Abstract
BackgroundStudies intending to measure drug-induced changes in learning and memory are challenged to parse out the effects of drugs on sensory, motor, and associative systems in the brain. In the context of conditioned taste aversion (CTA), drugs that alter the sensorium of subjects and affect their ability to taste and/or feel malaise may limit the ability of investigators to make conclusions about associative effects of these substances. Since the GABAergic system is implicated in inhibition, the authors were hopeful to use the GABA agonist, baclofen (BAC), to enhance extinction of a CTA, but first a preliminary evaluation of BAC's peripheral effects on animals' sensorium had to be completed due to a lack of published literature in this area.FindingsOur first experiment aimed to evaluate the extent to which the GABAB agonist, BAC, altered the ability of rats to differentiate between 0.3% and 0.6% saccharin (SAC) in a two bottle preference test. Here we report that 2 or 3 mg/kg (i.p.) BAC, but not 1 mg/kg BAC, impaired animals' gustatory discrimination abilities in this task. Furthermore, when SAC consumption was preceded by 2 or 3 mg/kg (i.p.) BAC, rats depressed their subsequent SAC drinking.A second experiment evaluated if the suppression of SAC and water drinking (revealed in Experiment 1) was mediated by amnesiac effects of BAC or whether BAC possessed US properties in the context of the CTA paradigm. The time necessary to reach an asymptotic level of CTA extinction was not significantly different in those animals that received the 3 mg/kg dose of BAC compared to more conventionally SAC + lithium chloride (LiCl, 81 mg/kg) conditioned animals.ConclusionsOur findings were not consistent with a simple amnesia-of-neophobia explanation. Instead, results indicated that 2 and 3 mg/kg (i.p.) BAC were capable of inducing a CTA, which was extinguishable via repeated presentations of SAC only. Our data indicate that, depending on the dose, BAC can alter SAC taste discrimination and act as a potent US in the context of a CTA paradigm.
Highlights
Studies intending to measure drug-induced changes in learning and memory are challenged to parse out the effects of drugs on sensory, motor, and associative systems in the brain
Results indicated that 2 and 3 mg/kg (i.p.) BAC were capable of inducing a conditioned taste aversion (CTA), which was extinguishable via repeated presentations of SAC only
We found that BAC (3 mg/kg) induced a conditioned taste aversion to SAC that extinguished in a time-course similar to that of a more conventional LiCl-induced SAC aversion [21]
Summary
Studies intending to measure drug-induced changes in learning and memory are challenged to parse out the effects of drugs on sensory, motor, and associative systems in the brain. GABAergic (g-Aminobutyric acid) systems play an important role in learning, memory, and inhibitory processes [1,2,3]. Baclofen [BAC; (±)-b-(Aminomethyl)-4- chlorobenzenepropanoic acid.] is a GABAB receptor agonist that has been used extensively in studies aimed at determining the role of GABA receptors in learning and memory. Rats injected intraperitoneally with BAC displayed both hyperdipsic and hyperphagic responses [10,11]. These behaviors were reversed, in rats, using systemic and intracerebroventricular injections of the GABAB antagonist, CGP35348 [11]. Infusions of BAC in the median raphe nuclei led to increased eating behaviors, but did not affect drinking behaviors [12]
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