Behavioral effects depression

Stimulants induce both tolerance and sensitization to their behavioral effects. Tolerance develops to the anorectic and euphoric effects of stimulants (Schuster 1981) however, chronic intermittent use of low doses of stimulants delays the development of tolerance. With the doses commonly used in clinical practice, patients treated for narcolepsy or for depressive or apathetic states find that the stimulant properties usually persist without development of tolerance however, the persistence of antidepressant effects remains a matter of controversy. Sensitization has been linked to the development of amphetamine-induced psychosis (Yui et al. 1999). Sensitization to the induction of psychosis is suggested because psychosis is induced by progressively lower doses and shorter periods of consumption of amphetamine following repeated use over time (Sato 1986). Sensitization for amphetamine-induced psychosis may persist despite long periods of abstinence. 

We then extended this approach to the study of LSD. The results were generally similar to those seen with 5-MeODMT but with two critical differences (89). First, a 50 /xg/kg dose of LSD produced a depression of raphe unit activity lasting, on the average, 3 to 4 hr, while the behavioral effects lasted for at least 6 to 8 hr. Second, when the 50 g/kg dose was readministered 24 hr later, it produced little or np behavioral effect (tolerance), but the effect on raphe unit activity was as large as that seen on the previous day. Based on those two... 

Electrical stimulation in the vicinity of the raphe nuclei has been reported to produce depressant effects on MSRs (32,142). These depressant effects could be attributed to activation of postsynaptic inhibitory receptors analogous to those characterized in the forebrain, except for the fact that the depression was blocked by 5-HT antagonists. The effectiveness of the antagonists suggests that the receptor is more akin to the excitatory 5-HT receptor characterized on motoneurons (134,184). The depressant behavioral effects could result from... 

Some of the depressant behavioral effects of hallucinogens may involve inhibitory postsynaptic 5-HT receptors. For example, depressant effects of hallucinogens on startle and locomotor activity may result from activation of these receptors, since 5-HT itself has similar effects. Studies on supersensitivity are lacking, however, and, again, the absence of selective antagonists prevents definitive conclusions. 

Disulfoton has also been studied for behavioral effects. Rats fed >0.5 mg/kg/day disulfoton for 90 days had significantly depressed brain acetylcholinesterase levels (59-74% below control), but the treated rats had shorter maze running times and made fewer mistakes than the controls (Clark and... 

Abstract In this chapter, the depression mechanism of five kinds of depressants is introduced respectively. The principle of depression by hydroxyl ion and hydrosulphide is explained which regulates the pH to make the given mineral float or not. And so the critical pH for certain minerals is determined. Thereafter, the depression by cyanide and hydrogen peroxide is narrated respectively which are that for cyanide the formation of metal cyanide complex results in depression of minerals while for hydrogen peroxide the decomposition of xanthate salts gives rise to the inhibitation of flotation. Lastly, the depression by the thio-organic such as polyhydroxyl and poly carboxylic xanthate is accounted for in detail including die flotation behavior, effect of pulp potential, adsorption mechanism and structure-property relation. 

Valproic acid causes hair loss in about 5% of patients, but this effect is reversible. Transient gastrointestinal effects are common, and some mild behavioral effects have been reported. Metabolic effects, including hyperglycemia, hyperglycinuria, and hyperammonemia, have been reported. An increase in body weight also has been noted. Valproic acid is not a CNS depressant, but its administration may lead to increased depression if it is used in combination with phenobarbital, primidone, benzodiazepines, or other CNS depressant agents. 

The behavioral effects of nicotine have been defined as both stimulant and depressant, effects that are influenced by the present mental status and expectations of the smoker. Smokers may feel alert and relaxed. Nicotine produces myriad effects on the central nervous system (CNS), almost all of which appear to be mediated through nicotinic receptors. Additionally, nicotine influences multiple neuronal systems. One of its most prominent effects is stimulated release of dopamine, particularly in the nucleus accumbens, which is a major component of the reward system. Nicotine also stimulates the release of endogenous opioids and glucocorticoids. 

The developmental neurotoxicity guideline, accepted by OECD in 2007, has added the important aspect of behavioral effects of pre- and postnatal exposure to chemicals. This development arose from the notion that behavioral disorders in man such as anxiety, depression, phobias, autism, and attention deficit hyperactivity disorder, which appear to show increasing prevalences in western societies, may have a perinatal origin (4, 5). In the absence of causal inferences with respect to chemicals it seems nevertheless prudent to assess in a risk assessment whether such causal relations may exist. 

May have additive sedative or behavioral effects with CNS depressants... 

CRH probably does not act alone. According to clinical neuroendocrinology, vasopressin is a prime candidate for the synergy of CRH effects at pituitary CRHj receptors, and it also has behavioral effects that are compatible with a role in depression. Chronic psychosocial stress enhances vasopressin expression and increases the number of hypothalamic neurons coexpressing CRH and vasopressin. Infusion of an antisense oligodeoxy-nucleotide, which corresponds to the mRNA of vasopressin type 1 receptor, into the septum led to reduced anxiety-related behavior that parallels decreases in vasopressin receptor binding (Landgraf et al. 1995). 

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