Synonyms for hypoactivity or Related words with hypoactivity


Examples of "hypoactivity"
Hypoactivity is an inhibition of behavioral or locomotor activity.
Theca cells with granulosa cells help form the corpus luteum. Theca cells are only correlated with developing ovarian follicles. They are the leading cause of endocrine-based infertility, as either hyperactivity or hypoactivity of the theca cells can lead to fertility problems; hyperactivity of theca cells causes hyperandrogenism, and hypoactivity leads to a lack of estrogen. Granulosa cell tumors, while rare (less than 5% of ovarian cancers), involve both the granulosa cells and the theca cells.
Studies in mice and rats indicated the symptoms of acute toxicity due to overdose included: hypoactivity, labored respiration, convulsion, diarrhea, tremor, and coma. A study in dogs indicated that a dose of 2000 mg/kg was not lethal.
Hypoactivity is a characteristic effect of sedative agents and many centrally acting anesthetics. Other drugs such as antipsychotics and mCPP also produce this effect, often as a side effect.
Sluggish cognitive tempo (SCT) is a cluster of symptoms that may comprise a novel attention disorder which is distinct from ADHD. It is characterized by dreaminess, mental fogginess, hypoactivity, sluggishness and a slow working speed.
Theories unifying neuroimaging findings have been proposed. The first model proposed is the "Limbic Cortical Model", which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing. Another model, the "Corito-Striatal model", suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures results in depression. Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.
The fearlessness theory of CU traits suggests that low amounts of cortisol lead to underarousal, causing impairments in fear processing, a trait seen in CU individuals. Hypoactivity in the hypothalamic-pituitary-adrenal axis in combination with CU traits seem to cause antisocial behavior even without external hardships.
In medicine, it can refer to a drug that can hold both antagonist (inhibitory) and agonist (excitatory) properties. For example, the antipsychotic Aripirazole causes antagonism of Dopamine D2 receptors in areas such as the Mesolimbic area of the brain (which show increased dopamine activity in psychosis), but also agonism of Dopamine receptors in areas of dopamine hypoactivity, such as the mesocortical area.
Similarly, in alcoholics, during withdrawal there is decreased activity in the OFC (compared to the OFCs of healthy controls) but, in addition, detoxified alcoholics have significantly lower levels of benzodiazepine receptors in the OFC (compared with healthy controls). Hypoactivity in the OFC of alcoholics is also supported by blunted metabolism in the OFC to response to both serotonogenic and GABA- ergic agents.
Sarcoidosis has paradoxical effects on inflammatory processes; it is characterized by increased macrophage and CD4 helper T-cell activation, resulting in accelerated inflammation, but immune response to antigen challenges such as tuberculin is suppressed. This paradoxic state of simultaneous hyper- and hypoactivity is suggestive of a state of anergy. The anergy may also be responsible for the increased risk of infections and cancer.
"S. cyanea" venom is strong enough to cause haemolytic activity, especially on O positive blood types. Rhabdomyolysis and hemorrhage may also occur. In mice, abdominal spasms, ataxia, defecation, dyspnoea, hyperactivity, hypoactivity, sweating, and throes were observed following venom injection. "S. cyanea" venom also contains some antibacterial activity.
Another region involved in the psychogenic tremor is the temporoparital junction depicted by a hypo-activation in patients that were functional imaging recorded during an episode of functional tremor or when the same patients were voluntarily mimicking their tremor. This region is thought to be a comparator region, comparing actual with predicted sensory feedback. This experiment suggests that the hypoactivity might represent a failure to match the actual and predicted sensory feedback, resulting in an inhibition of the movement. In addition, another functional imaging study in psychogenic movement disorder noted abnormally strong amygdala–supplementary motor area connectivity when patients were presented with emotionally stimuli and abnormally weak supplementary motor area–prefrontal cortex connectivity in a reaction time task. Scientists thus speculated that the hypoactivity may be due to the lack of an appropriate prediction outcome signal of the conversion tremor. Thus, without the predicted outcome signal, there would be no comparison between the predicted versus the actual sensory outcome of the conversion movement and hence the temporoparietal junction hypoactivity and the sensation that the movement is not under one’s control enabling the initiation of it.
Studies utilizing positron emission tomography (PET) have found during tasks that invoke disfluent speech, people who stutter show hypoactivity in cortical areas associated with language processing, such as Broca's area, but hyperactivity in areas associated with motor function. One such study that evaluated the stutter period found that there was over activation in the cerebrum and cerebellum, and relative deactivation of the left hemisphere auditory areas and frontal temporal regions.
Other mechanisms, however, may take place at the central level after peripheral nerve damage. The loss of afferent signals induces functional changes in dorsal horn neurons. A decrease in the large fiber input decreases the activity of interneurons inhibiting nociceptive neurons i.e. loss of afferent inhibition. Hypoactivity of the descending antinociceptive systems or loss of descending inhibition may be another factor. With the loss of neuronal input (deafferentation) the STT neurons begin to fire spontaneously, a phenomenon designated "deafferentation hypersensitivity."
A similar model termed "the limbic cortical model" has been proposed involving hyperactivity of ventral paralimbic regions and hypoactivity of dorsal limbic and prefrontal regions. This model and another termed "the cortical striatal model", consisting of abnormalities in the prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, caudate, putamen and globus pallidus, has been supported by more recent literature. The authors cited study bias, and lack of specificity of inclusion criteria and limiting factors.
Many of the obstacles that individuals with ASD face in terms of facial processing may be derived from abnormalities in the fusiform face area and amygdala, which have been shown to be important in face perception as discussed above. Typically, the fusiform face area in individuals with ASD has reduced volume compared to normally developed persons. This volume reduction has been attributed to deviant amygdala activity that does not flag faces as emotionally salient and thus decreases activation levels of the fusiform face area. This hypoactivity in the fusiform face area has been found in several studies.
In addition to the 5-HT receptor, buspirone is a weak antagonist of the dopamine D receptor, with approximately 15-fold lower affinity for this receptor relative to the 5-HT receptor. It preferentially blocks inhibitory presynaptic D autoreceptors, and antagonizes postsynaptic D receptors only at higher doses. In accordance, buspirone has been found to increase dopaminergic neurotransmission in the nigrostriatal pathway at low doses, whereas at higher doses, postsynaptic D receptors are blocked and antidopaminergic effects such as hypoactivity and reduced stereotypy, though notably not catalepsy, are observed in animals.
Studies of emotional processing in patients with MDD show various biases such as a tendency to rate happy faces more negatively. Functional neuroimaging has demonstrated hyperactivity of various brain regions in response to negative emotional stimuli, and hypoactivity in response to positive stimuli. Patients also showed decreased activity in the left dorsolateral prefrontal cortex in response to negative stimuli. Depressed people have impaired recognition of happy, angry, disgusted, fearful and surprised faces, but not of sad faces. The therapeutic lag of antidepressants has been suggested to be a result of antidepressants modifying emotional processing leading to mood changes. The observation that both acute and subchronic SSRI administration increases response to positive faces.
mCPP's strongest actions are at the 5-HT and 5-HT receptors and its discriminative cue is mediated primarily by 5-HT. Its negative effects such as anxiety, headaches, and appetite loss are likely mediated by its actions on the 5-HT receptor, whereas its psychedelic effects at high doses are caused by 5-HT activation. However, there is also evidence for mCPP antagonism of the 5-HT receptor, suggesting an indirect mechanism for the drug's psychedelic effects. Other effects of mCPP include nausea, hypoactivity, and penile erection, the latter two the result of increased 5-HT activity and the former likely via 5-HT stimulation.
Changes may also be associated with neuroplasticity, synaptic functionality and voltage gated calcium channels. Increased magnitude of hyperpolarization, possibly a result of dysfunctional calcium regulation, leads to decreased firing rate of neurons and decrease plasticity. This effect is particularly pronounced in the hippocampus of aged animals, and may be an important contributor to age associated memory deficits. The hyperpolarization of a neuron can be divided into three stages, the fast, medium and slow hyperpolarization. In aged neurons, the medium and slow hyperpolarization phases involving the opening of calcium dependent potassium channels appears to be prolonged. The prolonging of this phase has been hypothesized to be a result of deregulated calcium and hypoactivity of cholinergic, dopaminergic, serotonergic and glutaminergic pathways.