Hyperactive effects

Stypodiol, epistypodiol and stypotriol are secondary diterpene metabolites produced by the tropical brown algae Stypopodium zonaie. These compounds display diverse biological properties, including strong toxic, narcotic, and hyperactive effects upon the reef-dwelling fish. In the laboratory of A. Abad an efficient stereoselective synthesis of stypodiol and its C14 epimer, epistypodiol, was accomplished from (S)-(+)-carvone. The key transformations in the synthesis of these epimeric compounds were an intramolecular Diels-Alder reaction, a sonochemical Barbier reaction and an acid-catalyzed quinol-tertiary alcohol cyclization. 

Health and Safety Factors. Clinical side effects and LD q values of most commercially available analeptics have been summarized (2). Overdoses produce symptoms of extreme CNS excitation, including resdessness, hyperexcitabiUty, skeletal muscle hyperactivity, and ia some cases convulsions. 

For many years, there has been concern by medical professionals and nutritionists over the effects of dietary sugar on human health. Sucrose has been imphcated as a cause of juvenile hyperactivity, tooth decay, diabetes meUitus, obesity, atherosclerosis, hypoglycemia, and nutrient deficiencies. 

Other studies indicate that sucrose does not cause hyperactivity. Carbohydrate ingestion increases levels of serotonin (5-hydroxytryptamine), a brain neurotransmitter that promotes relaxation and sleep. Dietary sucrose should theoretically have a calming effect and reduce activity, manifestations which have been observed in case studies (63). To date, clinical investigations have failed to show a significant connection between sucrose consumption and aggressive or dismptive behavior (66). 

Cessation of prolonged heavy alcohol abuse may be followed by alcohol withdrawal or life-threatening alcohol withdrawal delirium. Typical withdrawal symptoms are autonomic hyperactivity, increased hand tremor, insomnia and anxiety, and are treated with benzodizepines and thiamine. Alcoholism is the most common cause of thiamine deficiency and can lead in its extreme form to the Wernicke s syndrome that can be effectively treated by high doses of thiamine. 

Psychostimulants are drugs that substantially influence cognitive and affective functioning and behaviors. Effects are increased motivational desire, agitation, heightened vigilance, euphoria, hyperactivity, and... 

The main indication for certain psychostimulants is ADHD in children and adults [4]. Recent research shows that the clinical effect and benefit are dramatic even in adults. About 60% of adult patients receiving stimulant medication showed moderate-to-marked improvement, as compared with 10% of those receiving placebo. The core symptoms of hyperactivity,... 

Psychostimulants. Figure 3 Effect of methylphenidate depending on baseline tonic (T) and phasic (P) dopamine levels. In a normal state only minimal changes are noted (which points to a rather low abuse potential). From a hypoactive state, methylphenidate increases both Tand P levels. However, this is much more true for the strongly lowered P tone. In contrast, in moderately hyperactive states and ADHD, T levels are increased and P levels are decreased, respectively, correlating with the baseline levels (adapted from [2]). 

The barbiturates are contraindicated in patients with known hypersensitivity to the drugs. The barbiturates are used cautiously in patients with liver or kidney disease and those with neurological disorders. The barbiturates (eg, phenobarbital) are used with caution in patients with pulmonary disease and in hyperactive children. When barbiturates are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. See Chapter 26 for additional information on the barbiturates. 

Acute exposure to large amounts of endosulfan results in frank effects manifested as hyperactivity, muscle tremors, ataxia, and convulsions. Possible mechanisms of toxicity include (a) alteration of neurotransmitter levels in brain areas by affecting synthesis, degradation, and/or rates of release and reuptake, and/or (b) interference with the binding of those neurotransmitter to their receptors. 

The effects of endosulfan have not been studied in children, but they would likely experience the same health effects seen in adults exposed to endosulfan. Data in adults, mostly derived from cases of accidental or intentional acute exposure (ingestion) to large amounts of endosulfan, indicate that the primary target of endosulfan toxicity is the nervous system. The effects are manifested as hyperactivity and convulsions and in some cases have resulted in death (Aleksandrowicz 1979 Blanco-Coronado et al. 1992 Boereboom et al. 1998 Cable and Doherty 1999 Lo et al. 1995 Terziev et al. 1974). These effects have been reproduced in experimental animals. 

The early report by Bradley (1937) on beneficial treatment effects with amphetamine in aggressive, destructive, irritable, and hyperactive boys was repeatedly eonfirmed by double-blind, placebo-controlled studies. Significant reductions in aggressive behavior and improvements in social interactions were found after treatment with 10 to 40 mg/day of d- or /-amphetamine for boys and girls, 5 to 14 years of age, who had been diagnosed as... 

In experiments with mice and squirrel monkeys, we confirmed and extended the antagonism of amphetamine-induced motor hyperactivity by naltrexone at the same time, however, amphetamine s disruption of aggressive and social behavior was not reversed by naltrexone (Winslow and Miczek, in press). Specifically, in mice, the resident s attack and threat behavior toward an intruder was even further reduced by amphetamine after naltrexone pretreatment (figure 7). Squirrel monkeys that are dominant within their social group exhibit significantly lower levels of aggressive display toward other group members and initiate fewer social interactions after amphetamine treatment naltrexone did not block these effects. The interactive effects of amphetamine and naltrexone on locomotor behavior are consistent with the proposed modulation of dopamine-mediated functions by opioids however, the interaction between amphetamine and naltrexone on social behavior appears to involve a different mechanism. 

Investigation of the neurochemical substrates for the psychostimulant effects of MDMA suggests a role for the mesolimbic dopamine system. Destruction of dopamine terminal fields in the nucleus accumbens significantly attenuated the locomotor activation produced by MDMA. A similar blockade of amphetamine-induced locomotor hyperactivity is known and was observed following amphetamine injection in these same rats. Such results support the hypothesis that at least one component of MDMA-induced hyperactivity is dopamine mediated and suggest that mesolimbic dopamine specifically is the critical substrate. In this way, MDMA resembles other classical psychostimulants like amphetamine and cocaine. Interestingly, evidence for functional cross-sensitization was suggested in the study in which an injection of amphetamine followed MDMA injection. 

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