Project description:We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects. There are three experimental groups: 1: pups with no infant shock and the adult forced swim test (FST)with no odor; 2. pups with infant odor-shock pairing and the adult forced swim test (FST) with no odor; 3. pups with infant odor-shock pairing and adult forced swim test with infant odor.
Project description:We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects.
Project description:Increasing evidence suggests microRNAs (miRNAs) control levels of mRNA expression during development of the nervous system and during sensory elicited remodelling of the brain. We used an associative olfactory learning paradigm (proboscis extension response) in the honeybee Apis mellifera to detect gene expression changes in the brain. Transcriptome analysis of bees trained to associate an odor with a reward and control bees exposed to air without reward, helped us abstract mRNA-miRNA interactions for empirical testing. Functional studies, feeding cholesterol-conjugated antisense RNA to bees resulted in the inhibition of miR-210 and of miR-932 that is embedded within the neuroligin 2 (Nlg2) gene involved in synapse development. Loss of miR-932 prevents long-term memory formation but not learning. We validated 3M-bM-^@M-^YUTR target site interactions of miR-932 and show miR-932 dysregulates actin, a key cytoskeletal molecule involved in neuronal development and activity-dependent plasticity of the brain. The analysis used Air group (no odor learning) as control sample for comparison to two groups of odor-conditioned bees: linalool and floral mix.
Project description:mRNA-seq of olfactory bulbs from odor-deprived and odor-stimulated mice (RNA-seq done in triplicates) Control mice were kept in a clean air environment (using an activated carbon filter). Stimulated mice were exposed to a cocktail of odorants for 30 minutes ("30 min" time point), or for 30 minutes followed by a period of 90 minutes of clean air ("120 min" time point.) Mice were sacrificed immediately at end of time point, and olfactory bulbs were dissected out for RNA extraction and RNA-FISH. Three adult mice (6-8 weeks of age or older) were used in each condition.
Project description:Phosphorylation of ribosomal protein S6 (pS6) serves as a molecular marker of neuronal activation by external stimuli. In this study, olfactory epithelium tissues were obtained from mice exposed to binary odor mixtures consisting of acetophenone–decanal or octanal–cis-3-hexenol. To examine how different delivery methods of odor presentation influence neural responses, two paradigms for binary mixtures were employed. In the “+” condition, the two odorants were directly combined on a single piece of filter paper, allowing interaction prior to volatilization. In contrast, in the “&” condition, the odorants were applied separately to two filter papers placed in close proximity (~1 mm apart), such that the components mixed only in the air upon evaporation. Using these approaches, four experimental odor groups were generated (A+D, A&D, O+C, and O&C), along with a no-odor control, resulting in a total of five groups. Following stimulation, pS6-associated ribosome complexes were isolated from olfactory epithelium lysates through immunoprecipitation, selectively enriching mRNAs undergoing active translation in odor-activated cells. RNA sequencing of these samples enabled transcriptomic profiling within activated neuronal populations, providing insights into gene expression programs associated with distinct delivery methods of binary odor stimulation.
2025-10-09 | GSE306619 | GEO
Project description:Identification of Odor-Causing Microbes in Papermaking Process