Central nervous system defined

In addition to the weU-defined opioid systems in the central nervous system, the three opioid peptides and their precursor mRNA have also been identified in peripheral tissues. ( -Endorphin is most abundant in the pituitary, where it exists in corticotroph cells with ACTH in the anterior lobe and in melanotroph cells with MSH in the intermediate lobe (59). Enkephalin and pre-pro-enkephalin mRNA have been identified in the adrenal medulla (60) and this has been the source of material for many studies of pro-enkephalin synthesis and regulation. Pre-pro-enkephalin mRNA has also been identified in the anterior and posterior lobes of the pituitary (61). mRNA for all three opioid precursors has been identified in the reproductive system (62—64). POMC... 

Extracellular adenosine acts through a class of G protein-coupled receptors (GPCRs), defined across mammalian species as Ab A2a, A2B, and A3ARs (adenosine receptors). Adenosine has a cytoprotective role in the body, both in the periphery and in the central nervous system. Following binding of adenosine, or another naturally occurring agonist, the receptor... 

Pituitary Adenylyl Cyclase-activating Polypeptide (PACAP) is a 38-amino acid peptide (PACAP-38), which is widely expressed in the central nervous system. PACAP is most abundant in the hypothalamus. It is also found in the gastrointestinal tract, the adrenal gland and in testis. Its central nervous system functions are ill-defined. In the periphery, PACAP has been shown to stimulate catecholamine secretion from the adrenal medulla and to regulate secretion from the pancreas. Three G-protein coupled receptors have been shown to respond to PACAP, PAQ (PACAP type I) specifically binds PACAP, VPACi and VPAC2 also bind vasoactive intestinal peptide (VDP). Activation of PACAP receptors results in a Gs-mediated activation of adenylyl cyclase. 

Impact on the body the impact on the body may be defined as local if the effect is confined to the site around the area of application of the device, or systemic if the effects may spread throughout the body, as is the case when the circulatory or central nervous systems are involved. 

B, Thiamin Coenzyme in pyruvate and a-ketoglutarate, dehydrogenases, and transketolase poorly defined function in nerve conduction Peripheral nerve damage (beriberi) or central nervous system lesions (Wernicke-Korsakoff syndrome)... 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Neuropathic pain is defined as spontaneous pain and hypersensitivity to pain associated with damage to or pathologic changes in the peripheral nervous system as in painful diabetic peripheral neuropathy (DPN), acquired immunodeficiency syndrome (AIDS), polyneuropathy, post-herpetic neuralgia (PHN) or pain originating in the central nervous system (CNS), that which occurs with spinal cord injury, multiple sclerosis, and stroke. Functional pain, a relatively newer concept, is pain sensitivity due to an abnormal processing or function of the central nervous system in response to normal stimuli. Several conditions considered to have this abnormal sensitivity or hyperresponsiveness include fibromyalgia and irritable bowel syndrome. 

Central nervous system myelin contains some unique proteins 58 Peripheral nervous system myelin also contains unique proteins 63 Some classically defined myelin proteins are common to both peripheral and central myelin 64... 

Defines the objective of safety pharmacology studies to Anon23 reveal functional effects on major physiological systems (e.g., cardiovascular, respiratory, renal, and central nervous systems)... 

Eric R. Kandel, a professor at Columbia University, is one of the world leaders in the science of the central nervous system, which he prefers to call the science of mind. A winner of the Nobel Prize in Medicine or Physiology in 2000, together with Arvid Carlsson and Paul Greengard, for his studies on the mechanism of learning, he has written the history of his life in science in an elegant book In Search of Memory. In this book, Kandel defines five principles of the science of mind. Here they are (and I quote directly) ... 

Exposure levels leading to effects on the central nervous systems of humans are not precisely defined. No symptoms of lightheadedness or nausea were experienced by humans exposed to 50 ppm for 70 minutes or 10 ppm for 3 hours (Stewart et al. 1961), but nausea, headache, and giddiness were found to be common symptoms in workers exposed to carbon tetrachloride for 8 hours a day at concentrations of 20-125 ppm (Elkins 1942 Heimann and Ford 1941 Kazantzis and Bomford 1960). Dizziness has also been reported in humans following short-term exposure (15 minutes) at a higher concentration (250 ppm) (Norwood et al. 1950). This suggests that the threshold for central nervous system effects in humans is probably in the range of 20-50 ppm for an 8-hour workday. 

As discussed in Section 2.2, the effects that are most often observed in humans exposed to carbon tetrachloride are liver and kidney injury and central nervous system depression. Exposure levels leading to these effects in humans are not well-defined. The threshold for central nervous system effects following exposures of 8 hours or more is probably in the range of 20-50 ppm (Elkin 1942 Heimann and Ford 1941 Kazantzis and Bomford 1960). On the other hand, kidney and liver effects can occur following exposure (15 minutes to 3 hours) to vapor concentrations of 200 and 250 ppm, respectively (Barnes and Jones 1967 Norwood et al. 1950). These doses correspond to an absorbed dose of approximately 100-200 mg/kg. 

The behavioral effects of nicotine have been defined as both stimulant and depressant, effects that are influenced by the present mental status and expectations of the smoker. Smokers may feel alert and relaxed. Nicotine produces myriad effects on the central nervous system (CNS), almost all of which appear to be mediated through nicotinic receptors. Additionally, nicotine influences multiple neuronal systems. One of its most prominent effects is stimulated release of dopamine, particularly in the nucleus accumbens, which is a major component of the reward system. Nicotine also stimulates the release of endogenous opioids and glucocorticoids. 

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