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Neuronal mechanism

Morphine and its salts are very valuable analgesic drugs but are highly addictive. In addition to suppression of pain, morphine causes constipation, decreases pupillary size and depresses respiration. Only the (-l-)-stereoisoraer is biologically active. They appear to produce their effects on the brain by activating neuronal mechanisms normally activated by... [Pg.266]

OT receptors in the hypothalamus are regulated by steroids. OT systems in the CNS are involved in homeostasis, reproduction, and related behavior. OT is also excitatory to neurons in the CNS at nanomolar concentrations (86), but relatively Httle is known about neuronal mechanisms and pharmacology. [Pg.580]

Groves, P.M.. and Tepper, J.M. Neuronal mechanisms of action of amphetamine. In Creese, I., ed. Stimulants Neurochemical,... [Pg.142]

Xi, M. C., Morales, F. R. Chase, M. H. (2004). Interactions between GABAergic and chohnergic processes in the nucleus pontis oralis neuronal mechanisms controlling active (rapid eye movement) sleep and wakefulness. J. Neurosci. 24, 10670-8. [Pg.108]

Terasawa E (2001) Luteinizing hormone-releasing hormone (LHRH) neurons mechanism of pulsatile LHRH release. Vitam Horm 63 91-129... [Pg.150]

Because of the low doses involved, these data are intriguing. However, classical conditioning procedures are, at present, of limited pharmacologic value to our knowledge, they have not yet been used to analyze underlying (neuronal) mechanisms. [Pg.46]

In this chapter, we have reviewed the effects of indolealkylamine and phen-ylalkylamine hallucinogens on respondent (classical or Pavlovian) and operant (instrumental) behavior. Both the classically conditioned NMR and bar pressing or licking that is simultaneously reinforced with food or water and suppressed by punishment appear to be particularly sensitive to low doses of LSD- or mescaline-like agents. To date, however, neither of these behaviors has provided substantial amounts of information regarding specific, underlying neuronal mechanisms. [Pg.52]

This chapter considers the effects of indolealkylamine (LSD-like) and phenyl-alkylamine (mescaline-like) hallucinogens on learned behavior. We concentrate on those approaches that have shed the most light on underlying neuronal mechanisms or that show promise of becoming useful (in vivo) animal models of hallucinogenic drug action. Thus we are selective rather than exhaustive, a luxury made possible in part because several more empirically oriented reviews have been published recently (14,16,34,35). [Pg.168]

Adler LE, Pachtman E, Eranks RD, et al Neurophysiological evidence for a defect in neuronal mechanisms involved in sensory gating in schizophrenia. Biol Psychiatry... [Pg.582]

Are there some basic neuronal mechanisms which are affected by all drugs of abuse ... [Pg.379]

NEURONAL MECHANISMS FOR PAIN-INDUCED AVERSION BEHAVIORAL STUDIES USING A CONDITIONED PLACE AVERSION TEST... [Pg.135]

Pain is comprised of sensory discriminative and negative affective components. Although the neural systems responsible for the sensory component of pain have been studied extensively, the neural basis of the affective component is not well understood. Recently, behavioral studies using the conditioned place paradigm have successfully elucidated the neural circuits and mechanisms underlying the negative affective component of pain. This review focuses on the behavioral studies that have used conditioned place aversion (CPA) tests to elucidate the neuronal mechanisms underlying pain-induced aversion. [Pg.136]

Cannabinoids may share at least some common neuronal mechanisms with opioid compounds. Studies of intracellular events associated with ligand binding to either cannabinoid or opiate receptors indicate that these receptors are linked via G proteins to the production of cAMP. Certain studies have also indicated that there may be some interaction between cannabinoid binding sites and opiate receptors in the reward pathway. In addition, there is increasing evidence that cannabinoids interact with opiate systems involved in the perception of pain. In fact, cannabinoids clearly produce analgesic effects in both experimental animals and humans, and of all the potential clinical uses of cannabinoids, the mediation of analgesia has received the most attention. Some evidence also indicates that the cannabinoid receptor system is an analgesic system. [Pg.200]

Freund J-H (1973) Neuronal mechanisms of the lateral geniculate body. Vol VIF3B pp. 177-246 in Jung R (ed). Handbook of sensory physiology Springer Berlin. [Pg.56]

Autonomic neuronal mechanisms also play an important role in regulating insulin release. In the sympathetic nervous system, o adrenergic agonists inhibit insulin release, whereas jS-adrenergic agonists stimulate the release of insulin. In Ihe parasympathetic nervous. system, cholinomimetic dmgs stimulate insulin release. [Pg.849]

The purpose of these neuronal mechanisms is to regulate BP and maintain homeostasis. Pathologic disturbances in any of the four major components (autonomic nerve fibers, adrenergic receptors, barore-ceptors, or central nervous system) conceivably could lead to chronically elevated BP. These systems are physiologically interrelated. A defect in one component may alter normal function in another, and such cumulative abnormalities then may explain the development of essential hypertension. [Pg.190]


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See also in sourсe #XX -- [ Pg.353 ]




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