Suppression of a hind limb flexion withdrawal reflex by microinjection of glutamate or morphine into the periaqueductal gray in the rat

Carstens, Earl; Hartung, Michael; Stelzer, B.; Zimmermann, M.

doi:10.1016/0304-3959(90)90055-i

Cited by 33 publications

(21 citation statements)

References 22 publications

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“…Besides the knowledge that PAG is involved in nociceptive transmission, it has been known for several years that electrical stimulation of or opiate microinjections into PAG of animals or humans also produce analgesia (see e.g. 11,17). It has therefore been proposed that in PAG there is some sort of interaction between afferent nociceptive and efferent nociceptive inhibiting transmission (39).…”

Section: Discussionmentioning

confidence: 99%

Reciprocal connections between the periaqueductal gray matter and other somatosensory regions of the cat mid brain: A possible mechanism of pain inhibition

Wiberg

1992

Upsala Journal of Medical Sciences

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Section: Discussionmentioning

confidence: 99%

Reciprocal connections between the periaqueductal gray matter and other somatosensory regions of the cat mid brain: A possible mechanism of pain inhibition

Wiberg

1992

Upsala Journal of Medical Sciences

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“…Descending control originating in the PAG has been shown to powerfully modulate withdrawal reflexes evoked by noxious mechanical and thermal (heat) stimuli (e.g., Mayer et al, 1971;Fardin et al, 1984;Carstens et al, 1990;McMullan and Lumb, 2006a;Leith et al, 2007). However whether this control extends to noxious cold stimulation remains unclear; therefore, the effect of VL-PAG stimulation on cold-evoked withdrawal thresholds and response magnitudes was investigated.…”

Section: Cold-evoked Withdrawal Reflexes Are Significantly Depressed mentioning

confidence: 99%

Spinal Processing of Noxious and Innocuous Cold Information: Differential Modulation by the Periaqueductal Gray

Leith¹,

Koutsikou²,

Lumb³

et al. 2010

J. Neurosci.

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In addition to cold being an important behavioral drive, altered cold sensation frequently accompanies pathological pain states. However, in contrast to peripheral mechanisms, central processing of cold sensory input has received relatively little attention. The present study characterized spinal responses to noxious and innocuous intensities of cold stimulation in vivo and established the extent to which they are modulated by descending control originating from the periaqueductal gray (PAG), a major determinant of acute and chronic pain. In lightly anesthetized rats, hindpaw cooling with ethyl chloride, but not acetone, was sufficiently noxious to evoke withdrawal reflexes, which were powerfully inhibited by ventrolateral (VL)-PAG stimulation. In a second series of experiments, subsets of spinal dorsal horn neurons were found to respond to innocuous and/or noxious cold. Descending control from the VL-PAG distinguished between activity in nociceptive versus non-nociceptive spinal circuits in that innocuous cold information transmitted by non-nociceptive class 1 and wide-dynamic-range class 2 neurons remained unaltered. In contrast, noxious cold information transmitted by class 2 neurons and all cold-evoked activity in nociceptive-specific class 3 neurons was significantly depressed. We therefore demonstrate that spinal responses to cold can be powerfully modulated by descending control systems originating in the PAG, and that this control selectively modulates transmission of noxious versus innocuous information. This has important implications for central processing of cold somatosensation and, given that chronic pain states are dependent on dynamic alterations in descending control, will help elucidate mechanisms underlying aberrant cold sensations that accompany pathological pain states.

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“…In the PAG and the spinal dorsal horn, the relay centers for pain and sensory information, glycine inhibits glutamate-evoked depolarization and represses the firing of neurons. Also, glutamate seems to be involved in PAG-mediated analgesia: microinjections of glutamate and glutamate agonists into the PAG have been shown to induce analgesia (Carstens et al, 1990). We have previously shown that COX-2 modulated PAG neuronal activity and involved with the regulation of the descending pain control system in the level of PAG neurons.…”

Section: Discussionmentioning

confidence: 97%

“…Several neurotransmitters in the PAG participate in the control of nociception. Among these, endogenous opioids, glycine, and glutamate seem to play a crucial role in the processing of painregulatory signals within this area (Carstens et al, 1990;Renno et al, 1992;Peng et al, 1996;Maione et al, 2000). Glycine is an important inhibitory transmitter in the brainstem and spinal cord.…”

Section: Introductionmentioning

confidence: 99%

“…The binding of glycine to its receptor produces a large increase in Cl − conductance, which causes membrane hyperpolarization (Min et al, 1996;Peng et al, 1996). Glutamate is a major excitatory neurotransmitter in the CNS where they participate in a great number of physiological and pathological states (Greenamyre et al, 1984;Carstens et al, 1990). Although amygdalin is known to be involved in inflammatory pain (Chang et al, 2005), the effect of amygdalin on neuronal activity at the level of PAG has not been reported, yet.…”

Section: Introductionmentioning

confidence: 99%

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Modulation of Amygdalin on Glycine- and Glutamate-induced Ion Currents in Rat Periaqueductal Gray Neurons

et al. 2008

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Amygdalin is known as vitamain B17, and it was called laetrile. Amygdalin is composed of two molecules of glucose, one molecule of benzaldehyde which induces an analgesic action, and one molecule of hydrocyanic acid which is an anti-neoplastic compound. Amygdalin had been used to treat cancers and relieve pain. In order to evaluate whether the analgesic action of amygdalin is related with descending pain control system, we performed patch clamp study. In the present study, the modulatory effects of amygdalin on glycine-and glutamate-induced ion currents in periaqueductal gray (PAG) neurons were investigated using the nystatin-perforated patch clamp method. Continuous application of lipopolysaccharides (LPS) on PAG neurons resulted in increased glycine-induced ion current, and in decreased glutamate-induced ion current. In contrast, continuous application of amygdalin with LPS resulted in decreased glycine-induced ion current increased by LPS, and increased glutamateinduced ion current decreased by LPS in concentration-and time-dependent fashion. These results demonstrate that amygdalin modulates neuronal activity of PAG by modulation of glycine and glutamate. Based on the present results, it can be suggested that amygdalin participates in the regulation of the descending pain control system in the level of PAG neurons. The present study demonstrated that activation of the descending pain control system is one of the possible analgesic mechanisms of amygdalin.

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Suppression of a hind limb flexion withdrawal reflex by microinjection of glutamate or morphine into the periaqueductal gray in the rat

Cited by 33 publications

References 22 publications

Reciprocal connections between the periaqueductal gray matter and other somatosensory regions of the cat mid brain: A possible mechanism of pain inhibition

Reciprocal connections between the periaqueductal gray matter and other somatosensory regions of the cat mid brain: A possible mechanism of pain inhibition

Spinal Processing of Noxious and Innocuous Cold Information: Differential Modulation by the Periaqueductal Gray

Modulation of Amygdalin on Glycine- and Glutamate-induced Ion Currents in Rat Periaqueductal Gray Neurons

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