Dopamine agonist Compound that activates dopamine receptors A dopamine agonist (DA) is a compound that activates dopamine receptors. There are two families of dopamine receptors, D2-like and D1-like, and they are all G protein-coupled receptors. D1- and D5-receptors belong to the D1-like family and the D2-like family includes D2, D3 and D4 receptors.[1] Dopamine agonists are primarily used in the treatment of Parkinson's disease, and to a lesser extent, in hyperprolactinemia and restless legs syndrome.[2] They are also used off-label in the treatment of clinical depression. The use of dopamine agonists is associated with impulse control disorders and dopamine agonist withdrawal syndrome (DAWS).[3] Medical uses[edit] Parkinson's disease[edit] There are two fundamental ways of treating Parkinson's disease, either by replacing dopamine or mimicking its effect.[1] Treatment of depression in Parkinson's patients[edit] Hyperprolactinemia[edit] Restless leg syndrome[edit] Adverse effects[edit] Side effects[edit]
Mitragyna speciosa Plant species, recreational drug (kratom) Mitragyna speciosa (commonly known as kratom[3]) is a tropical evergreen tree in the coffee family native to Southeast Asia. It is indigenous to Thailand, Indonesia, Malaysia, Myanmar, and Papua New Guinea,[4] where it has been used in herbal medicine since at least the nineteenth century.[5] Kratom has opioid properties and some stimulant-like effects.[6][7] As of 2018[update], the efficacy and safety of kratom are unclear, and the drug was unapproved as a therapeutic agent due to the poor quality of the research.[8][9] In 2019, the United States Food and Drug Administration (FDA) stated that there is no evidence that kratom is safe or effective for treating any condition.[10] Some people take it for managing chronic pain, for treating opioid withdrawal symptoms, or for recreational purposes.[4][8] The onset of effects typically begins within five to ten minutes and lasts for two to five hours.[4] Description[edit] Kratom flowers and foliage
James Gross James J. Gross is a psychologist best known for his research in emotion and emotion regulation. He is a professor at Stanford University and the director of the Stanford Psychophysiology Laboratory. [1] Education[edit] Gross received his B.A. in philosophy from Yale University in 1987. Work in psychology[edit] Gross' contributions to psychology lie primarily in the area of emotion regulation through psychophysiological research. Awards and fellowships[edit] James Gross has been the recipient of numerous academic awards from psychological and educational associations: References[edit] External links[edit] James Gross's homepage Mitragynine pseudoindoxyl Chemical compound Mitragynine pseudoindoxyl is a rearrangement product of 7-hydroxymitragynine.[1] It is an analgesic being more potent than morphine.[2][3] Pharmacology[edit] Mitragynine pseudoindoxyl is a μ opioid receptor agonist and δ opioid receptor antagonist and acts as a G protein biased agonist at μ opioid receptors and possesses a favourable side effect profile compared to conventional opioids.[4] See also[edit] Mitraphylline References[edit]
David Marr (neuroscientist) British neuroscientist and psychologist Biography[edit] Born in Woodford, Essex, and educated at Rugby School; he was admitted at Trinity College, Cambridge on 1 October 1963 (having been awarded an Open Scholarship and the Lees Knowles Rugby Exhibition). Work[edit] Theories of cerebellum, hippocampus, and neocortex[edit] Marr is best known for his work on vision, but before he began work on that topic he published three seminal papers proposing computational theories of the cerebellum (in 1969), neocortex (in 1970), and hippocampus (in 1971). Levels of analysis[edit] Stages of vision[edit] See also[edit] Publications[edit] References[edit] Further reading[edit] External links[edit] Extensive online biography Methylone Group of stereoisomers Methylone (also known as "3,4-methylenedioxy-N-methylcathinone", "MDMC", "βk-MDMA" and by the slang term "M1") is an empathogen and stimulant psychoactive drug. It is a member of the substituted amphetamine, substituted cathinone and substituted methylenedioxyphenethylamine classes. Methylone is the substituted cathinone analog of MDMA and the 3,4-methylenedioxy analog of methcathinone. The only structural difference of methylone with respect to MDMA is the substitution of 2 hydrogen atoms by 1 oxygen atom in the β position of the phenethylamine core, forming a ketone group.[2] Methylone was first synthesized by the chemists Peyton Jacob III and Alexander Shulgin in 1996 for potential use as an antidepressant.[3] Methylone has been sold for recreational use, taking advantage of the absence of legal prohibition of this compound in many countries[citation needed]. Effects[edit] Resemblance to MDMA[edit] Pharmacology[edit] Pharmacodynamics[edit] Pharmacokinetics[edit] Texas:
Paul Bach-y-Rita Paul Bach-y-Rita (April 4, 1934 – November 20, 2006) was an American neuroscientist whose most notable work was in the field of neuroplasticity. Bach-y-Rita was one of the first to seriously study the idea of neuroplasticity (although it was first proposed in the late 19th century), and to introduce sensory substitution as a tool to treat patients suffering from neurological disorders. Bach-y-Rita is known as "the father of sensory substitution".[1] Biography[edit] Bach-y-Rita was born on April 4, 1934, in New York City to Anne Hyman and Pedro Bach-y-Rita,[2] the latter a Catalan poet and teacher at City College of New York.[3] He studied at the Bronx High School of Science, from which he graduated at the age of fifteen before studying at Mexico City College (now the University of the Americas in Puebla). Work in Sensory Substitution and Neuroplasticity[edit] Bach-y-Rita's most notable work was in the field of neuroplasticity. Early research in Neuroscience[edit] See also[edit]
Morphine Pain medication of the opiate family Morphine is a pain medication of the opiate family that is found naturally in a dark brown resin in poppies (Papaver somniferum). It can be taken orally, sublingually, via inhalation, the trans-dermal route, inter-anally as well as via injection (both subcutaneously as well as more commonly intravenously.[7][9] It acts directly on the central nervous system (CNS) to induce analgesia and alter perception and emotional response to pain. Potentially serious side effects of morphine include decreased respiratory effort, vomiting, nausea, and low blood pressure.[7] Morphine is addictive and prone to abuse.[7] If one's dose is reduced after long-term use, opioid withdrawal symptoms may occur.[7] Common side effects of morphine include drowsiness, vomiting, and constipation.[7] Caution is advised for use of morphine during pregnancy or breast feeding, as it may affect the health of the baby.[7][2] Medical uses[edit] Pain[edit] Shortness of breath[edit]
Sensory substitution Sensory substitution is a change of the characteristics of one sensory modality into stimuli of another sensory modality. A sensory substitution system consists of three parts: a sensor, a coupling system, and a stimulator. The sensor records stimuli and gives them to a coupling system which interprets these signals and transmits them to a stimulator. Sensory substitution systems may help people by restoring their ability to perceive certain defective sensory modality by using sensory information from a functioning sensory modality. History[edit] Physiology[edit] In a regular visual system, the data collected by the retina is converted into an electrical stimulus in the optic nerve and relayed to the brain, which re-creates the image and perceives it. Technological support[edit] In order to achieve sensory substitution and stimulate the brain without intact sensory organs to relay the information, machines can be used to do the signal transduction, rather than the sensory organs. PSVA[edit]