PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8396783

Taste-potentiated odor aversion learning based on amphetamine.

P A Bryant·R A Boakes·I S McGregor
View original source ↗Export metadata ↓

Abstract

This study sought to determine whether a taste can potentiate a conditioned odor aversion based on amphetamine as well as those based on lithium. A taste-potentiated odor aversion (TPOA) based on lithium was obtained in Experiment 1 only with a low concentration of an almond odor. This concentration was used in Experiment 2 where the taste, 0.1% saccharin, potentiated an odor aversion based on 1 mg/kg d-amphetamine. This was replicated in Experiment 3 where potentiation was found with doses of both 1 and 3 mg/kg amphetamine, and no effect of dose was detected. It was concluded that TPOA learning is not restricted to drugs such as lithium that produce conditioned unpalatability as well as conditioned aversions to a taste, because amphetamine does not produce conditioned unpalatability at the doses used here. Furthermore, because in Experiment 3 postconditioning extinction of the saccharin aversion removed the potentiation effect, it appears that this form of TPOA may depend on an association between the odor and taste, as proposed by within-compound theory.

Explore related subjects

AmphetamineAnimalsAssociation LearningAvoidance LearningChloridesConditioning, ClassicalDose-Response Relationship, DrugDrinkingDrug SynergismExtinction, PsychologicalLithiumLithium ChlorideMaleRatsRats, WistarSmellTasteJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P A Bryant, R A Boakes, I S McGregor. 1993. Taste-potentiated odor aversion learning based on amphetamine.. https://doi.org/10.1016/0031-9384(93)90128-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Delta opioid receptors regulate calcium-dependent, amphetamine-evoked glutamate levels in the rat striatum: an in vivo microdialysis study.

Blockade of opioid receptors decreases amphetamine-induced behaviors and dopamine release in the striatum. Use of selective opioid receptor ligands has indicated that these effects are mediated by delta opioid receptors (DORs). However, the site of action of delta receptors and the influence of delta receptor antagonists on other neurotransmitters released by amphetamine are unknown. Therefore, the effect of reverse microdialysis of the selective delta opioid antagonist, naltrindole, on extracellular striatal glutamate levels evoked by amphetamine (2.5 mg/kg, i.p.) was investigated. Naltrindole (10-100 microM) decreased amphetamine-evoked glutamate levels in a concentration-dependent manner. The selective delta agonist, [D-Pen(2,5)]-enkephalin (100, 500 microM), reversed the effect of naltrindole, confirming that delta receptors mediated this effect. The amphetamine-evoked increase in extracellular glutamate levels was determined to be 39% calcium-sensitive by lowering the calcium concentration in the perfusate. Under these conditions, naltrindole had no effect on the calcium-independent component of amphetamine-evoked glutamate levels. These data indicate that intrastriatal DORs modulate a calcium-dependent, amphetamine-evoked component of extracellular glutamate levels that may depend on activation of a transsynaptic basal ganglia-thalamo-cortical loop.

Amphetamine↗
PubMed2000

Chronic food restriction increases fos-like immunoreactivity (FLI) induced in rat forebrain by intraventricular amphetamine.

Chronic food restriction enhances behavioral responsiveness to amphetamine and other abused drugs. Because this effect is evident when drugs are administered intracerebroventricularly (i.c.v.) as well as systemically, it would seem to reflect increased sensitivity of a neural substrate rather than a change in drug disposition. In the present study, c-Fos immunohistochemistry was used to evaluate whether the magnitude and pattern of cellular activation induced by i.c.v. amphetamine is altered by a regimen of food restriction previously shown to potentiate amphetamine reward. In the absence of amphetamine challenge, there was generally no difference in brain Fos-like immunoreactivity (FLI) between ad libitum fed and food-restricted rats. In response to amphetamine (50 microg), both groups displayed increased FLI in caudate-putamen, nucleus accumbens, bed nucleus of the stria terminalis, ventral pallidum, central nucleus of the amygdala, and cingulate cortex. With the exception of cingulate cortex and caudal caudate-putamen, a significantly greater response was observed in brain regions of food-restricted rats. These results indicate that food restriction augments a cellular immediate early gene (IEG) response to acute amphetamine in brain regions known to mediate rewarding and other behavioral effects of psychostimulants. The difference between these results and those produced by sensitizing regimens of psychostimulant exposure are discussed, as are possible endocrine factors that could be involved in the modulatory effect of food restriction on cellular and behavioral responses to amphetamine.

Amphetamine↗
PubMed2000

Cocaine- and amphetamine-regulated transcript-immunoreactivity in the rat sympatho-adrenal axis.

Distribution of cocaine- and amphetamine-regulated transcript-like immunoreactivity (CART-LI) was studied in the rat spinal cord, sympathetic ganglia and adrenal glands by immunohistochemical methods, utilizing a polyclonal antiserum raised against the CART peptide fragment 55-102. CART-LI was detected in nerve fibers and in basket-like terminals surrounding many postganglionic neurons of the superior cervical ganglion (SCG), stellate, paravertebral and prevertebral ganglia. Postganglionic neurons exhibited low or non-detectable levels of CART-LI. Surgical sectioning of the cervical sympathetic trunk for 6-7 days resulted in a nearly complete loss of CART-LI fibers and terminals in the SCG. In the adrenal gland, CART-LI nerve fibers formed a plexus underneath the capsule, some of which bifurcated and made a sharp turn toward the adrenal medulla, where clusters of chromaffin cells were intensely labeled. The detection of CART-LI in sympathetic ganglia and adrenal glands extends the previous observation of the presence of CART-LI in sympathetic preganglionic neurons and further supports the notion that CART peptide(s) may function as a signaling molecule in the sympatho-adrenal axis.

Amphetamine↗