Search

Background We previously showed that the infralimbic medial prefrontal cortex (IL-mPFC) plays an important role in recent and remote memory retrieval and extinction of conditioned odor aversion (COA) and contextual fear conditioning (CFC) in adult rats. Because the mPFC undergoes maturation during post-weaning, here, we aimed to explore (1) whether post-weanling rats can form recent and remote COA and CFC memory, and (2) the role of the IL-mPFC in mediating these processes. Methods To investigate the retrieval process, we transiently inactivated the IL-mPFC with lidocaine prior to the retrieval test at either recent or remote time points. To target the consolidation process, we applied the protein synthesis inhibitor after the retrieval at recent or remote time points. Results Our results show that the post-weanling animals were able to develop both recent and remote memory of both COA and CFC. IL-mPFC manipulations had no effect on retrieval or extinction of recent and remote COA memory, suggesting that the IL has no effect in COA at this developmental stage. In contrast, the IL-mPFC played a role in (1) the extinction of recent, but not remote, CFC memory, and (2) the retrieval of remote, but not recent, CFC memory. Moreover, remote, but not recent, CFC retrieval enhanced c-Fos protein expression in the IL-mPFC. Conclusions Altogether, these results point to a differential role of the IL-mPFC in recent and remote CFC memory retrieval and extinction and further confirm the differences in the role of IL-mPFC in these processes in post-weanling and adult animals. [ABSTRACT FROM AUTHOR]

Predation is a key factor in prey population dynamics and could impact population recovery. One common means employed to recover prey populations is that of translocations, but most fail owing to high predation during the early stages. We tested whether conditioned odor aversion can reduce predation during animal translocations by using the predation of the European rabbit Oryctolagus cuniculus by the red fox Vulpes vulpes as a case study. Following a before‐after control‐impact design (BACI), we deployed bait stations monitored using camera‐traps in two zones to which rabbits were translocated. One week before the rabbits were released, microencapsulated levamisole was added to rabbit baits located in the treatment zones, along with vanilla essence as an odor cue. A total of 148 rabbits were distributed in artificial warrens with the odor cue and 68 of them were fitted with radio collars in order to determine their survival rates. The response to the treatment and translocation as regards subsequent rabbit abundance was evaluated using N‐mixture models, while rabbit establishment was evaluated using a warren use index (WUI). The treatment decreased the proportion of baits consumed by foxes, but this decrease was partially compensated by other predators. WUI and rabbit population growth increased significantly more after translocations in the treatment zones than in the control zones. The short‐term survival of translocated rabbits was also higher in the treatment zones than in the control zones. Our study showed that conditioned odor aversion reduced rabbit predation by foxes, and had a positive effect on rabbit population growth after translocation, since there was an increase in rabbit survival and warren establishment. This method could be used as a non‐lethal tool for the recovery of a key prey when carrying out programs concerning the reintroduction of endangered predators or for other vulnerable species requiring translocations. [ABSTRACT FROM AUTHOR]

Childhood obesity increases the risk of health and cognitive disorders in adulthood. Consuming high-fat diets (HFD) during critical neurodevelopmental periods, like childhood, impairs cognition and memory in humans and animals, affecting the function and connectivity of brain structures related to emotional memory. However, the underlying mechanisms of such phenomena need to be better understood. This study aimed to investigate the neurochemical profile of the amygdala and hippocampus, brain structures involved in emotional memory, during the acquisition of conditioned odor aversion in male rats that consumed a HFD from weaning to adulthood. The rats gained weight, experienced metabolic changes, and reduced insulin sensitivity and glucose tolerance. Rats showed enhanced odor aversion memory, contrary to the expected cognitive impairments. This memory enhancement was accompanied by increased noradrenergic and glutamatergic neurotransmission in the amygdala and hippocampus. Importantly, this upregulation was specific to stimuli exposure, as basal neurotransmitter levels remained unaltered by the HFD. Our results suggest that HFD modifies cognitive function by altering neurochemical signaling, in this case, upregulating neurotransmitter levels rendering a stronger memory trace, demonstrating that metabolic dysfunctions do not only trigger exclusively detrimental plasticity processes but also render enhanced plastic effects depending on the type of information., (© 2024 The Author(s). Journal of Neuroscience Research published by Wiley Periodicals LLC.)

Abstract: Conditioned odor aversion (COA) corresponds to the avoidance of an odorized-tasteless solution (conditioned stimulus, CS) previously paired with toxicosis. COA occurs only when the interstimulus interval (ISI) is kept short, suggesting that the memory trace of the odor is subject to rapid decay. Previous experiments have shown that the entorhinal cortex (EC) is involved in the acquisition of COA, since lesion of the EC rendered COA tolerant to long ISI. Because EC lesions induce a septo-hippocampal cholinergic sprouting, the present experiment investigated whether COA tolerance to long ISI may be linked to this sprouting reaction. In a first experiment, male Long-Evans rats subjected to bilateral excitotoxic EC lesions combined to intracerebroventricular infusions of the selective cholinergic immunotoxin 192 IgG-saporin were exposed to odor-toxicosis pairing using a long ISI (120min). Results showed that EC-lesioned rats displayed COA with the long ISI but not the control groups. In rats with EC combined to 192 IgG-saporin lesions, histological analysis demonstrated no evidence for cholinergic septo-hippocampal sprouting. In a second experiment, animals with 192-IgG saporin lesion showed a marked COA with a short ISI (5min). These results suggest that the COA with the long ISI found in rats with EC lesions might involve a functional activity related to the EC lesion-induced hippocampal cholinergic sprouting. As the injection of 192 IgG-saporin alone did not affect COA with a short ISI, our data also point to a possible role of hippocampal cholinergic neurons in the modulation of memory processes underlying COA. [Copyright &y& Elsevier]

Evidence from the effect of aspiration lesions of the entorhinal cortex (EC) has shown that this region is involved in conditioned odor-aversion (COA) learning--that is, the avoidance of an odorized tasteless solution the ingestion of which precedes toxicosis--by rendering COA tolerant to long odor--toxicosis delay. The present study examined whether neurotoxic lesions restricted to the lateral or medial parts of the EC, in comparison with large aspiration lesions, were sufficient to produce this effect. Male Long--Evans rats received odor--intoxication pairing with either a short (5-min) or long (120-min) delay between the presentation of the odor and toxicosis. All groups, including sham-lesioned controls, showed COA at the 5-min odor--toxicosis delay interval, but only rats with lateral EC damage displayed COA at the longer delay. These data show that the lateral EC is part of the substrate involved in the control of the olfactory memory trace during COA. [ABSTRACT FROM AUTHOR]

• NMDA receptors activity in the Central Amygdala is required for Acquisition of Conditioned Odor Aversion. • NMDA receptors activity is required for up to 15 min after conditioning for Long-term odor aversion Memory formation. • Nitric Oxide Synthase activity is required for both acquisition and consolidation of Conditioned Odor Aversion. • Neither NMDA receptors nor Nitric Oxide Synthase activity is necessary for aversion memory retrieval. Rats readily learn to avoid a tasteless odorized solution if they experience visceral malaise after consuming it. This phenomenon is referred to as conditioned odor aversion (COA). Several studies have shown that COA depends on the functional integrity of the amygdala, with most studies focusing on the basolateral nucleus. On the other hand, the role of the central amygdala (CeA) which is known to be involved in the consolidation of conditioned taste aversion (CTA) remains to be established. To address this issue, we evaluated the effect of inhibiting NMDA receptor activity in this structure on COA memory formation. Intra-CeA infusions of non-competitive NMDA receptor inhibitor MK-801 prevented memory formation both when administered before and up to 15 min after COA conditioning, while no effect of this drug was observed when given before long-term memory test. We next evaluated the role of one of the main downstream effectors of brain NMDA receptor signaling, nitric oxide synthase (NOS), known to play a key role in a wide variety learning tasks including some types of olfactory conditioning. Similar results were obtained with inhibition of either NOS or neuron-specific NOS; which proved to be required both during and after COA training, though for a shorter time span than NMDA receptors. Also, neither isoform showed to be required to memory retrieval. These results suggest that the US signaling during acquisition and the initial consolidation step of COA depends on glutamate-NO system activation in the CeA. [ABSTRACT FROM AUTHOR]

The retrieval of odor-related memories shapes animal behavior. The anterior piriform cortex (aPC) is the largest part of the olfactory cortex, and it plays important roles in olfactory processing and memory. However, it is still unclear whether specific cellular mechanisms in the aPC control olfactory memory, depending on the appetitive or aversive nature of the stimuli involved. Cannabinoid-type 1 (CB1) receptors are present in the aPC (aPC-CB1), but their potential impact on olfactory memory was never explored. Here, we used a combination of behavioral, genetic, anatomical, and electrophysiological approaches to characterize the functions of aPC-CB1 receptors in the regulation of appetitive and aversive olfactory memory. Pharmacological blockade or genetic deletion of aPC-CB1 receptors specifically impaired the retrieval of conditioned odor preference (COP). Interestingly, expression of conditioned odor aversion (COA) was unaffected by local CB1 receptor blockade, indicating that the role of aPC endocannabinoid signaling is selective for retrieval of appetitive memory. Anatomical investigations revealed that CB1 receptors are highly expressed on aPC GABAergic interneurons, and ex vivo electrophysiological recordings showed that their pharmacological activation reduces miniature inhibitory post-synaptic currents (mIPSCs) onto aPC semilunar (SL), but not pyramidal principal neurons. COP retrieval, but not COA, was associated with a specific CB1-receptor-dependent decrease of mIPSCs in SL cells. Altogether, these data indicate that aPC-CB1 receptor-dependent mechanisms physiologically control the retrieval of olfactory memory, depending on odor valence and engaging modulation of local inhibitory transmission. • CB1 receptors are highly expressed in anterior piriform cortex (aPC) interneurons • aPC-CB1 receptors control retrieval of conditioned odor preference (COP) • aPC-CB1 receptors are not involved in retrieval of conditioned odor aversion • COP retrieval is linked to CB1-dependent reduction of aPC inhibitory transmission Terral et al. explore the role of the endocannabinoid system in olfactory memory functions. They show that cannabinoid type-1 (CB1) receptors control the retrieval of appetitive, but not aversive, olfactory memory, associated with a modulation of local inhibitory transmission onto specific principal neurons of the anterior piriform cortex. [ABSTRACT FROM AUTHOR]

Previous work has shown that β-adrenergic and GABAergic systems in the basolateral amygdala (BLA) are involved in the acquisition of conditioned odor aversion (COA) learning. The involvement of α 2 -adrenoreceptors, however, is poorly documented. In a first experiment, male Long-Evans rats received infusions of 0.1 μg of the selective α 2 -antagonist dexefaroxan (Dex) in the BLA before being exposed to COA learning. In a second experiment, levels of norepinephrine (NE) were analyzed following Dex retrodialysis into the BLA. While microdialysis data showed a significant enhancement of NE release in the BLA with Dex, behavioral results showed that pre-CS infusion of Dex impaired, rather than facilitated, the acquisition of COA. Our results show that the NE system in the BLA is involved in the acquisition of COA, including a strong α 2 -receptor modulation until now unsuspected. Supported by the recent literature, the present data suggest moreover that the processes underlying this learning are probably mediated by the balanced effects of NE excitatory/inhibitory signaling in the BLA, in which interneurons are highly involved.