CNS effect

In humans, the hypothalamic-derived protein and the hormone noncovalent complexes are packaged in neurosecretory granules, then migrate along axons at a rate of 1 4 mm/h until they reach the posterior pituitary where they are stored prior to release into the bloodstream by exocytosis (67). Considerable evidence suggests that posterior pituitary hormones function as neurotransmitters (68) vasopressin acts on the anterior pituitary to release adrenocorticotropic hormone [9002-60-2] (ACTH) (69) as well as on traditional target tissues such as kidneys. Both hormones promote other important central nervous system (CNS) effects (9,70). 

Dmg receptors represent another type of receptor family. The central nervous system (CNS) effects of the anxiolytic, diazepam, and the psychotropic actions of the caimabiaoids and phencycUdine have resulted ia the identification of specific receptors for these molecules. This has resulted ia the search for an endogenous ligand for these receptors. Thus, ia these situations, the pharmacological action has preceded the discovery of the receptor which, ia turn, has provided clues ia several iastances to the endogenous ligand. 

Agent or class CNS effects Orthostatic hypotension Arrhythmias Anticholinergic effects Weight change... 

Isoxazoles (630a) have reported diuretic activity (75JAP(K)7595272), while (630b) have reported hypolipemic activity (77USP4032644) and (630c) have CNS effects. 

The long-term OES is 50 ppm (8 hr TWA), set to protect against CNS effects, which will also protect against liver or kidney damage and initation. The short-term OES is 1000 ppm (15 minute reference period) to minimize exposures at initant levels. 

The solvent has a sweetish odour similar to chloroform detectable at about 30 ppm. It is primarily a depressant of tlie central nervous system (CNS). Significant impairment of performance in behavioural tests and some CNS effects have occuiTed at 1000 ppm but not at 300 ppm prenarcotic symptoms have occuired at mean levels of 200 ppm to 300 ppm. 

The most important fluorinated benzodiazepine, flurazepam (21) has found considerable use (and abuse) as a hypnotic [I4 Flumazenil (22) is a fast-acting antidote in the treatment of benzodiazepine intoxication and m the reversal of the CNS effects of benzodiazepines dunng anesthesia [f<5,19]... 

There is an increased risk for bone marrow suppression when levamisole or hydroxyurea are administered witii other antineoplastic dni. Use of levamisole witii phenytoin increases die risk of phenytoin toxicity. Pegaspargase may alter drug response of the anticoagulants. When procarbazine is administered with other central nervous system (CNS) depressants, such as alcohol, antidepressants, antihistamines, opiates, or the sedatives, an additive CNS effect may be seen. Procarbazine may potentiate hypoglycemia when administered witii insulin or oral antidiabetic dru . ... 

CNS effect Known change in DA function Neuroleptic effect Presumed change in DA function... 

The Phase I study explored i.v. administration of BB-83698 at single dose-escalating levels up to 475 mg and systemic exposures were reportedly linear in both animals and humans [84]. While dose-limiting CNS effects... 

Dose-related reversible CNS effects have also been reported in children receiving long-term therapy in which propylene glycol was a cosolvent [57],... 

The most likely explanation for these results is that simple phenolics inhibit a very large array of enzymes in vitro. The most likely explanation for the CNS effects of Uncaria rynchophylla would be that indole alkaloids, such as dihydrocorynanteine or hirsutine (32), interact with the central neurotransmission and possibly the serotonin ergic system. 

The acute CNS effects of MDMA administration are mediated by the release of monoamine transmitters, with the subsequent activation of presynaptic and postsynaptic receptor sites.40 As specific examples in rats, MDMA suppresses 5-HT cell firing, evokes neuroendocrine secretion, and stimulates locomotor activity. MDMA-induced suppression of 5-HT cell firing in the dorsal and median raphe involves activation of presynaptic 5-HT1A autoreceptors by endogenous 5-HT.4142 Neuroendocrine effects of MDMA include secretion of prolactin from the anterior pituitary and corticosterone from the adrenal glands 43 Evidence supports the notion that these MDMA-induced hormonal effects are mediated via postsynaptic 5-HT2 receptors in the hypothalamus, which are activated by released 5-HT. MDMA elicits a unique profile of locomotor effects characterized by forward locomotion and elements of the 5-HT behavioral syndrome such as flattened body posture, Straub tail, and forepaw treading.44 6 The complex motor effects of MDMA are dependent on monoamine release followed by activation of multiple postsynaptic 5-HT and DA receptor subtypes in the brain,47 but the precise role of specific receptor subtypes is still under investigation. 

Phenmetrazine Clinically used for short-term appetite suppression in the longer term its supposed benefits for weight control are very doubtful recreational use is rare, with weaker CNS effects than amphetamine, but it is still addictive. 

These findings are of considerable interest since, as we discuss in detail below, the AUH protein is a protein known to bind to AU-rich motifs in the 3 -untrans-lated region (3 -UTR) of various transcripts, thereby stabilizing them [54—56]. Thus, via their effects on the expression of the AUH protein, lithium and VPA could potentially regulate the temporal and spatial patterns of the expression of multiple genes in the CNS, effects which could potentially underlie their therapeutic effects in an illness as complex as BD. 

Asparaginase -enzyme that inhibits protein synthesis -anaphylaxis -hepatotoxicity -CNS effects (lethargy, confusion, somnolence, depression) -coagulopathy -pancreatitis... 

Dexamethasone -corticosteroid -leukocytosis -nausea and vomiting -anorexia or increased appetite -CNS effects (psychosis, confusion) -fluid retention -hyperglycemia -osteoporosis... 

Parathyroid hormone (PTH) produces CNS effects in normal subjects and neuropsychiatric symptoms are frequently encountered in patients with primary hyperparathyroidism, where EEG changes resemble those described in acute renal failure. Circulating PTH is not removed by hemodialysis. In uremic patients both EEG changes and neuropsychiatric symptoms are improved by either parathyroidectomy or medical suppression of PTH. The mechanism whereby PTH causes disturbances of CNS function is not well understood, but it has been suggested that increased PTH might facilitate the entry of Ca2+ into the cell resulting in cell death. 

Pregnant women, alcoholics, and patients with poor diets who are treated with INH should receive pyridoxine, 10 to 50 mg daily, to reduce the incidence of CNS effects or peripheral neuropathies. 

Tolerance to the daytime CNS effects (e.g., drowsiness, psychomotor impairment, decreased concentration) may develop in some individuals. 

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