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]
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
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
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]
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]
Neuroplasticity
Neuroplasticity, also known as brain plasticity, neuroelasticity, or neural plasticity, is the ability of the brain to change continuously throughout an individual's life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time. The aim of neuroplasticity is to optimize the neural networks during phylogenesis, ontogeny, and physiological learning, as well as after a brain injury.[1] Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are "plastic") even through adulthood.[2][3][4][5] However, the developing brain exhibits a higher degree of plasticity than the adult brain.[6][7]:30 Neurobiology[edit] JT Wall and J Xu have traced the mechanisms underlying neuroplasticity. Applications and example[edit] The adult brain is not entirely "hard-wired" with fixed neuronal circuits. Treatment of brain damage[edit]
How BrainPort Works
A blind woman sits in a chair holding a video camera focused on a scientist sitting in front of her. She has a device in her mouth, touching her tongue, and there are wires running from that device to the video camera. The woman has been blind since birth and doesn't really know what a rubber ball looks like, but the scientist is holding one. Well, not exactly through her tongue, but the device in her mouth sent visual input through her tongue in much the same way that seeing individuals receive visual input through the eyes. Most of us are familiar with the augmentation or substitution of one sense for another. ... we do not see with the eyes; the optical image does not go beyond the retina where it is turned into spatio-temporal nerve patterns of [impulses] along the optic nerve fibers. The multiple channels that carry sensory information to the brain, from the eyes, ears and skin, for instance, are set up in a similar manner to perform similar activities.
Circadian Rhythm Abnormalities
Tryptophan
Tryptophan (symbol Trp or W)[2] is an α-amino acid that is used in the biosynthesis of proteins. It contains an α-amino group, an α-carboxylic acid group, and a side chain indole, making it a non-polar aromatic amino acid. It is essential in humans, meaning the body cannot synthesize it: it must be obtained from the diet. Tryptophan is also a precursor to the neurotransmitter serotonin and the hormone melatonin.[3] It is encoded by the codon UGG. Like other amino acids, tryptophan is a zwitterion at physiological pH where the amino group is protonated (–NH3+; pKa = 9.39) and the carboxylic acid is deprotonated ( –COO−; pKa = 2.38).[4] Function[edit] Metabolism of L-tryptophan into serotonin and melatonin (left) and niacin (right). The disorder fructose malabsorption causes improper absorption of tryptophan in the intestine, reduced levels of tryptophan in the blood,[10] and depression.[11] Recommended dietary allowance[edit] In 2002, the U.S. Dietary sources[edit] Side effects[edit]
