The topographical distribution of serotoninergic terminals in the spinal cord of the cat: biochemical mapping by the combined use of microdissection and microassay procedures

Olivéras, Jean-Louis; Bourgoin, S.; Héry, F.; Besson, Jean‐Marie; Hamon, Michel

doi:10.1016/0006-8993(77)90680-1

Cited by 174 publications

(38 citation statements)

References 32 publications

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“…With regard to the terminals from which the monoamines may originate, it is known that all serotonin terminals in the spinal cord originate in brain stem nuclei (Dahlstrom & Fuxe, 1965;Anderson, 1972;Oliveras, Bourgoin, Hery, Besson & Hamon, 1977). In contrast, there are two possible sources for spinal noradrenaline.…”

Section: Discussionmentioning

confidence: 99%

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Tyce¹,

Yaksh²

1981

The Journal of Physiology

156

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SUMMARY1. Superfusates taken from spinal cords of cats anaesthetized with chloralose and urethane were assayed for endogenous serotonin and noradrenaline by high-pressure liquid chromatography with electrochemical detection.2. Stimulating the dorsolateral funiculus, caudal to a spinal transaction, enhanced in a frequency-dependent manner the levels of monoamines in the spinal superfusate.3. Tyramine added to the superfusate enhanced the release of noradrenaline and serotonin. 4. In cats with intact neuraxes, stimulation of the sciatic nerve at high, but not low intensities produced a 2-to 3-fold increase in the levels of monoamines in the spinal superfusate. This evoked monoamine efflux was attenuated by cold block of the cervical spinal cord.5. Stimulation of the infraorbital branch of the trigeminal nerve evoked the release of noradrenaline and serotonin from the lumbar cord in animals with intact neuraxes. Cold block of the cervical cord blocked trigeminal-evoked release of lumbar serotonin and noradrenaline.6. That the monoamine efflux was not due to elevations in blood pressure was indicated by the failure of vasoxyl, an a-agonist producing hypertension, to evoke any changes in spinal monoamine levels. 7. The monoamine release was not dependent upon either an opiate-sensitive link or upon the activation of the sympathetic ganglia, because systemic administration of naloxone (an opiate antagonist) and chlorisondamine (a ganglionic blocking agent) failed to antagonize the evoked release of amines.8. These results suggest the existence of a spinopetal monoamine system which is activated by peripheral stimuli. The modulatory influence associated with increasing monoamine tone in the spinal cord clearly indicated that somatic stimuli may activate a descending monoamine pathway which serves to modulate the magnitude of the ascending sensory message.

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Section: Discussionmentioning

confidence: 99%

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Tyce¹,

Yaksh²

1981

The Journal of Physiology

156

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“…The RVM contains a number of nuclei, including the nucleus raphe magnus (NRM). The NRM is a major serotonergic nucleus that supplies the spinal cord with the majority of its 5-hydroxytryptamine (serotonin) (5-HT) (Oliveras et al, 1977). It has been hypothesized that -opioids stimulate RVM serotonergic neurons, leading to inhibition of spinal dorsal horn neurons through 5-HT release.…”

mentioning

confidence: 99%

Activation of μ-Opioid Receptors Inhibits Synaptic Inputs to Spinally Projecting Rostral Ventromedial Medulla Neurons

Finnegan

Li²,

Chen³

et al. 2004

J Pharmacol Exp Ther

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The rostral ventromedial medulla (RVM) is a major locus for the descending control of nociception and opioid analgesia. However, it is not clear how opioids affect synaptic inputs to RVM neurons. In this study, we determined the effect of -opioid receptor activation on excitatory and inhibitory synaptic transmission in spinally projecting RVM neurons. RVM neurons were retrogradely labeled with a fluorescent tracer injected into the dorsal horn of the spinal cord in rats. Whole-cell voltage-clamp recordings were performed on labeled RVM neurons in brain slices in vitro. The -receptor agonist [D-Ala 2 ,N-Me-Phe 4 ,Gly 5 -ol]-enkephalin (DAMGO, 1 ⌴) significantly decreased the amplitude of evoked excitatory postsynaptic currents (EPSCs) in 52% (9 of 17) of labeled cells. DAMGO also significantly reduced the amplitude of evoked inhibitory postsynaptic currents (IPSCs) in 69% (11 of 16) of cells examined. Furthermore, DAMGO significantly decreased the frequency of miniature EPSCs in 55% (15 of 27) of cells and significantly decreased the frequency of miniature IPSCs in all 12 cells studied. Although most EPSCs and IPSCs were mediated by glutamate and GABA, the nicotinic and glycine receptor antagonists attenuated EPSCs and IPSCs, respectively, in some labeled RVM neurons. Immunocytochemical labeling revealed that only 35% of recorded RVM neurons were tryptophan hydroxylase-positive, and 15% cells had GABA immunoreactivity. Thus, this study provides important functional evidence that activation of -opioid receptors decreases the release of both excitatory and inhibitory neurotransmitters onto most spinally projecting RVM neurons.The rostral ventromedial medulla (RVM) plays an important role in the descending modulation of nociceptive information and opioid analgesia (Fields et al., 1983a;Jones and Gebhart, 1988;Urban and Smith, 1994). The RVM receives synaptic inputs from the periaqueductal gray (PAG) and relays information to the dorsal horn of the spinal cord through the dorsolateral funiculus. The analgesia produced by microinjection of morphine into the PAG is dependent upon the connection to the RVM (Urban and Smith, 1994;Pan and Fields, 1996). Direct stimulation of the RVM also can produce potent analgesia. For example, medullary electrical stimulation or microinjection of glutamate and morphine into the RVM results in either an increase in the tail-flick latency or a decrease in spinal dorsal horn neuronal activity (Llewelyn et al., 1986;Jones and Gebhart, 1988;McGowan and Hammond, 1993;Urban and Smith, 1994). However, the cellular mechanisms of the action of opioids in the RVM remain unclear.Three classes of RVM neurons have been identified, including ON-, OFF-, and NEUTRAL-cells, that show, respectively, increases, decreases, and no changes in the firing activity in response to noxious stimuli (Fields et al., 1983b(Fields et al., , 1995. Furthermore, activation of -opioid receptors inhibits ON-cells, but stimulates OFF-cells during the application of noxious stimulation (Fields et al., 1983b). Althoug...

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“…Serotonergic neurons comprise less than a quarter of the cells in the rat medullary raphe magnus and adjacent reticular formation (collectively referred to as RM here), but are the major source of serotonin in the spinal and medullary dorsal horns (Dahlstrom and Fuxe 1964;Oliveras et al 1977;Potrebic et al 1994). Serotonergic RM cells have been implicated in a number of physiological processes including pain modulation, sleep-wake control, and cold defense.…”

Section: Introductionmentioning

confidence: 99%

Serotonergic Raphe Magnus Cell Discharge Reflects Ongoing Autonomic and Respiratory Activities

Mason¹,

Gao²,

Genzen³

2007

Journal of Neurophysiology

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Serotonergic cells are located in a restricted number of brainstem nuclei, send projections to virtually all parts of the central nervous system, and are critical to normal brain function. They discharge tonically at a rate modulated by sleep/wake cycle and, in the case of medullary serotonergic cells in raphe magnus and the adjacent reticular formation (RM), are excited by cold challenge. Yet, beyond behavioral state and cold, endogenous factors that influence serotonergic cell discharge remain largely mysterious. The present study in the anesthetized rat investigated predictors of serotonergic RM cell discharge by testing whether cell discharge correlated to three rhythms observed in blood pressure recordings that averaged >30 minutes in length. A very slow frequency rhythm with a period of minutes, a respiratory rhythm, and a cardiac rhythm were derived from the blood pressure recording. Cross correlations between each of the derived rhythms and cell activity revealed that the discharge of 38 of the 40 serotonergic cells studied was significantly correlated to the very slow and/or respiratory rhythms. Very few serotonergic cells discharged in relation to the cardiac cycle and those that did, did so weakly. The correlations between serotonergic cell discharge and the slow and respiratory rhythms cannot arise from baroreceptive input. Instead we hypothesize that they are by-products of on-going adjustments to homeostatic functions that happen to alter blood pressure. Thus, serotonergic RM cells integrate information about multiple homeostatic activities and challenges and can consequently modulate spinal processes according to the most pressing need of the organism.

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The topographical distribution of serotoninergic terminals in the spinal cord of the cat: biochemical mapping by the combined use of microdissection and microassay procedures

Cited by 174 publications

References 32 publications

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

Activation of μ-Opioid Receptors Inhibits Synaptic Inputs to Spinally Projecting Rostral Ventromedial Medulla Neurons

Serotonergic Raphe Magnus Cell Discharge Reflects Ongoing Autonomic and Respiratory Activities

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