Depression stimulants and

See Chap. 68, Substance-Related Disorders Overview and Depressants, Stimulants, and Hallucinogens, authored by Paul L. Doering and Lisa Boothby, and Chap. 69, Substance-Related Disorders Alcohol, Nicotine, and Caffeine, authored by Paul L. Doering, W. Klugh Kennedy, and Lisa A. Boothby, for a more detailed discussion of the topic. 

Kefauver-Harris Drug Amendments passed to ensure drug efficacy and greater drug safety in response to the thalidomide birth defects disaster. 1965 Drug Abuse Control Amendments are enacted to deal with problems of abuse of depressants, stimulants, and hallucinogens. 

Drug Abuse Control Amendments are enacted to deal with problems caused by abuse of depressants, stimulants, and hallucinogens. 

The Department of Health, Education, and Welfare s Bureau of Drug Abuse Control was responsible for the control of dangerous drugs, including depressants, stimulants, and hallucinogens, such as lysergic acid diethylamide (LSD). 

Patients receiving monoamine oxidase inhibitors (MAOI) as antidepressant therapy have been especially subject to the hypertensive effects of vasoactive amines (52). These dietary amines have also been impHcated as causative agents ia migraine. Other aaturaHy occurring alkaloids (qv) have been recognized for centuries as possessing neurological stimulant and depressant properties. 

General types of physiological functions attributed to quaternary ammonium compounds are curare action, muscarinic—nicotinic action, and ganglia blocking action. The active substance of curare is a quaternary that can produce muscular paralysis without affecting the central nervous system or the heart. Muscarinic action is the stimulation of smooth-muscle tissue. Nicotinic action is primary transient stimulation and secondary persistent depression of sympathetic and parasympathetic ganglia. 

According to Georgadze the three sophora alkaloids sophocarpine (a), sophocarpidine (h) and sophoridine (c) only differ in degree and not in character of their pharmacological activity thus on intravenous injection each causes a rise and then a fall i i blood pressure and their activity in this direction is in decreasing order (a), (c), (b). In small doses they stimulate, and in larger doses depress, the isolated heart of either cold- or warm-blooded animals and then their decreasing order of activity is (c), (b), (a). 

Ephedra is used in diet products as an appetite depressant and stimulant, and in sports drinks to mask fatigue. It is also used as a bronchial stimulator, and to relieve symptoms of the common cold. 

The rates of comorbid psychiatric disorders such as depression, ADHD, and antisocial personality disorder are significantly higher in stimulant abusers... 

Drawing all this evidence together, Schildkraut (1965) concluded that depression was caused by a functional deficit of noradrenergic transmission in the brain. He also thought that the rebound depression and fatigue, which are experienced after the arousing effects of amphetamine have worn off, were due to depletion of neuronal stores of noradrenaline. However, Schildkraut made a clear distinction between the effects of antidepressants and the arousal induced by amphetamine, describing the latter as stimulation and excitement . To this day, there is controversy over whether or not amphetamine has a beneficial effect in depression. 

This behavioural syndrome, rather emotively called learned helplessness", is widely believed to share many features of depression, not least because both culminate in psychomotor retardation and both are linked with experience of uncontrollable, unpredictable stress. Whether or not learned helplessness really is an analogue of depression remains controversial (Maier 1993). Nevertheless, escape deficits in rats are prevented by pretreatment with antidepressants from different generic groups. Other psychotropic agents, such as CNS stimulants and neuroleptics, are generally ineffective. 

In this chapter, consideration will be given to two categories, which are well known CNS depressants (anticholinergics) and CNS stimulants (LSD). Although cannabinols and psylocibin, for instance, have been considered in the past, their effective dose is too high for these to be regarded as likely agents for use in the field. 

It will dissolve and eapet Tumors from the Uterus in an early cage of development. The tendency to cancerous humors there is checked very speedily by its use. It removes faintness, flatulency, destroys all craving for stimulants, and relieves weakness of the ttomach, It cures Bloating, Headaches, Nervous Prostration, Gen cral Debility, Sleeplessness, Depression and Indigestion,... 

Jewet R. E., Norton S. (1966). Effects of some stimulants and depressant drugs on the sleep cycle of the cat. Exp. Neurol 15, 463-74. 

The observed Li+-induced stimulation of corticotropin (ACTH) secretion from cells in culture, requiring extracellular Ca2+, involves a corresponding and apparently associated increase in the concentration of Ins(l)P, indicating some interaction with phosphoinositide metabolism [176], Pretreatment with Li+ desensitizes the cells, reducing this Li+-induced stimulation of ACTH secretion. Li+ initially raises plasma cortisol levels in manic-depressives however the levels are subsequently reduced with chronic Li+ treatment in both patients and controls [177]. This effect is probably secondary to the stimulation and subsequent desensitization of ACTH secretion by Li+, as observed in cultured cells. 

MDMA stimulates the CNS, causes euphoria and relaxation, and produces a mild hallucinogenic effect. It can cause muscle tension, nausea, faintness, chills, sweating, panic, anxiety, depression, hallucinations, and paranoid thinking. It increases heart rate and blood pressure and destroys serotonin (5-HT)-producing neurons in animals. It is considered to be neurotoxic in humans. 

In addition to the excitatory effects described above, there is some evidence that administration of hallucinogens can depress MSRs and PSRs in intact animals. These depressant effects, however, do not appear to be simply mediated by stimulation of inhibitory postsynaptic 5-HT receptors in the spinal cord, since they are blocked by 5-HT antagonists. 

Several semisynthetic derivatives of yohimbine alkaloids show interesting pharmacological activity. For example, 17-methylthiomethoxyyohimbane stereoisomers (612 and 613) are valuable central nervous system depressants (349) and several hydrazides of yohimbinecarboxylic acid (614 and 615-type compounds) are useful cardiac stimulants, respiratory analeptics, and antihypertensives (350-353). 

In this rapidly evolving field, the detection of PDE enzymes in the central nervous system (CNS) has stimulated interest in exploring potential applications of PDE inhibitors for treating CNS disorders such as Alzheimer s disease and other cognitive malfunctions, depression, anxiety, and schizophrenia. This review will focus on these therapeutic opportunities as well as new developments in the medicinal chemistry and biology associated with selected members of the PDE family, in particular PDEs 2, 4, 9, and 10. There have been a number of other reviews in this field in the past year that have covered selected individual PDE enzymes and potential pharmacologic applications of PDE inhibitors in CNS disorders [3,7,8]. 

Due to the large number of references which appeared to be worth mentioning, it became necessary to divide this review into two parts. The present part deals mainly with pyridazines as chemotherapeutics, antithrombotics, antise-cretory and anti-ulcer agents, analgesic and anti-inflammatory agents as well as with various central nervous system stimulants and depressants. Part 2 of this review, which is planned for a future volume of this Series, will be devoted mainly to compounds which act on the cardiovascular system and to a discussion of miscellaneous additional pharmacological activities of pyridazine derivatives. 

Nickel ions have been shown to depress the in vivo and in vitro release of prolactin [336], while the release of growth hormone was stimulated, and only at relatively high ion concentrations. Hyperglycemia occurs in rats following intraperitoneal or intratracheal injections of NiCl2 [265, 337, 338], The mechanism of action of nickel appears to be inhibition of insulin release this inhibition could be related to the extremely high concentration of nickel found in the pituitary and the effect on the secretion of the pituitary hormones (growth hormone and adrenocorticotropic hormone). 

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