Analgesia produced by electrical stimulation of catecholamine nuclei in the rat brain

Segal, Menachem; Sandberg, David E.

doi:10.1016/0006-8993(77)90488-7

Cited by 227 publications

(34 citation statements)

References 13 publications

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“…Furthermore, nerve injury affects descending inhibitory controls from brain stem nuclei. In the intact nervous system, stimulation of the locus coeruleus (Segal and Sandberg 1977) or the nucleus raphe magnus (Oliveras et al 1979) produces an inhibition of dorsal horn neurons. Following dorsal rhizotomy, however, stimulation of these areas produces excitation, rather than inhibition, in half the cells studied (Hodge et al 1983).…”

Section: Denercation Hypersensitidty and Neuronal Hyperactivitymentioning

confidence: 99%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,829

703

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SummaryPeripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also playa significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (eNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in eNS function which influence subsequent pain experience.

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Section: Denercation Hypersensitidty and Neuronal Hyperactivitymentioning

confidence: 99%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,829

703

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“…Electrical stimulation of the locus coeruleus produces analgesia (Segal & Sandberg, 1977). Unlike the case for the dorsal raphe, there is a direct projection from the locus coeruleus to spinal cord (Basbaum & Fields, 1977).…”

Section: Introductionmentioning

confidence: 99%

Serotonergic innervation of the locus coeruleus from the dorsal raphe and its action on responses to noxious stimuli.

Segal¹

1979

The Journal of Physiology

243

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SUMMARYThe connexions between the dorsal raphe nucleus and the nucleus locus coeruleus were studied in urethane anaesthetized rats.1. (Cells in the locus coeruleus gave an excitatory response to a noxious stimulus, e.g. leg pinch.2. This excitatory response was blocked by either a parenteral or an ionophoretic injection of morphine and recovered after an injection of naloxone.3. Electrical stimulation in the region of the dorsal raphe blocked excitatory locus coeruleus responses to noxious stimuli.4. While naloxone did not antagonize the effects of the dorsal raphe stimulation towards locus coeruleus activity, these effects were absent in rats pretreated with a serotonin synthesis inhibitor, PCPA or with 5,7-DHT which destroys serotonincontaining terminals, and were reduced by the serotonin antagonist methysergide.5. A serotonin-containing inhibitory pathway between the dorsal raphe and the locus coeruleus is proposed to account for these results.

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“…Because clonidine is an a,-adrenoceptor agonist, the descending (bulbospinal and pontospinal) noradrenergic system is considered to inhibit physiologically the transmission of nociceptive information through az adrenoceptors located on the primary afferent terminals and/or the dorsal horn neurons (Segal and Sandberg, 1977;Ramana Reddy and Yaksh, 1980;Howe et al, 1983). Moreover, the surface superfusion experiment of the spinal cord reveals that the noxious stimulievoked release of substance P is regulated by local application of noradrenaline, suggesting that the release-regulating receptors are located on the primary afferent terminal (Kuraishi et al, 19856).…”

mentioning

confidence: 99%

Presynaptic α₂ Adrenoceptors Inhibit Glutamate Release from Rat Spinal Cord Synaptosomes

Kamisaki

Hamada

Maeda

et al. 1993

Journal of Neurochemistry

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Abstract:The presynaptic regulation of amino acid release from nerve terminals was investigated using synaptosomes prepared from the rat spinal cord. The basal releases of endogenous glutamate (Glu), aspartate (Asp), and y-aminobutyric acid (GABA) were 34.6, 21.5, and 10.0 pmol/min/ mg of protein, respectively. Exposure to a depolarizing concentration of KCl (30 mkI) evoked 2.7-, 1 . 5 , and 2.9-fold increases in Glu, Asp, and GABA release, respectively. Clonidine reduced the K+-evoked overflow of Glu to 56% of the control overflow with a potency (1C5J of 17 nM, but it did not affect K+-evoked overflow of Asp, GABA, and their basal releases. Similarly, noradrenaline inhibited the K' -evoked overflow of Glu, although phenylephrine and isoproterenol showed no effect. The inhibitory effect of clonidine was counteracted by a,-adrenoceptor antagonists, rauwolscine, yohimbine, and idazoxan, regardless of the imidazoline structures. Because Glu is considered a neurotransmitter of primary afferents that transmit both nociceptive and nonnociceptive stimuli in the spinal cord, these data suggest that part of Glu release may be regulated by the noradrenergic system through a2 adrenoceptors localized on the primary afferent terminals. The primary afferents that transmit peripheral signals to the second-order neurons in the spinal cord are differentiated by the diameters of the nerve fibers, corresponding to the conducting information. For example, pain is mediated by nociceptive nerves (A6

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Analgesia produced by electrical stimulation of catecholamine nuclei in the rat brain

Cited by 227 publications

References 13 publications

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Serotonergic innervation of the locus coeruleus from the dorsal raphe and its action on responses to noxious stimuli.

Presynaptic α₂ Adrenoceptors Inhibit Glutamate Release from Rat Spinal Cord Synaptosomes

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Analgesia produced by electrical stimulation of catecholamine nuclei in the rat brain

Cited by 227 publications

References 13 publications

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Serotonergic innervation of the locus coeruleus from the dorsal raphe and its action on responses to noxious stimuli.

Presynaptic α2 Adrenoceptors Inhibit Glutamate Release from Rat Spinal Cord Synaptosomes

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Presynaptic α₂ Adrenoceptors Inhibit Glutamate Release from Rat Spinal Cord Synaptosomes