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Serotonergic fibers

Morrison, J.H. Foote, S.L. Molliver, M.E. Bloom, F.E. and Lidov, H.G.W. Noradrenergic and serotonergic fibers innervate complementary layers in monkey primary visual cortex An immunohistochemi-cal study. Proc Natl Acad Sci USA 79 2401-2405, 1982. [Pg.301]

Zhou, F.C., and Azmitia, E.C. Induced homotypic sprouting of serotonergic fibers in hippocampus. II. An immunocytochemistry study. Brain Res 373 337-348, 1986. [Pg.305]

Serotonergic and non-serotonergic fibers originating in the RVM terminate predominantly in dorsal horn laminae I, II (substantia gelatinosa), and V, which are the main targets... [Pg.273]

Morizumi T, Tsukatani H, Miwa T. 1994. Olfactory disturbance induced by deafferentation of serotonergic fibers in the olfactory bulb. Neuroscience 61 733-738. [Pg.196]

Intrathecal administration of the o-agonist clonidlne attenuated nociceptive responses in rats and cats. Attempts to characterize further the receptors involved as or 02 gave inconclusive results. Studies with monoamine depletors indicated that intact spinal adrenergic and serotonergic fibers are involved in a complex way in expression of morphine analgesia in rats.Adrenergic systems may mediate foot shock analgesia (rats, tail flick).A study in terminal cancer patients... [Pg.5]

Most injection studies have been performed in projection areas of the serotonergic system and in the raph nuclei from which serotonergic fibers emanate. HiUegaart et al. [42] reported that 8-OH-DPAT ii jected into the nucleus accumbens produced a facilitation of the male rat sexual behavioiir, as evidenced by a decrease in number of mounts and intromissions to ejaculation, as well as by a decrease in the postejaculatory interval. Injections into the olfactory tubercle had no effects on sexual behaviour. Femdndez-Guasti et al. [43] confirmed the stimulatory effects of 8-OH-DPAT after local application into the nuclear accumbens, but edso found similar effects for medial preoptic area injections. They foimd no effects after dorsal raph4 administration, in line with HiUegaart et al. [Pg.76]

This chapter will review some recently completed studies on the long-term effects of MDMA in nonhuman primates. The goals of these studies were to (1) determine if the neurotoxic effects of MDMA, which have been well documented in the rodent (see below), generalize to the primate (2) compare the relative sensitivity of primates and rodents to the neurotoxic effects of MDMA (3) ascertain if the toxic effects of MDMA in the monkey are restricted to nerve fibers (as they are in the rat), or if they involve cell bodies as well (4) evaluate how closely toxic doses of MDMA in the monkey approximate those used by humans and (5) examine whether 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) can be used to detect MDMA-induced serotonergic damage in the CNS of primates. Before presenting the results of these studies, previous results in the... [Pg.306]

The results of the studies reviewed here show that the neurotoxic effects of MDMA generalize to the primate. Further, they indicate that monkeys are considerably more sensitive than rats to the serotonin-depleting effects of MDMA, and that the dose-response curve of MDMA in the monkey is much steeper than in the rat. Perhaps as a consequence of this, the toxic effects of MDMA in the monkey involve serotonergic nerve fibers as well as cell bodies, whereas in the rat, only nerve fibers are affected. The present studies also show that the toxic dose of MDMA in the monkey... [Pg.316]

The fact that most serotonergic dorsal raphe neurons are dependent on extrinsic excitatory or facilitatory inputs to express their characteristic spontaneous activity may seem to contradict previous studies suggesting that these neurons may function as autonomous pacemakers (42) with an endogenous rhythm (31) attributable to the presence of pacemaker potentials (8). Such a contradiction exists only if one insists that endogenous rhythms and pacemaker potentials must, by definition, be totally autonomous, i.e., completely independent of all extrinsic synaptic or neurohumoral influences. Such a definition would seem too restrictive in view of the fact that some invertebrate neurons display pacemaker potentials only when certain afferent fibers are stimulated (38) or when exposed to certain neurohumoral substances (18,28). [Pg.94]

Opioid-induced antinociception depends, to some degree, on monoaminergic signaling in the spinal dorsal horn. While opioids can act directly on dorsal horn terminals of primary afferent nociceptive fibers or on excitatory interneurons in lamina II of the dorsal horn to reduce the release of excitatory transmitters (Glaum et al., 1994), the supraspinally mediated analgesic effects of opioids, at least in part, involve interactions with central and spinal serotonergic and noradrenergic transmission. [Pg.275]

DA modulates in the STh neurons the activity of the glutamatergic cortical afferents and GABAergic pallidal afferents (Hamani et al., 2004). Dopaminergic terminals, which contact mainly the neck of dendritic spines, establish synaptic contacts with the distal dendrites of STh neurons. These receive synaptic input also from thalamic fibers deriving from the intralaminar nuclei, serotonergic input deriving from the dorsal raphe nucleus and glutamatergic input from the motor cortex. Inhibitory pallidal afferents innervate mostly the proximal dendrites and the cell body of STh neurons. [Pg.52]

Neuromodulatory transmitter inputs to MOB. Darkfield photomicrographs showing the distribution of cholinergic (a), noradrenergic (b), and serotonergic (c) fibers revealed respectively with immunohistochemistry for choline acetyltransferase (ChAT), dopamine-jS-hydroxylase (DBH), and serotonin (5-HT). Reprinted from Handbook of Chem. Neuroanat. Integrated Sys. CNS, Vol. 12, Part III, Chapter III, The Olfactory System, M. Shipley et al., pp. 469-573, 1996, with permission from Elsevier, Ltd... [Pg.168]

McLean JH, Shipley MT. 1987b. Serotonergic afferents to the rat olfactory bulb II. Changes in fiber distribution during development. J Neurosci 7 3029-3039. [Pg.195]


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See also in sourсe #XX -- [ Pg.368 ]




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