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"disinhibit" Definitions
  1. disinhibit somebody to help somebody to stop feeling shy so that they can relax and show their feelings

17 Sentences With "disinhibit"

How to use disinhibit in a sentence? Find typical usage patterns (collocations)/phrases/context for "disinhibit" and check conjugation/comparative form for "disinhibit". Mastering all the usages of "disinhibit" from sentence examples published by news publications.

"Our data suggest that alcohol sustains fundamental appetite signals, (and does) not just disinhibit their behavioral manifestation," wrote Denis Burdakov, who led the study at the Francis Crick Institute in London.
"While pot can help bring out our most sexy selves, disinhibit us, or relax us during sex, I would highly recommend that people learn to be in the moment and deeply feel and connect with their partners without using enhancing drugs," Prosterman says.
Every day, we wake up and are exposed to some new dumbass saying dumbass shit about, for instance, the truth of the existence of carbon-affected climate change that will probably disinhibit the world if we don't do something about it, or the legal status of a group of refugees seeking shelter in the United States, or "Concerned editorials" about demographic shifts in the United States making the country less white, or any number of other terrifying and important real world issues.
Anethole has estrogenic activity. It has been found to significantly increase uterine weight in immature female rats. Fennel, which contains anethole, has been found to have a galactagogue effect in animals. Anethole bears a structural resemblance to catecholamines like dopamine and may displace dopamine from its receptors and thereby disinhibit prolactin secretion, which in turn may be responsible for the galactagogue effects.
Alcohol is believed to disinhibit urges normally considered socially unacceptable. The sober brain is able to utilize the frontal cortex to make executive decisions and restrain these impulses. However, the drunk brain is unable to regulate the urges for excessive behavior. By leading the brain to overreact to present cues and disregard the implications of one's actions, alcohol often provokes aggressive behavior.
But if a society believes that intoxication leads to relaxation and tranquil behavior, then it usually leads to those outcomes. Alcohol expectations vary within a society, so these outcomes are not certain. People tend to conform to social expectations, and some societies expect that drinking alcohol will cause disinhibition. However, in societies in which the people do not expect that alcohol will disinhibit, intoxication seldom leads to disinhibition and bad behavior.
In men, raloxifene has been found to disinhibit the hypothalamic–pituitary–gonadal axis (HPG axis) and thereby increase total testosterone levels. Due to the simultaneous increase in sex hormone-binding globulin (SHBG) levels however, free testosterone levels often remain unchanged in men during therapy with raloxifene. Raloxifene has estrogenic effects on liver protein synthesis. It increases SHBG levels in both pre- and postmenopausal women as well as in men.
By blocking 5-HT1A autoreceptors at doses that are selective for them over postsynaptic 5-HT1A receptors, pindolol may be able to disinhibit serotonin release and thereby improve the antidepressant effects of SSRIs. The results of augmentation therapy with pindolol have been encouraging in early studies of low quality. However, a 2015 systematic review and meta- analysis of five randomized controlled trials found no overall significant benefit. There were also no significant differences in tolerability or safety.
In other words, this branch of the vagus is said to inhibit or disinhibit defensive limbic circuits, depending on the situation. Note: Attributing defensive behaviours purely to the limbic system is an oversimplification, as these are triggered by _perceived_ threats, thus requiring an interplay of brain areas performing sensory integration, memory and semantic knowledge with the limbic system to be elicited. Similarly, the regulation of emotions requires a complex interplay of higher cognitive areas with limbic ones. The vagus nerve mediates control of supradiaphragmatic visceral organs, such as the esophagus, bronchi, pharynx, and larynx.
While epilepsy- induced hypergraphia is usually lateralized to the left cerebral hemisphere in the language areas, hypergraphia associated with lesions and other brain damage usually occurs in the right cerebral hemisphere. Lesions to the right side of the brain usually cause hypergraphia because they can disinhibit language function on the left side of the brain. Hypergraphia has also been known to be caused by right hemisphere strokes and tumors. Lesions to Wernicke's area (in the left temporal lobe) can increase speech output, which can sometimes manifest itself in writing.
Hu and her colleagues then explored the potential of using ketamine to target the burst firing/hyperactivity in lateral habenula neurons that was leading to depressive phenotypes. Ketamine has been previously shown to be effective as a rapid antidepressant, yet the mechanisms of action have not yet been completely elucidated. They showed that blocking the NMDAR-dependent burst firing in the LHb, through ketamine administration, is able to alleviate symptoms of depression in rodent models. The blocking of LHb hyperactivity appears to disinhibit downstream monoaminergic reward centers thereby exerting antidepressant effects on habenular circuitry.
Due to its selectivity for and competitive inhibition of the AR, BOMT has been described as a pure or "true" antiandrogen, similarly to benorterone, cyproterone, and flutamide. Like other steroidal antiandrogens, BOMT may actually be a weak partial agonist of the AR, as it appears to have the potential for weak androgenic effects in specific situations. On the basis of animal research, BOMT does not appear to act as an AR antagonist in central nervous system tissues, and in relation to this, does not disinhibit the hypothalamic–pituitary–gonadal axis or increase testosterone levels.
Aromatase inhibitors like anastrozole prevent the conversion of testosterone into estradiol by aromatase. As only a very small fraction of testosterone is converted into estradiol, this does not affect testosterone levels, but it can prevent estrogenic side effects like gynecomastia that can occur when testosterone is administered at relatively high dosages. However, estradiol exerts negative feedback on the hypothalamic–pituitary–gonadal axis and, for this reason, prevention of its formation can reduce this feedback and disinhibit gonadal production of testosterone, which in turn can increase levels of endogenous testosterone. Testosterone therapy is sometimes combined with an aromatase inhibitor for men with secondary hypogonadism who wish to conceive children with their partners.
Several studies in brain traumas and insults have demonstrated significant associations between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices, affecting visuospatial functions, somatosensation, and spatial memory, motoric, instinctive, affective, and intellectual behaviours. Disinhibition syndromes have also been reported with mania-like manifestations in old age with lesions to the orbito-frontal and basotemporal cortex involving limbic and frontal connections (orbitofrontal circuit), especially in the right hemisphere. Behavioural disinhibition as a result of damage to frontal lobe could be seen as a result of consumption of alcohol and central nervous system depressants drugs, e.g., benzodiazepines that disinhibit the frontal cortex from self-regulation and control.
Cannabinoids usually contain a 1,1'-di-methyl-pyran ring, a variedly derivatized aromatic ring and a variedly unsaturated cyclohexyl ring and their immediate chemical precursors, constituting a family of about 60 bi-cyclic and tri-cyclic compounds. Like most other neurological processes, the effects of cannabis on the brain follow the standard protocol of signal transduction, the electrochemical system of sending signals through neurons for a biological response. It is now understood that cannabinoid receptors appear in similar forms in most vertebrates and invertebrates and have a long evolutionary history of 500 million years. The binding of cannabinoids to cannabinoid receptors decrease adenylyl cyclase activity, inhibit calcium N channels, and disinhibit K+A channels.
Alcohol myopia is a cognitive-physiological theory on alcohol abuse in which many of alcohol's social and stress-reducing effects, which may underlie its addictive capacity, are explained as a consequence of alcohol's narrowing of perceptual and cognitive functioning. The alcohol myopia modelSteele & Josephs, "Alcohol Myopia It's Prized and Dangerous Effects",American Psychologist,1990 posits that rather than disinhibit, alcohol produces a myopia effect that causes users to pay more attention to salient environmental cues and less attention to less salient cues. Therefore, alcohol's myopic effects cause intoxicated people to respond almost exclusively to their immediate environment. This "nearsightedness" limits their ability to consider future consequences of their actions as well as regulate their reactive impulses.
Chemical structure of agomelatine (Valdoxan), the prototypical NDDI. Norepinephrine and dopamine disinhibitors (NDDIs) are a class of drugs which act at specific sites to disinhibit downstream norepinephrine and dopamine release in the brain. Agomelatine, an antidepressant which disinhibits norepinephrine and dopamine release in the frontal cortex by antagonizing 5-HT2C receptors, was the first drug to be described as an NDDI. While many other drugs also antagonize 5-HT2C receptors to some degree or another, they tend to be very non-specific in their actions, and as a result, the term "NDDI" has generally, though not always (for instance, fluoxetine has been called an NDDI in addition to SSRI due to its (weak) blockade of 5-HT2C), been reserved for describing newer, more selective agents in which disinhibition of norepinephrine and dopamine release is their primary mechanism of action.

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