Lesion of the lateral entorhinal cortex amplifies odor‐induced expression of c‐fos, junB, and zif 268 mRNA in rat brain

Abstract

Paradoxical facilitation of olfactory learning following entorhinal cortex (EC) lesion has been described, which may result from widespread functional alterations taking place within the olfactory system. To test this hypothesis, expression of the immediate early genes c-fos, junB, and zif 268 was studied in response to an olfactory stimulation in several brain areas in control and in EC-lesioned rats. Olfactory stimulation in control rats induced the expression of the three genes in the granular/mitral and glomerular layers of the olfactory bulb, as well as c-fos and junB expression in the piriform cortex. However EC lesion was devoid of effects in nonstimulated animals; it significantly amplified the odor-induced expression of the three genes in these areas, as well as in the amygdala, hippocampus, and parietal-temporal cortices. The data suggest that EC lesion modifies the neural processing of odor by suppressing an inhibitory influence on brain areas connected to this cortex.

Lateral Entorhinal Modulation of Piriform Cortical Activity and Fine Odor Discrimination

“…The results are consistent with earlier reports using electrolytic or aspiration lesions of the entorhinal/perirhinal cortex suggesting a top-down entorhinal cortex suppression of piriform cortical activity (Bernabeu et al, 2006; Mouly and Di Scala, 2006) Figure 7. Bilateral infusion of muscimol into the aPCX impaired gross odor discrimination (10c vs 10cR1).…”

“…cillations were enhanced, we hypothesize that the loss of LEC top-down suppression enhances OB-PCX excitability and thus enhances OB-PCX LFP beta oscillatory activity. This potential enhanced aPCX responsiveness to OB input could also contribute to the previously observed enhancement in odor-evoked c-fos activation in the PCX following entorhinal cortex lesions (Bernabeu et al, 2006), and enhancement of simple odor learning (Ferry et al, 1996;Wirth et al, 1998). Interestingly, the enhancement in the aPCX single-unit firing rate following LEC silencing was associated with a disruption in firing entrainment to locally recorded LFP beta oscillations (Fig.…”

Cortical Odor Processing in Health and Disease

“…These prior studies have in part interpreted their findings in the context of entorhinal cortex as the major afferent of the hippocampal formation, and odor quality differences were not closely controlled. However, as described above, the entorhinal cortex is also a major feedback afferent to the olfactory system (Canto et al, 2008; Haberly and Price, 1978) and robustly modulates odor-evoked activity in the piriform cortex (Bernabeu et al, 2006; Chapuis et al, 2013; Kay et al, 1996; Mouly and Di Scala, 2006), which could contribute importantly to these effects. For example, recent work using reversible silencing of the entorhinal cortex with muscimol infusions demonstrates that loss of entorhinal feedback enhances piriform cortical single-unit activity and odor-evoked LFP oscillations.…”

“…It must be noted that the emergence of hyperexcitability within the olfactory system emerges before Aβ plaque formation, suggesting an important role for soluble Aβ oligomers or potentially AICD in this dysfunction. Finally, recall that loss of entorhinal cortical function also induces hyperexcitability in piriform cortex (Bernabeu et al, 2006; Chapuis et al, 2013). It is presently unclear how Aβ deposition within the entorhinal cortex may contribute to piriform cortical functional pathology.…”

The Olfactory Mosaic: Bringing an Olfactory Network Together for Odor Perception

“…In addition to these coherence studies, the lateral entorhinal cortex has also been demonstrated to influence the PCX activity. Aspiration lesions of the entorhinal cortex increase odor-evoked PCX activity [e.g., immediate early gene labeling; (Bernabeu, Thiriet, Zwiller, & Di Scala, 2006)] and enhance simple odor learning such as conditioned odor aversion (Ferry, Oberling, Jarrard, & Di Scala, 1996). These results suggest a strong top-down suppression of PCX activity by the entorhinal cortex.…”