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Clinical neurochemistry
Clinical neurochemistry is the field of neurological biochemistry which relates biochemical phenomena to clinical symptomatic manifestations in humans. While neurochemistry is mostly associated with the effects of neurotransmitters and similarly-functioning chemicals on neurons themselves, clinical neurochemistry relates these phenomena to system-wide symptoms. Clinical neurochemistry is related to neurogenesis, neuromodulation, neuroplasticity, neuroendocrinology, and neuroimmunology in the context of associating neurological findings at both lower and higher level organismal functions.
==Neuropharmacology and drug action==
The integration of knowledge concerning the molecular and cellular actions of a drug within the brain circuitry leads to an overall understanding of a neurological drug's action mechanisms. This understanding of drug action in turn can be extrapolated to account for system-wide or clinical manifestations which are observed as symptoms. The clinical effects of a neural drug are due to both immediate changes in homeostasis and long-term neural adaptations characterized by the phenomena neural plasticity.〔
The most basic and fundamental neurological phenomena in neuropharmacology is the binding of a drug or neurologically active substance to a cellular target. One assay to determine the extent at which a ligand binds to its receptor is the radioligand binding assay (RBA), in which specific binding of a radioactively-labeled ligand is denoted by the difference between saturated and non-saturated tissue samples. While the RBA assay assumes that the tissue prepared has just one molecular target per ligand, in actuality this may not be the case. For example, serotonin binds to many diverse serotonin receptors which makes the RIA assay quite difficult to interpret. Because many receptors are essentially enzymes, the field of pharmakinetics utilizes the Michaelis-Menten equation to describe drug affinity (dissociation constant Kd) and total binding (Bmax). Although Kd and Bmax can be determined pictorally in a normal or logarithmic plot of ligand binding vs drug concentration, Scatchard plots allow for mathematical representation of several ligand binding sites, each with its own Kd.〔
Drug potency is the measure of binding strength between a drug and a specific molecular target, whereas drug efficacy describes the biological effect exerted by the drug itself, at either a cellular or organismal level. Because drugs range widely in their potency and efficacy, drugs have been categorized on the spectrum of agonists and antagonists. ''Agonists'' bind to receptors and elicit the same effects as an endogenous neurotransmitter. For example, morphine is an agonist of the opioid receptor family. Conversely, ''antagonists'' bind to a receptor and elicit no cellular change.〔 Naloxone, an antagonist of the opioid receptors, exerts a biological effect only be interfering with endogenous neurotransmitter (morphine) binding.〔 ''Inverse agonists'' bind to receptors and elicit the opposite effect that an agonist would. The spectrum of drug continuum also includes ''partial agonists'' and ''partial inverse agonists'', which comprise the wide majority of neurological clinical treatments. The ultimate clinical effect of a drug can be analyzed with a dose-response curve.〔
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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