Hypothalamus-olfactory system crosstalk: orexin a immunostaining in mice.

Short title: Orexin in miceInternational audienceIt is well known that olfaction influences food intake, and conversely, that an individual's nutritional status modulates olfactory sensitivity. However, what is still poorly understood is the neuronal correlate of this relationship, as well as the connections between the olfactory bulb and the hypothalamus. The goal of this report is to analyze the relationship between the olfactory bulb and hypothalamus, focusing on orexin A immunostaining, a hypothalamic neuropeptide that is thought to play a role in states of sleep/wakefulness. Interestingly, orexin A has also been described as a food intake stimulator. Such an effect may be due in part to the stimulation of the olfactory bulbar pathway. In rats, orexin positive cells are concentrated strictly in the lateral hypothalamus, while their projections invade nearly the entire brain including the olfactory system. Therefore, orexin appears to be a good candidate to play a pivotal role in connecting olfactory and hypothalamic pathways. So far, orexin has been described in rats, however, there is still a lack of information concerning its expression in the brains of adult and developing mice. In this context, we revisited the orexin A pattern in adult and developing mice using immunohistological methods and confocal microscopy. Besides minor differences, orexin A immunostaining in mice shares many features with those observed in rats. In the olfactory bulb, even though there are few orexin projections, they reach all the different layers of the olfactory bulb. In contrast to the presence of orexin projections in the main olfactory bulb, almost none have been found in the accessory olfactory bulb. The developmental expression of orexin A supports the hypothesis that orexin expression only appears post-natally

Somatostatin Serves a Modulatory Role in the Mouse Olfactory Bulb: Neuroanatomical and Behavioral Evidence

Somatostatin (SOM) and somatostatin receptors (SSTR1–4) are present in all olfactory structures, including the olfactory bulb (OB), where SOM modulates physiological gamma rhythms and olfactory discrimination responses. In this work, histological, viral tracing and transgenic approaches were used to characterize SOM cellular targets in the murine OB. We demonstrate that SOM targets all levels of mitral dendritic processes in the OB with somatostatin receptor 2 (SSTR2) detected in the dendrites of previously uncharacterized mitral-like cells. We show that inhibitory interneurons of the glomerular layer (GL) express SSTR4 while SSTR3 is confined to the granule cell layer (GCL). Furthermore, SOM cells in the OB receive synaptic inputs from olfactory cortical afferents. Behavioral studies demonstrate that genetic deletion of SSTR4, SSTR2 or SOM differentially affects olfactory performance. SOM or SSTR4 deletion have no major effect on olfactory behavioral performances while SSTR2 deletion impacts olfactory detection and discrimination behaviors. Altogether, these results describe novel anatomical and behavioral contributions of SOM, SSTR2 and SSTR4 receptors in olfactory processing

Etude de l’activation cérébrale induite par le comportement via la cartographie de l’expression de la protéine FOS chez le rongeur

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Suppression of c-fos expression in the amygdala impairs the retrieval of taste potentiated odor aversion

Suppression of c-fos expression in the amygdala impairs the retrieval of taste potentiated odor aversion. 18. Congress of european chemoreception research organization, ECR

Cerveaux de lapereaux : circuits mis en jeu par un signal phéromonal et un odorant phéromone-appris

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Inactivation of the basolateral amygdala impairs the retrieval of recent and remote taste-potentiated odor aversion memory

International audienceMemory reorganization as a time-dependent process can be investigated using various learning tasks such as the taste-potentiated odor aversion (TPOA). In this paradigm rats acquire a strong aversion to an olfactory cue presented simultaneously with a gustatory cue. Together these cues are paired with a delayed visceral illness. The basolateral amygdaloid nucleus (BLA) plays a key role in TPOA acquisition but its involvement in retrieval remains unclear. We investigated the involvement of the BLA in either recent or remote retrieval of TPOA. In each case, the number of licks observed in response to the presentation of either the odor or the taste was used to assess retrieval. Before the retrieval test, rats received a bilateral infusion of lidocaine to inactivate the BLA. We observed that both recent and remote TPOA retrieval tests induced by the odor presentation were disrupted in the lidocaine-injected rats. By contrast, the BLA inactivation had no effect upon the aversion towards the taste cue regardless of the time of retrieval. The present study provides evidence that BLA functioning is necessary for retrieval of aversive odor memory, even with a long post-acquisition delay

Does the olfactory cue activate the same brain network during aging in the rat after taste potentiated odor aversion retrieval?

International audienceDepending on the brain networks involved, aging is not accompanied by a general decrease in learning and memory capabilities. We demonstrated previously that learning and retrieval of taste potentiated odor aversion (TPOA) is preserved, and even slightly improved, in senescent rats showing some memory deficiencies in cognitive tasks (Dardou, Datiche, & Cattarelli, 2008). TPOA is a particular behavior in which the simultaneous presentation of odor and taste cues followed by a delayed visceral illness leads to a robust aversion towards both conditioned stimuli, which permits diet selection and animal survival. The present experiment was performed in order to investigate the stability or the evolution of the brain network underlying TPOA retrieval during aging. By using immunocytochemical detection of Fos and Egr1 proteins we mapped the cerebral activation induced by TPOA retrieval elicited by the odor presentation in the young, the adult and the senescent rats. The pattern of brain activation changed and the number of activated areas decreased with age. Nevertheless, the piriform cortex and the basolateral amygdala nucleus were always activated and seemed essential for TPOA retrieval. The hippocampus and the neocortical areas could have different implications in TPOA memory in relation to age. The patterns of expression of Fos and Egr1 were different, suggesting their differential involvement in TPOA retrieval. Data are discussed according to the possible roles of the brain areas studied and a model of schematic brain network subtending TPOA retrieval induced by the odor cue is proposed

Fos and Egr1 expression in the rat brain in response to olfactory cue after taste-potentiated odor aversion retrieval

When an odor is paired with a delayed illness, rats acquire a relatively weak odor aversion. In contrast, rats develop a strong aversion to an olfactory cue paired with delayed illness if it is presented simultaneously with a gustatory cue. Such a conditioning effect has been referred to as taste-potentiated odor aversion learning (TPOA). TPOA is an interesting model for studying neural mechanisms of plasticity because of its robustness and rapid acquisition. However, the neural substrate involved in TPOA retrieval has not been well characterized. To address this question, we used immunocytochemical detection of inducible transcription factors encoded by the immediate-early genes Fos and Egr1. Thirsty male rats were conditioned to TPOA learning, and they were submitted to retrieval in the presence of the learned odor 3 d later. Significant increases in both Fos and Egr1 expressions were observed in basolateral amygdala, insular cortex, and hippocampus in aversive rats in comparison with the all the control groups. The pattern of neuronal activity seemed unlikely to be related to the sole LiCl injection. Lastly, opposite patterns of Fos and Egr1 were noted in the entorhinal cortex and the central nucleus of amygdala, suggesting a differential involvement of these markers in retrieval of TPOA