Neuroscience letters
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Neuroscience letters · Mar 2001
Differential antinociceptive effect of transcutaneous electrical stimulation on pain behavior sensitive or insensitive to phentolamine in neuropathic rats.
The effects of transcutaneous electrical stimulation and systemic injection of phentolamine, a non-specific alpha-adrenergic antagonist, on the behavioral signs of mechanical allodynia and cold hyperalgesia in rats with nerve injury were investigated. Mechanical allodynia and cold hyperalgesia were evaluated by measuring the paw withdrawal frequency (PWF) resulting from repetitive application of a von Frey hair and the paw lift duration (PLD) at a cold temperature, respectively. After a unilateral nerve injury, both PWF and PLD increased in the injured hind paw. ⋯ Naloxone reversed the LFHI-TES produced depression of PWF. Intraperitoneal administration of phentolamine depressed the injury-induced increased PLD without affecting the injury-induced increased PWF. Our results suggest that LFHI-TES, which activates the endogenous opioid systems, produces an antinociceptive effect that appears to be related to whether or not the pain is mediated by sympathetic activity.
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Neuroscience letters · Jan 2001
The role of peripheral N-methyl-D-aspartate receptors in Freund's complete adjuvant induced mechanical hyperalgesia in rats.
We investigated the role of excitatory amino acid receptors in mechanical hyperalgesia induced by subcutaneous injection of Freund's complete adjuvant (FCA) into the rat hind paw. In normal rats, an intraplantar (i.pl.) injection of L-glutamate, but not of D-glutamate (3 pmol/0.1 ml each) produced a mechanical hyperalgesia in the hind paw with a lowered paw-withdrawal threshold to pressure. ⋯ The results suggest that NMDA, but not non-NMDA receptors play a substantial role in mediating the development of mechanical hyperalgesia induced in the inflamed paw following i.pl. FCA injection.
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Neuroscience letters · Dec 2000
Reduced production of lactate during hypoxia and reoxygenation in astrocytes isolated from stroke-prone spontaneously hypertensive rats.
Lactate production and expressions of monocarboxylate transporter 1 (MCT1) and lactate dehydrogenase (LDH) mRNA after hypoxia and reoxygenation (H/R) were examined by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) using astrocytes in culture isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY). The basal production of lactate in SHRSP was the same as that observed in WKY. ⋯ In addition LDH and MCT1 mRNA expressions in SHRSP were significantly less strong compared with those in WKY during H/R. These findings indicate that decreased production and slow transport of lactate in SHRSP astrocytes are involved in neuronal energy depletion and possibly encourage neuronal damage, although hereditary weakness of cortical neurons is also related to cell death during H/R.
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Neuroscience letters · Dec 2000
The N-methyl-D-aspartate antagonistic and opioid components of d-methadone antinociception in the rat spinal cord.
The d-enantiomer of the opioid methadone is a weak opioid with low micromolar affinity to the N-methyl-D-aspartate (NMDA) receptor. We have investigated the antinociception and in vivo NMDA antagonism after systemic administration of d-methadone in the rat spinal cord. d-Methadone caused antinociception in the Randall-Selitto model of inflammatory pain and inhibited the responses of hindlimb single motor units to noxious electrical and mechanical stimulation (ED(50) 6.6, 6.8 and 7.2 mg/kg intravenous (i.v.), respectively); the wind-up of these responses was only inhibited at the dose almost completely abolishing the baseline responses. d-Methadone inhibited the activity of spinal dorsal horn neurones evoked by both iontophoretic NMDA and (R, S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA, ED(50) 5.7 and 8.2 mg/kg i.v., respectively). After pre-treatment with naloxone, d-methadone was unable to inhibit nociception in the Randall-Selitto model, the NMDA- or AMPA-evoked neuronal activity or the motoneurone wind-up. Thus, in the antinociceptive dose range, the NMDA antagonism does not appear to contribute to the mechanism of d-methadone antinociception.
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Neuroscience letters · Nov 2000
Bradykinin B1 receptor is constitutively expressed in the rat sensory nervous system.
Using immunocytochemistry with an antibody raised to a specific rat bradykinin B1 receptor sequence, we showed that the B1 receptor was expressed in the naive rat sensory nervous system. B1 immunoreactivity was seen in laminae 1 and 2 of the dorsal horn of the spinal cord, where primary afferents terminate, and on peripheral nerve terminals in the bladder. ⋯ B1 activation has an important role in the hyperalgesia associated with inflammation, but the site of action of B1 antagonists has generally been believed to be on peripheral, non-neuronal cells. The striking distribution of B1 receptors on sensory neurones suggests that a direct action of B1 activators on the nervous system may also contribute to hyperalgesia.