses of the hypothalamic‐pituitary‐adrenocortical system than of the sympathetic nervous system. The sympathetic noradrenergic system is active even when the individual is at rest and maintains tonic levels of cardiovascular performance. Adrenoceptors in the membranes of effector cells determine the physiological and metabolic effects of catecholamines.
- Noradrenaline and adrenaline are catecholamines.
- Noradrenaline is the main neurotransmitter of the sympathetic nerves in the cardiovascular system.
- Adrenaline is the main hormone secreted by the adrenal medulla.
- The sympathetic noradrenergic system plays major roles in tonic and reflexive changes in cardiovascular tone.
- Adrenaline is a major determinant of responses to metabolic or global challenges to homeostasis.
- Adrenaline responses to stressors are more closely linked to responses of the hypothalamic‐pituitary‐adrenocortical system than of the sympathetic nervous system.
- The sympathetic noradrenergic system is active even when the individual is at rest and maintains tonic levels of cardiovascular performance.
- Adrenoceptors in the membranes of effector cells determine the physiological and metabolic effects of catecholamines.
- Beta‐adrenoceptors mediate stimulatory effects of catecholamines on the rate and force of the heartbeat; stimulation of vascular alpha‐adrenoceptors produces vasoconstriction and increases blood pressure, and stimulation of vascular beta‐adrenoceptors – especially beta‐2 adrenoceptors in skeletal muscle – produces vasodilation.
- Catecholamines affect cardiovascular functions by actions at adrenoceptors on cardiovascular cells, in the nervous system, and in the kidneys. ref
by S Ho, … J Chung, in Innovation and Technology of Women’s Intimate Apparel, 2006
Noradrenaline (norepinephrine), often referred to as one of the ‘stress hormones’ that normally causes an increased heart rate, increased blood pressure, dilation of pupils, dilation of air passages in the lungs, vasoconstriction (narrowing of blood vessels) in non-essential organs and strengthens the force of the heart’s contraction. Lee et al. studied the effects of skin pressure by wearing foundation garments (bra plus girdle) whilst awake on the circadian rhythms of urinary noradrenaline. The urinary noradrenaline level was lowered whilst wearing foundation garments throughout the day and night. Wearing foundation garments during wakefulness and sleep was suggested to influence the noradrenaline secretion. Sugimoto found that urinary norepinephrine was increased by wearing a girdle regardless of the type or the pressure of girdle. A girdle with a larger area of body compression resulted in a greater increase in urinary norepinephrine than a narrow area of compression. The urinary epinephrine level did not change when wearing a girdle. The results indicated that the girdles had a stimulating effect on urinary norepinephrine, suggesting some level of stress on the body. The findings showed inconsistent results in the effect of girdles on urinary stress hormone, therefore future research is needed to establish the effect of wearing girdles. ref
from Alkaloids, 2015
Noradrenaline (NAdr = norepinephrine, NE) is formed by the stereospecific oxidation of the β-carbon of dopamine, which itself is formed by the decarboxylation of l-DOPA (L-3,4-dihydroxyphenylalanine). Epinephrine (Adr) is formed by the N-methylation of norepinephrine. Thus, a compound that blocks the enzyme dopa decarboxylase (responsible for the decarboxylation of dopa) causes a decline in the level of catecholamines, such as dopamine and norepinephrine, and hypotensive activity is expected. The absolute stereostructures of norepinephrine and epinephrine were determined by the transformation of each of these alkaloids into R-mandelic acid. ref
by K. Wiedemann, in International Encyclopedia of the Social & Behavioral Sciences, 2001
Considering a large body of clinical and preclinical findings, the monoamine transmitters serotonin and noradrenaline and the neuropeptide corticotropin-releasing factor are most important in the regulation of the neuroanatomical structures involved in anxiety and fear. Regarding serotonergic neurotransmission, several findings support its involvement in mediating anxiety: serotonin neurons in the raphe nuclei have an inhibitory effect on noradrenergic neurons at the locus coeruleus. In addition, these neurons act at the periaquaeductal gray modifying the escape responses and are also thought to inhibit the hypothalamic release of CRF. From a clinical point of view, these findings are supported by the effects of serotonin reuptake inhibitors, that is, pharmaceuticals which inhibit the uptake of serotonin back into the presynaptic neuron and increase the amount of serotonin in the synapse to bind both to pre- and postsynaptic sites where more than 13 subtypes of serotonin receptors coupled to different membranous and intracellular effector systems have been identified (Kent et al. 1998). Overall, a long-term increase of serotonergic transmission by these compounds exerts antipanic and anxiolytic effects. The other important neurotransmitter system involved in anxiety disorders is the noradrenergic system (Sullivan et al. 1999). Noradrenalin neurons largely originate in the locus coeruleus and some other nuclei in the medulla and pons. Projection sites include the prefrontal cortex, the amygdala, the hippocampus, the hypothalamus, the thalamus, and the nucleus tractus solitarius. Conversely, the locus coeruleus is innervated by the amygdala. Therefore, the locus coeruleus seems to integrate external sensory and visceral afferents influencing a wide range of neuroanatomical structures related to fear and stress. Clinically it has been proven that noradrenergic alpha-2 receptor antagonists such as yohimbine can be used to provoke panic attacks acting via an increase in synaptic availability of noradrenaline. In contrast, clonidine, an alpha-2 adrenergic agonist, exerts anxiolytic-like effects in experimentally induced panic attacks such as lactate infusions. Both transmitter systems, the serotonergic and the noradrenergic, interact with the release of CRF, a 41 amino acid neuropeptide (Arborelius et al. 1999, Koob 1999). Neurons containing CRF and its receptors have been shown to be distributed throughout the brain and CRF has emerged as a neurotransmitter that plays a central role not only in stress regulation but also in anxiety and depression. CRF neurons are found in the amygdala, the hypothalamus, and the locus coeruleus. Their activity is regulated by adaptive responses. CRF neurons also project from the amygdala to the locus coeruleus. Hence CRF could act as a modulator of cognitive and physiological symptoms of anxiety. This factor initiates, on the one hand, a humoral cascade which enhances via the secretion of corticotropin the release of glucocorticoids, which in turn act at central gluco- and mineralocorticoid receptors. CRF is on the other hand involved in the modulation of anxiety and depression. Stress results in increased CRF concentrations in the locus coeruleus and CRF increases the firing rate noradrenergic neurons. In contrast, noradrenaline also potently stimulates the release of CRF. The involvement of CRF is interesting also with respect to respiratory alterations during panic attacks which have led to the ‘suffocation false alarm theory’ (Klein 1993), since CRF seems to be an important modulator of respiratory centers in the brain stem. Several studies support the contention that antagonists and inhibitors of the synthesis of CRF exert anxiolytic-like effects. A CRF-1 receptor-deficient mouse showed a significantly lowered anxiety behavior in comparison with controls. Antagonists of CRF receptors have also been examined in clinical trials for their anxiolytic and antidepressant potency. Since serotonin reuptake inhibitors are involved in the inhibitory regulation of noradrenergic neurons of the locus coeruleus and since serotonin reuptake inhibitors are thought to reduce the hypothalamic release of CRF, these complex interactions suggest that noradrenergic, serotonergic, and CRF-regulated neurotransmission are linked together mediating the responses to anxiety, fear, and stress (see Peptides and Psychiatry). ref
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