Neuroscience letters
-
Neuroscience letters · May 2001
Low dose aspirin attenuates escape/avoidance behavior, but does not reduce mechanical hyperalgesia in a rodent model of inflammatory pain.
The present experiment examined the effect of aspirin on the escape/avoidance behavioral response to a mechanical stimulus (476 mN von Frey monofilament) in the place escape avoidance paradigm (PEAP) following subcutaneous administration of carrageenan (CARR). Forty-one male Sprague-Dawley rats received subcutaneous injection of CARR or saline in the left hindpaw and 3 1/2 h later were administered aspirin (0, 50 or 150 mg/kg). Thirty minutes later, animals were tested in the PEAP and then the mechanical paw withdrawal threshold was measured. ⋯ The shift from a preferred dark side of the chamber to the light side was attenuated by pre-treatment with both doses of aspirin (50 and 150 mg/kg). The lack of anti-hyperalgesia and avoidance behavior with 50 mg/kg aspirin suggests a decrease in the aversive nature of mechanical stimulation of the afflicted paw. It is suggested that the mechanisms underlying the affective/motivational dimension of nociception (escape/avoidance) can be dissociated from the processing of nociceptive information related to withdrawal responding.
-
Neuroscience letters · May 2001
Excitotoxic injury stimulates pro-drug-induced 7-chlorokynurenate formation in the rat striatum in vivo.
Peripheral administration of L-4-chlorokynurenine (4-Cl-KYN), which is enzymatically converted in astrocytes to form the glycine(B) receptor antagonist 7-chlorokynurenic acid (7-Cl-KYNA), has been shown to provide neuroprotection against excitotoxic damage. The present study was designed to examine the metabolic fate of 4-Cl-KYN after systemic injection, and to study its brain uptake and subsequent transamination during the acute phase following an excitotoxic insult. To this end, adult rats received intrastriatal injections of vehicle (1 microl) or quinolinic acid (QUIN) (240 nmol/1 microl), and were administered 50 mg/kg 4-Cl-KYN (intraperitoneally) immediately after surgery. ⋯ The contralateral, QUIN-injected striatum contained 212+/-39 and 97+/-27 nM 7-Cl-KYNA, respectively. This injury-induced increase was accompanied by slightly higher 4-Cl-KYN levels in the QUIN-treated striatum, indicating that better pro-drug availability in part accounts for the enhanced 7-Cl-KYNA formation. These data demonstrate that systemic 4-Cl-KYN application, by targeting reactive glial cells during the early, reversible stage of excitotoxic neurodegeneration, produces disproportionately large amounts of the neuroprotectant 7-Cl-KYNA at the site of the emerging lesion.
-
Neuroscience letters · May 2001
Striatal dopaminergic metabolism is increased by deep brain stimulation of the subthalamic nucleus in 6-hydroxydopamine lesioned rats.
Deep brain stimulation of the subthalamic nucleus is an established therapeutic strategy for patients with Parkinson's disease. Although the exact mechanisms of action remain unknown, it is noteworthy that dopaminergic medication can be markedly reduced after neurostimulation of the subthalamic nucleus. ⋯ Deep brain stimulation of the subthalamic nucleus was followed by a delayed increase of extracellular 3,4-dihydroxyphenylacetic and homovanillic whereas dopamine levels were unchanged in stimulated rats and controls. Our results indicate that deep brain stimulation of the subthalamic nucleus affects significantly striatal dopaminergic metabolism in 6-hydroxydopamine lesioned rats.
-
Neuroscience letters · Apr 2001
Clinical TrialA new method for measuring the conduction velocities of Abeta-, Adelta- and C-fibers following electric and CO(2) laser stimulation in humans.
The conduction velocities of Abeta-, Adelta- and C-fibers of a peripheral nerve of the upper limb in normal subjects were measured by a combination of conventional electric stimulation, painful CO(2) laser stimulation and non-painful CO(2) laser stimulation of a tiny skin surface area, respectively. The values obtained were 69.1+/-7.4 m/s, 10.6+/-2.1 and 1.2+/-0.2 m/s, respectively. These findings demonstrated that the combined methods are useful for experimental and clinical exploration of the physiological function and pathophysiological role of Abeta-, Adelta- and C-fibers of a given peripheral nerve.
-
Neuroscience letters · Mar 2001
The alterations of N-Methyl-D-aspartate receptor expressions and oxidative DNA damage in the CA1 area at the early time after ischemia-reperfusion insult.
Delayed neuronal death in the CA1 of the hippocampus following global ischemia has been evoked by both the activation of N-methyl-D-aspartate receptor (NR) and the generate reactive oxygen species in the neurons. In the present study, we investigated whether oxidative DNA damages may be correlated with NR subunits (NR1 and NR2A/B) expression following ischemia insults in vivo. ⋯ However, NR2A/B and 8-OHdG immunoreactivities were enhanced in CA1 over 24 h after ischemia although NR1 immunoreactivity was decreased. These results suggest that oxidative stress and excitotoxicity in the CA1 may simultaneously trigger neuronal damages at early time after ischemia, and free radical damage including oxidative DNA damage may eventually promote the delayed neuronal death in this region.