Matching Items (5)

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Neuromodulation of olfactory learning by serotonergic signaling at glomerular synapses reveals a peripheral sensory gating mechanism

Description

Sensory gating is a process by which the nervous system preferentially admits stimuli that are important for the organism while filtering out those that may be meaningless. An optimal sensory

Sensory gating is a process by which the nervous system preferentially admits stimuli that are important for the organism while filtering out those that may be meaningless. An optimal sensory gate cannot be static or inflexible, but rather plastic and informed by past experiences. Learning enables sensory gates to recognize stimuli that are emotionally salient and potentially predictive of positive or negative outcomes essential to survival. Olfaction is the only sensory modality in mammals where sensory inputs bypass conventional thalamic gating before entering higher emotional or cognitive brain regions. Thus, olfactory bulb circuits may have a heavier burden of sensory gating compared to other primary sensory circuits. How do the primary synapses in an olfactory system "learn"' in order to optimally gate or filter sensory stimuli? I hypothesize that centrifugal neuromodulator serotonin serves as a signaling mechanism by which primary olfactory circuits can experience learning informed sensory gating. To test my hypothesis, I conditioned genetically-modified mice using reward or fear olfactory-cued learning paradigms and used pharmacological, electrophysiological, immunohistochemical, and optical imaging approaches to assay changes in serotonin signaling or functional changes in primary olfactory circuits. My results indicate serotonin is a key mediator in the acquisition of olfactory fear memories through the activation of its type 2A receptors in the olfactory bulb. Functionally within the first synaptic relay of olfactory glomeruli, serotonin type 2A receptor activation decreases excitatory glutamatergic drive of olfactory sensory neurons through both presynaptic and postsynaptic mechanisms. I propose that serotonergic signaling decreases excitatory drive, thereby disconnecting olfactory sensory neurons from odor responses once information is learned and its behavioral significance is consolidated. I found that learning induced chronic changes in the density of serotonin fibers and receptors, which persisted in glomeruli encoding the conditioning odor. Such persistent changes could represent a sensory gate stabilized by memory. I hypothesize this ensures that the glomerulus encoding meaningful odors are much more sensitive to future serotonin signaling as such arousal cues arrive from centrifugal pathways originating in the dorsal raphe nucleus. The results advocate that a simple associative memory trace can be formed at primary sensory synapses to facilitate optimal sensory gating in mammalian olfaction.

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Created

Date Created
  • 2012

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Scents of efficiency: discovering how olfactory stimuli affect caregiver performance in a simulated emergency department

Description

Research has shown that the ability to smell is the most direct sense an individual can experience. With every breath a person takes, the brain recognizes thousands of molecules and

Research has shown that the ability to smell is the most direct sense an individual can experience. With every breath a person takes, the brain recognizes thousands of molecules and makes connections with our memories to determine their composition. With the amount of research looking into how and why we smell, researchers still have little understanding of how the nose and brain process an aroma, and how emotional and physical behavior is impacted. This research focused on the affects smell has on a caregiver in a simulated Emergency Department setting located in the SimET of Banner Good Samaritan Medical Center in Phoenix, Arizona. The study asked each participant to care for a programmed mannequin, or "patient", while performing simple computer-based tasks, including memory and recall, multi-tasking, and mood-mapping to gauge physical and mental performance. Three different aromatic environments were then introduced through diffusion and indirect inhalation near the participants' task space: 1) a control (no smell), 2) an odor (simulated dirty feet), and 3) an aroma (one of four true essential oils plus a current odor-eliminating compound used in many U.S. Emergency Departments). This study was meant to produce a stressful environment by leading the caregiver to stay in constant movement throughout the study through timed tasks, uncooperative equipment, and a needy "patient". The goal of this research was to determine if smells, and of what form of pleasantness and repulsiveness, can have an effect on the physical and mental performance of emergency caregivers. Findings from this study indicated that the "odor eliminating" method currently used in typical Emergency Departments, coffee grounds, is more problematic than helpful, and the introduction of true essential oils may not only reduce stress, but increase efficiency and, in turn, job satisfaction.

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Agent

Created

Date Created
  • 2013

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Calcium-mediated excitation and plasticity in primary olfactory pathways of the honey bee antennal lobe

Description

Spatiotemporal processing in the mammalian olfactory bulb (OB), and its analog, the invertebrate antennal lobe (AL), is subject to plasticity driven by biogenic amines. I study plasticity using honey bees,

Spatiotemporal processing in the mammalian olfactory bulb (OB), and its analog, the invertebrate antennal lobe (AL), is subject to plasticity driven by biogenic amines. I study plasticity using honey bees, which have been extensively studied with respect to nonassociative and associative based olfactory learning and memory. Octopamine (OA) release in the AL is the functional analog to epinephrine in the OB. Blockade of OA receptors in the AL blocks plasticity induced changes in behavior. I have now begun to test specific hypotheses related to how this biogenic amine might be involved in plasticity in neural circuits within the AL. OA acts via different receptor subtypes, AmOA1, which gates calcium release from intracellular stores, and AmOA-beta, which results in an increase of cAMP. Calcium also enters AL interneurons via nicotinic acetylcholine receptors, which are driven by acetylcholine release from sensory neuron terminals, as well as through voltage-gated calcium channels. I employ 2-photon excitation (2PE) microscopy using fluorescent calcium indicators to investigate potential sources of plasticity as revealed by calcium fluctuations in AL projection neuron (PN) dendrites in vivo. PNs are analogous to mitral cells in the OB and have dendritic processes that show calcium increases in response to odor stimulation. These calcium signals frequently change after association of odor with appetitive reinforcement. However, it is unclear whether the reported plasticity in calcium signals are due to changes intrinsic to the PNs or to changes in other neural components of the network. My studies were aimed toward understanding the role of OA for establishing associative plasticity in the AL network. Accordingly, I developed a treatment that isolates intact, functioning PNs in vivo. A second study revealed that cAMP is a likely component of plasticity in the AL, thus implicating the AmOA-beta; receptors. Finally, I developed a method for loading calcium indicators into neural components of the AL that have yet to be studied in detail. These manipulations are now revealing the molecular mechanisms contributing to associative plasticity in the AL. These studies will allow for a greater understanding of plasticity in several neural components of the honey bee AL and mammalian OB.

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Created

Date Created
  • 2014