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A neurotransmitter is a signaling molecule secreted by a neuron to affect another cell across a synapse. The cell receiving the signal, or target cell, may be another neuron, but could also be a gland or muscle cell.
Empathogens or entactogens are a class of psychoactive drugs that induce the production of experiences of emotional communion, oneness, relatedness, emotional openness—that is, empathy or sympathy—as particularly observed and reported for experiences with 3,4-methylenedioxymethamphetamine (MDMA). This class of drug is distinguished from the classes of hallucinogen or psychedelic, and amphetamine or stimulants. Major members of this class include MDMA, MDA, MDEA, MDOH, MBDB, 5-APB, 5-MAPB, 6-APB, 6-MAPB, methylone, mephedrone, GHB, αMT, and αET, MDAI among others. Most entactogens are phenethylamines and amphetamines, although several, such as αMT and αET, are tryptamines. When referring to MDMA and its counterparts, the term MDxx is often used. Entactogens are sometimes incorrectly referred to as hallucinogens or stimulants, although many entactogens such as ecstasy exhibit psychedelic or stimulant properties as well.
Neurochemistry is the study of chemicals, including neurotransmitters and other molecules such as psychopharmaceuticals and neuropeptides, that control and influence the physiology of the nervous system. This particular field within neuroscience examines how neurochemicals influence the operation of neurons, synapses, and neural networks. Neurochemists analyze the biochemistry and molecular biology of organic compounds in the nervous system, and their roles in such neural processes including cortical plasticity, neurogenesis, and neural differentiation.
Neuroplasticity, also known as neural plasticity or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It is when the brain is rewired to function in some way that differs from how it previously functioned. These changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping or neural oscillation. Other forms of neuroplasticity include homologous area adaptation, cross modal reassignment, map expansion, and compensatory masquerade. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, information acquisition, environmental influences, pregnancy, caloric intake, practice/training, and psychological stress.
Tianeptine, sold under the brand names Stablon, Tatinol, and Coaxil among others, is an atypical tricyclic antidepressant which is used mainly in the treatment of major depressive disorder, although it may also be used to treat anxiety, asthma, and irritable bowel syndrome.
Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic, G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad, long-lasting signal. This modulation can last for hundreds of milliseconds to several minutes. Some of the effects of neuromodulators include altering intrinsic firing activity, increasing or decreasing voltage-dependent currents, altering synaptic efficacy, increasing bursting activity and reconfiguring synaptic connectivity.
5,7-Dihydroxytryptamine (5,7-DHT) is a monoaminergic neurotoxin used in scientific research to decrease concentrations of serotonin in the brain. The mechanism behind this effect is not well understood, but it is speculated to selectively destroy serotonergic neurons, in a manner similar to the dopaminergic neurotoxicity of 6-hydroxydopamine (6-OHDA). What is known is that this compound is in fact not selective in depleting serotonin content, but also depletes norepinephrine. To selectively deplete serotonin stores, it is commonly administered in conjunction with desmethylimipramine (desipramine), which inhibits the norepinephrine transporter.
Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules during increased neuronal activity.
Indeloxazine (INN) is an antidepressant and cerebral activator that was marketed in Japan and South Korea by Yamanouchi Pharmaceutical Co., Ltd for the treatment of psychiatric symptoms associated with cerebrovascular diseases, namely depression resulting from stroke, emotional disturbance, and avolition. It was marketed from 1988 to 1998, when it was removed from the market reportedly for lack of effectiveness.
Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.
para-Chloroamphetamine (PCA), also known as 4-chloroamphetamine (4-CA), is a substituted amphetamine and monoamine releaser similar to MDMA, but with substantially higher activity as a monoaminergic neurotoxin, thought to be due to the unrestrained release of both serotonin and dopamine by a metabolite. It is used as a neurotoxin by neurobiologists to selectively kill serotonergic neurons for research purposes, in the same way that 6-hydroxydopamine is used to kill dopaminergic neurons.
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.
Malleability of intelligence describes the processes by which intelligence can increase or decrease over time and is not static. These changes may come as a result of genetics, pharmacological factors, psychological factors, behavior, or environmental conditions. Malleable intelligence may refer to changes in cognitive skills, memory, reasoning, or muscle memory related motor skills. In general, the majority of changes in human intelligence occur at either the onset of development, during the critical period, or during old age.
Research into the mental disorder of schizophrenia, involves multiple animal models as a tool, including in the preclinical stage of drug development.
The development of an animal model of autism is one approach researchers use to study potential causes of autism. Given the complexity of autism and its etiology, researchers often focus only on single features of autism when using animal models.
Willardiine (correctly spelled with two successive i's) or (S)-1-(2-amino-2-carboxyethyl)pyrimidine-2,4-dione is a chemical compound that occurs naturally in the seeds of Mariosousa willardiana and Acacia sensu lato. The seedlings of these plants contain enzymes capable of complex chemical substitutions that result in the formation of free amino acids (See:#Synthesis). Willardiine is frequently studied for its function in higher level plants. Additionally, many derivates of willardiine are researched for their potential in pharmaceutical development. Willardiine was first discovered in 1959 by R. Gmelin, when he isolated several free, non-protein amino acids from Acacia willardiana (another name for Mariosousa willardiana) when he was studying how these families of plants synthesize uracilyalanines. A related compound, Isowillardiine, was concurrently isolated by a different group, and it was discovered that the two compounds had different structural and functional properties. Subsequent research on willardiine has focused on the functional significance of different substitutions at the nitrogen group and the development of analogs of willardiine with different pharmacokinetic properties. In general, Willardiine is the one of the first compounds studied in which slight changes to molecular structure result in compounds with significantly different pharmacokinetic properties.
LIT-001 is a small-molecule oxytocin receptor agonist and vasopressin receptor mixed agonist and antagonist that was first described in the literature in 2018. Along with TC OT 39 and WAY-267464, it is one of the first small-molecule oxytocin receptor agonists to have been developed. LIT-001 has greatly improved pharmacokinetic properties relative to oxytocin, reduces social deficits in animal models, and may have potential as a therapeutic agent in the treatment of social disorders like autism in humans.
References
- 1 2 3 4 5 6 7 "Research programme: autism therapeutic (KM-391) - Innovation Pharmaceuticals". AdisInsight. 9 June 2017. Retrieved 10 November 2024.
Cellceutix (now Innovation Pharmaceuticals) was developing KM 391, an orally active, small molecule serotonin uptake modulator, for the treatment of autism. [...]
- 1 2 3 "Delving into the Latest Updates on KM-391 with Synapse". Synapse. 1 November 2024. Retrieved 10 November 2024.
- 1 2 3 4 5 6 Webb S (August 2010). "Drugmakers dance with autism". Nat Biotechnol. 28 (8): 772–774. doi:10.1038/nbt0810-772. PMID 20697394.
Cellceutix, a biotech company in Beverly, Massachusetts, is also testing a preclinical compound for autism, KM-391, in a rodent model of autism developed by researchers at the Kennedy Krieger Institute in Baltimore. The autism-like symptoms are induced by injecting the chemical 5,7-dihydroxytryptamine (5,7-DHT) into the forebrain of newborn rat pups, leading to neonatal serotonin depletion, reduced brain plasticity and abnormal behaviors. In an initial study, KM-391 given over 90 days restored normal behaviors, and near-normal serotonin levels and increased brain plasticity relative to a nontreatment group and a group given Prozac. Another study measuring serotonin levels in three regions of the rat brain has confirmed the restoration of normal serotonin levels. Another small study added an oxytocin antagonist to the mix. The antagonist alone intensified the autism-related behaviors, such as repetitive behaviors and sensitivity to touch, but when given with KM-391, the frequency and intensity of these behaviors were reduced.
- ↑ Kumar B, Prakash A, Sewal RK, Medhi B, Modi M (2012). "Drug therapy in autism: a present and future perspective". Pharmacol Rep. 64 (6): 1291–1304. doi:10.1016/s1734-1140(12)70927-1. PMID 23406740.
Tab. 3. Drugs under different phases of development #: [...] [Drug:] KM 391: Action: Acts on serotonin uptake. Developmental stage: Preclinical stage. [...] # Source: http://clinicaltrials.gov/
- ↑ Majhi S, Kumar S, Singh L (2023). "A Review on Autism Spectrum Disorder: Pathogenesis, Biomarkers, Pharmacological and Non-Pharmacological Interventions". CNS Neurol Disord Drug Targets. 22 (5): 659–677. doi:10.2174/1871527321666220428134802. PMID 36915952.
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