Biomedical subjects

C J LaBuda

Publications and source records attributed to C J LaBuda.

9 recordsLinked to original sources

PubMed2001

A comparison of chronic aspartame exposure to aspirin on inflammation, hyperalgesia and open field activity following carrageenan-induced monoarthritis.

The purpose of the present study was to investigate whether chronic aspartame exposure possesses analgesic and anti-inflammatory actions in the carrageenan-induced monoarthritis model similar to those properties of aspirin. Prior research demonstrated that aspartame can reduce second phase formalin pain and increase motor activity in arthritic patients. Fifty-eight male Sprague-Dawly rats were treated with aspartame (25, 50, 100 mg/kg) or saline for six days. An additional group of animals received daily injections of saline and on the sixth treatment day, received a 150-mg/kg dose of aspirin 30-minutes prior to behavioral testing. On Day 6, animals received an intra-articular (i.a.) injection of 2% lambda carrageenan (CARR) or an equal volume of saline and were tested four hours later on threshold to mechanical and thermal stimuli, open field activity, and knee joint diameter. Aspirin-treated arthritic animals exhibited significantly less mechanical hyperalgesia and knee joint inflammation compared with vehicle treated arthritic animals. However, aspirin did not reverse thermal hyperalgesia or increase motor activity to control levels. Aspartame did not reduce inflammation, increase motor activity, or attenuate thermal allodynia, but at 50 mg/kg did attenuate mechanical allodynia compared with vehicle treated arthritic animals. The anti-hyperalgesic effect on mechanical hyperalgesia was not seen at 25 mg/kg or 100 mg/kg aspartame. These results suggest that a certain amount of aspartame may provide relief of arthritic pain to a similar degree as aspirin in some individuals. The specific effect of aspartame and aspirin on mechanical hyperalgesia should be considered when these agents are used for the therapeutic treatment of arthritic conditions.

Animals↗

PubMed2001

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. Compared with Saline vehicle-treated controls, all CARR-treated animals displayed hyperalgesia, as reflected by enhanced responding to mechanical stimulation applied to the CARR-injected paw. Mechanical hyperalgesia was significantly reduced by the pre-treatment of 150 mg/kg, but not 50 mg/kg aspirin. In the PEAP, CARR vehicle-treated animals avoided a preferred location of the test chamber that was associated with mechanical stimulation of the hyperalgesic paw. 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.

Animals↗

PubMed2001

The anxiolytic effect of acute ethanol or diazepam exposure is unaltered in mu-opioid receptor knockout mice.

Previous researchers demonstrate an opioidergic involvement in the anxiolytic and rewarding actions of ethanol and diazepam. Therefore, to further characterize the role of the opioid system in the anxiolytic action of ethanol and diazepam, normal (C57BL/6J), hybrid (B6129F1) and mu-opioid receptor knockout mice were given i.p. ethanol (0, 1.0 or 1.6 g/kg) or diazepam (1.5 mg/kg). The anxiolytic properties of these agents were then tested in the elevated plus-maze. Additional ethanol-treated mu-opioid receptor knockout mice (1 g/kg) were pretreated with the kappa-opioid receptor antagonist nor-BNI (0 or 3 mg/kg) to assess the involvement of kappa-opioid activity in ethanol's anxiolytic actions. The anxiolytic action of ethanol and diazepam in the mu-opioid receptor knockout mouse did not differ from the effects obtained in normal mice and pretreatment with nor-BNI did not significantly attenuate ethanol's actions in mu-opioid receptor knockout mice. Thus, the anxiolytic actions of ethanol and diazepam appear to be independent of opioid system activity in the mu-opioid receptor knockout mouse.

Animals↗

PubMed2000

Morphine and gabapentin decrease mechanical hyperalgesia and escape/avoidance behavior in a rat model of neuropathic pain.

A behavioral test paradigm that measures the aversive quality of stimulus-evoked pain in an animal model of neuropathic pain (L5 ligation) was tested for sensitivity to (1) different forces (476 and 202 mN) and frequencies (once every 15 or 30 s) of mechanical stimulation to the hyperalgesic paw and (2) different doses of the common antinociceptive compounds morphine (1 and 10 mg/kg) and gabapentin (30 and 90 mg/kg). Compared to non-ligated controls, the greater force (476 mN) and frequency (every 15 s) of mechanical stimulation of the hyperalgesic paw was associated with the greatest degree of escape/avoidance behavior. There was not a significant degree of escape/avoidance behavior at the lowest force (202 mN) and frequency (every 30 s) of mechanical stimulation. Compared to ligated vehicle treated controls, morphine (1 mg/kg) and gabapentin (90 mg/kg) decreased mechanical hyperalgesia and also attenuated the escape/avoidance behavior. The antinociceptive and antiaversive effects were found at doses that did not produce evidence of decreased motor activity. It is concluded that the behavioral test paradigm used to measure the aversiveness of stimulus-evoked nociceptive behavior is sensitive to different degrees of evoked pain and traditional analgesic compounds.

Acetates↗

PubMed2000

Mechanical and thermal hypersensitivity develops following kainate lesion of the ventral posterior lateral thalamus in rats.

Damage to the ventral-posterior lateral nucleus (VPL) of the thalamus or its afferent pathways can produce moderate to severe on-going pain and pain in response to normally innocuous stimuli (allodynia) and hypersensitivity to mildly noxious stimuli (hyperalgesia). The present study measured the responses to mechanical and thermal stimuli before and 2, 8, 24 and 48 h after a kainate-induced lesion of the VPL in male rats. Compared with control animals, hypersensitivity to mechanical stimulation of the hindpaw was apparent by 24 h post-lesion. At 48 h, the frequency of mechanical response increased from a baseline response frequency of 17+/-4.7 to 46+/-11.6%. Thermal withdrawal latencies 48 h after the lesion decreased from a baseline latency of 9.9+/-1.8 to 5.3+/-0.4 s. It is concluded that a neurotoxic lesion of the VPL results in a delayed onset of mechanical and thermal hyperalgesia. This study suggests a potential model for studying the basic mechanisms and potential therapies for central pain syndrome.

Afferent Pathways↗

PubMed2000

Stress-induced analgesia in mu-opioid receptor knockout mice reveals normal function of the delta-opioid receptor system.

Stress-induced analgesia (SIA) was examined in wildtype and mu-opioid receptor knockout mice. We used thermal paw withdrawal (TPW) latency following a continuous 3-min swim in 20 degrees C water, and found a significant increase in TPW latency in both wild-type and knockout mice. Pre-treatment prior to the swim with naltrindole, a selective delta-opioid receptor antagonist, blocked the increase in TPW latency in knockout mice. These results demonstrate an intact delta-receptor-mediated function of a physiologically-released endogenous agonist in the mu-opioid receptor knockout mouse. The present findings are in contrast with previous reports that analgesia induced by exogenous delta agonists is reduced in the knockout mice.

Analgesia↗

PubMed2000

A behavioral test paradigm to measure the aversive quality of inflammatory and neuropathic pain in rats.

The present experiment assessed the aversive quality of neuropathic and inflammatory pain in rats. Compared to sham-treated animals, L5 ligated (neuropathic) and complete Freund's adjuvant (inflammatory)-treated animals displayed an initial period of escape followed by avoidance of a preferred location of the test chamber that was associated with mechanical stimulation of the hyperalgesic paw. The onset of the avoidance behavior occurred during the first 10-15 min of behavioral testing and was maximal at 30 min. It is concluded that animals find mechanical stimulation of the hyperalgesic paw aversive and that this behavioral test paradigm is an additional method that may be used to assess nociception in rat neuropathic and inflammatory models.

Animals↗

PubMed2000

Aspirin attenuates the anxiolytic actions of ethanol.

The present study examined the effect of aspirin on the anxiolytic action of ethanol. Previous research has shown that ethanol reliably produces an anxiolytic effect on rodent's plus-maze performance while aspirin has been demonstrated to attenuate several of ethanol's behavioral actions. Female Sprague-Dawley rats were given s.c. aspirin doses of 0 or 150 mg/kg, followed 30 min later by s.c. ethanol doses of 0, 1.0 or 1.6 g/kg. After 5 min, animals were tested in the elevated plus-maze. Although aspirin did not have a significant effect on anxiety-related behavior, it did attenuate the anxiolytic action of ethanol at the dose of 1.0 g/kg, but not at the 1.6 g/kg dose. Thus, aspirin by itself does not appear to possess anxiolytic actions, but does modify the anxiolytic actions of 1.0 g/kg, but not 1.6 g/kg ethanol.

Animals↗

PubMed2000

Anxiety in mice following acute aspartame and ethanol exposure.

The purpose of the present study was to look at the effect of aspartame on the anxiolytic actions of ethanol. Previous research has shown that ethanol reliably produces an anxiolytic effect on rodent's plus-maze performance. There have been anecdotal reports that aspartame increases anxiety. CD-1 male mice were given i.p. aspartame doses of vehicle, 1000, or 2000 mg/kg, followed 30 min later by i.p. ethanol doses of 1.6 g/kg or vehicle. Animals were then placed in an open field, then tested in the plus-maze. Results determined that the aspartame condition had no significant effect on anxiety-related behavior, nor did it alter the anxiolytic actions of ethanol. Thus, acute high dose exposure to aspartame does not appear to affect anxiety-related behaviors.

Animals↗