Neural representations of odors get associated with other stimuli through experience. Are action potentials the neural representation that directly gets associated with reinforcement during conditioning? In Manduca , I found that odor presentations elicited only one or two spikes at odor onset (and sometimes offset) in each of a small portion of Kenyon cells, a population of neurons known to be crucial for olfactory associative learning. By using a series of odor-taste associative conditioning paradigms with various sucrose presentation timings, I carefully controlled the temporal overlap between Kenyon cell spiking and sucrose reinforcement timing. I found that in paradigms that led to learning, spiking in Kenyon cells ended well before the reinforcement was given. Further, increasing the temporal overlap between Kenyon cell spiking and sucrose reinforcement actually reduced learning efficacy. Therefore, spikes in Kenyon cells are not the neural representation that gets directly reinforced, and Hebbian spike timing--dependent plasticity in Kenyon cells alone cannot underlie this learning. / Two important focuses in neuroscience are to study how animals process sensory stimuli, and how such stimuli get associated with other sensory modalities through experience. Often, sensory stimuli elicit the oscillatory synchronization of neurons in different parts of the brain, and thus may constitute an important stage in sensory processing. Odor-evoked oscillatory synchronization has been observed in a wide variety of animals, including mammals and insects. Despite differences in details of anatomical structure, animals from widely different phyla appear to use similar strategies to encode odors. Here, using the moth Manduca sexta, I examined the factors that cause odor-evoked oscillatory synchronization of olfactory neurons and that determine the frequency of these oscillations. I found that frequency of oscillations decreased from ∼40 Hz to ∼20 Hz during the course of a lengthy odor pulse. This decrease in oscillatory frequency appeared in parallel with a decrease in net olfactory receptor output, suggesting that the intensity of olfactory receptor neuron input to the antennal lobe, the first olfactory relay center, may determine oscillatory frequency. However, I found that changing odor concentration had little effect on oscillatory frequency. Combining the results of recordings made in vivo and computational models, I found that increasing odor concentration recruited additional, but less well-tuned olfactory receptor neurons to respond to the odor. Firing rates of these neurons were tightly constrained by adaptation and saturation. My work established that, in the periphery, odor concentration is mainly encoded by the size of the olfactory receptor neuron population that responded to the odor, whereas oscillatory frequency is determined by the adaptation and saturation of this response. / Ong, Chik Ying Rose. / Advisers: Siu Kai Kong; Mark Stopfer. / Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 132-147). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

The initial step in odor recognition by the nose is the binding of odorant molecules to receptor sites embedded in the dendritic membranes of olfactory receptor cells. Despite considerable interest and experimentation into the nature of these receptor sites, little is known of their specificity to different types of odorant molecules. This lack of knowledge partially stems from the fact that the nature of receptor proteins is most effectively studied when specific and irreversible inhibitors are available for use as chemical probes, yet no such agents have been discovered for use in the olfactory system. A series of alkylating agents and other chemically active odorants were tested to determine whether they might react with specific odorant receptors and modify olfactory responses. Electroolfactogram (EOG) recordings were obtained before, during, and after treatment of the olfactory mucosae of grass frogs (Rana pipiens) with a chemically active odorant.

The behavioural and electrophysiological consequences of two newly developed aniracetam analogues were investigated in male Long-Evans rats. Results indicate that an intraperitoneal (i.p.) injection of LD38.2 significantly improved retention in a two odour olfactory discrimination task. However, three different dosages of LN1 did not facilitate memory in the task. In rats with chronically implanted electrodes, both compounds rapidly crossed the blood brain barrier (BBB) after an i.p. injection and influenced several parameters of the field excitatory postsynaptic potential (EPSP) in the CA1 and dentate gyrus regions of the hippocampus. The enhancement of the field EPSP following LD38.2 administration may be related to the drug's ability to facilitate memory in the olfactory discrimination task. Compounds, like LD38.2, that enhance both hippocampal transmission and performance in learning/memory tasks in laboratory rodents may have implications for the treatment of clinical memory disorders.

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