Changes in the biogenic amine content of the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens of rats submitted to single and repeated sessions of the elevated plus-maze test

Abstract

It has been demonstrated that exposure to a variety of stressful experiences enhances fearful reactions when behavior is tested in current animal models of anxiety. Until now, no study has examined the neurochemical changes during the test and retest sessions of rats submitted to the elevated plus maze (EPM). The present study uses a new approach (HPLC) by looking at the changes in dopamine and serotonin levels in the prefrontal cortex, amygdala, dorsal hippocampus, and nucleus accumbens in animals upon single or double exposure to the EPM (one-trial tolerance). The study involved two experiments: i) saline or midazolam (0.5 mg/kg) before the first trial, and ii) saline or midazolam before the second trial. For the biochemical analysis a control group injected with saline and not tested in the EPM was included. Stressful stimuli in the EPM were able to elicit one-trial tolerance to midazolam on re-exposure (61.01%). Significant decreases in serotonin contents occurred in the prefrontal cortex (38.74%), amygdala (78.96%), dorsal hippocampus (70.33%), and nucleus accumbens (73.58%) of the animals tested in the EPM (P < 0.05 in all cases in relation to controls not exposed to the EPM). A significant decrease in dopamine content was also observed in the amygdala (54.74%, P < 0.05). These changes were maintained across trials. There was no change in the turnover rates of these monoamines. We suggest that exposure to the EPM causes reduced monoaminergic neurotransmission activity in limbic structures, which appears to underlie the "one-trial tolerance" phenomenon.

Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi

“…As it was previously said, NAS has been early involved in anxiety processes by us and another group [37,44,45], and after it, an important number of laboratories are showing additional evidences on the role of NAS in anxiety, citing our findings [12,15,16,43,65]. All these studies give support to a previous study using immunohistochemical staining for fos-like activity, mapping functional activation of discrete brain areas induced by anxiogenic situations.…”

Effect of long-term aspartame (artificial sweetener) on anxiety, locomotor activity and emotionality behavior in Wistar Albino rats

“…Our earlier report [46] also clearly indicates the increase in blood methanol level was associated with a marked increase in the free radical generation in brain regions of aspartame-treated MTX animals. Exposure to the EPM causes reduced monoaminergic neurotransmission activity in several limbic structures, such as dorsal hippocampus [47], which has been considered to be part of the so-called behavioral inhibition system and exerts a key role in the control of anxiety [48][49][50].…”

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

“…Based on this, drug effects on anxiety-like behaviours and aversive learning with subsequent long-term effects on memory in 24 h were tested. It has been reported that the prior experience of an undrugged EPM testing session may alter the behavioural responses in an undrugged retest session [13,74]. The injury caused by the injection might change the expression of messenger RNAs and proteins.…”