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Taste recognition memory is evident in rodents because the initial neophobia to novel tastes attenuates across exposures as the taste becomes familiar and safe. This attenuation of taste neophobia (AN) is context-dependent and an auditory background change could induce the recovery of the neophobic response. The AN auditory context-dependency requires the hippocampal integrity but the neurochemical mechanisms underlying the interaction with the taste memory circuit remain unexplored. We have applied pharmacological intervention by 6-hidroxydopamine (6-OHDA) hippocampal lesion for assessing the role of catecholamines in the hippocampal system to Wistar rats that drank a novel 3% vinegar solution for several consecutive days. Additionally, we manipulated the auditory background as a context that could either change or remain constant across all the drinking sessions. We found that a disruption of the context-dependent AN was induced by intracerebral administration of 6-OHDA targeted to the ventral CA1 hippocampus (vCA1). We conclude that the ability of the auditory context to modulate taste recognition memory involves the catecholaminergic activity in the ventral hippocampal circuit for the proper acquisition of safe taste memory., (Copyright © 2021 Elsevier B.V. All rights reserved.)

In two experiments adult rats (aged at least 6 months at the start of the procedure) received a diet enriched with added choline for a period of 10 weeks; control subjects were maintained on a standard diet during this time. All rats then underwent the spontaneous object recognition (SOR) procedure in which they were exposed to a pair of objects and then tested, after a retention interval, to a display with one object changed. Exploration of the changed object indicates retention and use of information acquired during the exposure phase. All subjects showed retention with a 24-h interval (Experiments 1 and 2) and when retested after a further 24 h (Experiment 1). But when tested for the first time after a 48-h interval (Experiment 2), control subjects showed no evidence of retention, exploring both objects equally, whereas those given the dietary supplement continued to show a preference for the changed object. This supports the conclusion that dietary choline supplementation can enhance performance on a task regarded as a test of declarative memory, and will do so even when the supplementations is given in adulthood., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Prior alcohol use is associated with impaired response inhibition in humans, including in laboratory go/no-go discrimination tasks. In two experiments, we determined whether chronic intermittent access to alcohol would alter go/no-go discrimination learning. Rats received 4-6 weeks of chronic intermittent access to 20% alcohol (alone or accompanied by saline or 1.5g/kg alcohol injections) or water. Rats then began discrimination training 4-5days after the end of the alcohol access. Each lever was available for 40s with one lever intermittently reinforced ("active lever") and the other lever non-reinforced ("inactive lever"). The rats given access to alcohol without concurrent alcohol injections drank ∼10g/kg/24-h on average during the last three weeks of alcohol access. The groups given alcohol injections (Alcohol+Injection groups) exhibited suppressed drinking, but the Alcohol+Injection groups exhibited higher blood alcohol spikes than all other alcohol groups (195 vs. 85-90mg/dl, respectively). We found no evidence for impaired go/no-go discrimination learning in either experiment. However, the alcohol access groups with moderate-to-high average alcohol consumption (>3g/kg/24-h) exhibited over-responding to the active lever compared to the water-only groups. One group given alcohol injections (Alcohol+Injection group) that exhibited very low voluntary drinking (<1g/kg/24-h) did not exhibit the over-responding effect, suggesting that the total 24-h alcohol dose matters more than short-lived blood alcohol spikes. Our findings are in accord with previous research showing that repeated alcohol withdrawal causes over-responding for responses that lead to limited reinforcement. Future work will determine the psychological and neurobiological basis of this behavioral change., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Previous results indicated that damage and pharmacological inactivation of the basolateral amygdala (BLA) interfere with the attenuation of taste neophobia. A similar disruption of safe taste memories formation induced by the inhibition of protein synthesis in the perirhinal cortex (PRh) has been reported. Thus, we have assessed the effect of bilateral BLA neurotoxic lesions on PRh activity after novel and familiar taste exposure. Wistar male rats with NMDA lesions of the BLA and SHAM-operated received two consecutive exposures to a 3% cider vinegar solution. Fos-like immunoreactivity (FLI) was examined as a marker of neuronal activity in PRh. As expected the BLA lesioned group showed no evidence of neophobia attenuation. A similar number of PRh Fos-positive cells were found in SHAM and BLA groups exposed to the novel taste solution. However, the BLA-lesioned group exhibited a lower number of Fos stained cells than the SHAM-lesioned group after being exposed to the familiar taste solution. This supports the notion of BLA and PRh as components of a neural circuit involved in safe taste recognition memory and suggests a role of PRh in various forms of recognition memory., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Lesion studies of the role of the gustatory insular cortex (GC) and amygdala (Am) in conditioned taste aversion (CTA) are confounded by the irreversibility of the intervention. Functional ablation methods allow more specific influencing of different phases of CTA acquisition and retrieval. Bilateral tetrodotoxin (TTX) blockade of GC (10 ng) or Am (3 ng) before or after saccharin drinking in rats with chronically implanted intracerebral cannulae showed that GC is indispensable for the initial processing of the taste stimulus but not for the association of the gustatory trace with the symptoms of LiCl poisoning. Gustatory signals can by-pass the blocked Am, the inactivation of which, however, impairs the gustatory trace-poisoning association. TTX injection into both GC and Am impairs CTA retrieval more than isolated blockade of either of these structures. It is argued that GC and Am implement processing of gustatory and visceral signals, respectively, but that formation and consolidation of the CTA engram proceeds outside forebrain, probably at the level of the brainstem.

Existing data on the effects of area postrema (AP) lesions on body rotation-induced emesis as well as on the participation of this zone in the acquisition of taste aversion learning (TAL) with other emetic agents suggest a possible role for the AP in learned aversions induced by body rotation. Nevertheless, earlier studies have shown that AP lesions do not prevent learned aversions induced by body rotation. The present experiments were performed in male Wistar rats in order to explore the effects of AP lesions on body rotation-induced flavor aversions as a function of the paradigm employed. Flavor aversions were induced by 30 min of circular body rotation (90 r.p.m.) using two different paradigms: a standard one including one trial learning, delay and single stimulus test and a three trials paradigm (with and without interstimulus delay) including both single stimulus test and choice test. AP lesions disrupt acquisition provided that the paradigm used includes interstimulus delay, i.e. when body rotation is applied 15 min after flavor intake. However, the AP seems to play no essential role when body rotation is applied immediately after flavor intake in a three-trial paradigm, as no effects were observed following AP lesions. In addition, subdiaphragmatic vagotomy plus simultaneous AP lesions leads to no interference in the acquisition of learned aversions induced by body rotation applied immediately after intake. It is concluded that body rotation may trigger a variety of aversive effects capable of inducing learned aversions, each apparently involving independent neural systems.

The structural characteristics of the area postrema, its anatomical connections, participation in the detection of emesis-provoking substances and the effects of area postrema lesions on taste aversion learning acquisition, are all factors which speak in favor of a role as a chemoreceptor zone involved in the detection of aversive agents which act as effective inducers of taste aversion learning. The feasibility of substituting electrical intracerebral stimulation of the area postrema for the aversive stimulus was investigated in a taste aversion learning paradigm. In Expt. 1, 0.1-ms rectangular pulses of 50 Hz, delivered intermittently or continuously for 4 h after a 15-min delay following ingestion of the gustatory stimulus, produced reliable learning. Expt. 2 showed the learning thus induced to reflect all the characteristics features attributed to taste aversion learning: one-trial learning, long interstimulus delay and cue-consequence specificity. These results suggest that the area postrema could participate in the detection of the aversive consequences of particular taste aversion learning-inducing agents.