Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
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#51 SYMPOSIUM:<br />
EXPERIENCE DRIVEN PLASTICITY<br />
OF THE OLFACTORY SYSTEM<br />
#53 SYMPOSIUM:<br />
EXPERIENCE DRIVEN PLASTICITY<br />
OF THE OLFACTORY SYSTEM<br />
Understanding Plasticity in the Olfactory Intrabulbar Map<br />
Leonardo Belluscio<br />
National Institutes of Health / NINDS Bethesda, MD, USA<br />
In the mammalian olfactory system sensory neurons project<br />
their axons to the surface in the olfactory bulb generating a<br />
pair of glomerular maps that reflect odorant receptor identity.<br />
These maps are further connected through a set of reciprocal<br />
intrabulbar projections that are mediated by tufted cells that<br />
specifically link iso-functional odor columns to produce a second<br />
order map called the intrabulbar map. We have shown that<br />
intrabulbar projections are established postnatally and undergo<br />
continuously refinement through an activity dependent process<br />
that has no critical period. Here we present that both loss of<br />
olfactory sensory input and broad odorant stimulation are<br />
capable of disrupting the intrabulbar map specificity, while<br />
re-introduction of normal activity restores the map to proper<br />
order. We also reveal that the regenerating interneurons<br />
are central to intrabulbar circuit plasticity and that proper<br />
connectivity depends specifically upon new neurons from<br />
the rostral migratory stream. Together these data illustrate<br />
that olfactory bulb plasticity is a balance between activity,<br />
regeneration and remodeling. Acknowledgements: National<br />
Institute of Neurological Disorders and Stroke, Intramural<br />
Research Program.<br />
#52 SYMPOSIUM:<br />
EXPERIENCE DRIVEN PLASTICITY<br />
OF THE OLFACTORY SYSTEM<br />
Long-term imaging of odor representations in awake mice<br />
Takaki Komiyama<br />
University of Cali<strong>for</strong>nia, San Diego, CNCB, La Jolla CA 92093 USA<br />
How are sensory representations in the brain influenced by the<br />
state of an animal? Here we use chronic two-photon calcium<br />
imaging to explore how wakefulness and experience shape odor<br />
representations in the mouse olfactory bulb. Comparing the<br />
awake and anesthetized state, we show that wakefulness greatly<br />
enhances the activity of inhibitory granule cells and makes<br />
principal mitral cell odor responses more sparse and temporally<br />
dynamic. In awake mice, brief repeated odor experience leads<br />
to a gradual and long-lasting (months) weakening of mitral cell<br />
odor representations. This mitral cell plasticity is odor specific,<br />
recovers gradually over months, and can be repeated with<br />
different odors. Furthermore, the expression of this experiencedependent<br />
plasticity is prevented by anesthesia. Together, our<br />
results demonstrate the dynamic nature of mitral cell odor<br />
representations in awake animals, which is constantly shaped by<br />
recent odor experience.<br />
Olfactory Experience Shapes Insect Olfactory Centres<br />
Jean-Marc Devaud<br />
Research Center on Animal Cognition, Université Paul Sabatier<br />
Toulouse, France<br />
Insects provide excellent models to study how neural<br />
networks dedicated to olfactory processing are <strong>for</strong>med during<br />
development, and how they work in the adult. However, their<br />
organisation is not fixed once development is achieved.<br />
On the contrary, as in vertebrates, the connectivity and functional<br />
organisation of insect olfactory systems are not fixed: they<br />
exhibit clear plastic properties, as shown in various species over<br />
the recent years. In our work, we have been focusing on the<br />
plastic changes affecting the anatomy of the olfactory centres as<br />
a consequence of olfactory experience, be it the mere exposure<br />
to environmental odorants or associative learning and memory.<br />
In particular, we have been looking <strong>for</strong> structural rearrangements<br />
in two main olfactory centres known <strong>for</strong> their role in olfactory<br />
learning and memory in the insect brain: the antennal lobes and<br />
the mushroom bodies. The modular organization of these two<br />
neuropils allows quantifying the changes affecting their structure<br />
in the brains of animals submitted to different treatments.<br />
By doing so, and by focusing mostly on the honeybee (Apis<br />
mellifera) as a model species, we have been able to show that<br />
the <strong>for</strong>mation of long-term memories of previous olfactory<br />
experience is associated with structural modifications in insect<br />
olfactory networks. Interestingly, such modifications vary with<br />
the nature of the experience undergone by the animal, and<br />
may be considered as supports of olfactory memories. Thus,<br />
they are likely to contribute to the acquisition and retention of<br />
behavioural responses adapted to changing environments.<br />
#53.5 CLINICAL LUNCHEON:<br />
TASTE RECEPTORS IN GUT AND PANCREAS<br />
REGULATE ENDOCRINE FUNCTION<br />
Robert F. Margolskee<br />
Monell Chemical Senses Center, Philadelphia, PA, USA<br />
Many of the receptors and downstream signalling proteins<br />
involved in taste detection and transduction are expressed also<br />
in intestinal and pancreatic endocrine cells where they underlie<br />
certain chemosensory responses. Intestinal endocrine cells<br />
express T1r taste receptors, the taste G-protein gustducin, and<br />
several other taste transduction elements. So too do pancreatic<br />
islet endocrine cells. Knockout mice lacking alpha-gustducin<br />
or the sweet taste receptor subunit T1r3 have deficiencies in<br />
intestinal secretion of glucagon-like peptide-1 (GLP-1) and in<br />
the regulation of plasma levels of insulin and glucose. Glucosedependent<br />
insulin release from mouse pancreatic islets ex vivo<br />
is stimulated by sucralose and other sweeteners. Islets from T1r3<br />
knockout mice release insulin normally in response to glucose,<br />
but show no enhanced release of insulin in response to noncaloric<br />
sweeteners. Thus, there appear to be two mechanisms<br />
ORAL ABSTRACTS<br />
<strong>Abstracts</strong> are printed as submitted by the author(s).<br />
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