Olfactory interference in the honey bee: histamine pharmacology, calcium imaging and modeling

DACHER M; LOCATELLI F; SMITH B

San Diego, EEUU

Congreso; Society for Neuroscience 2007; 2007

American Society for Neuroscience

Title: Olfactory interference in the honey bee: histamine pharmacology, calcium imaging and modeling Location: San Diego Convention Center: Halls B-H Presentation Start/End Time: Tuesday, Nov 06, 2007, 8:00 AM - 9:00 AM Authors: *M. DACHER, F. LOCATELLI, B. H. SMITH; Schl Life Sci., Arizona State Univ., Tempe, AZ The honey bee (Apis mellifera) is a valuable model for studying plasticity of olfactory coding in the Antennal Lobe (AL), which is the analog of the vertebrate Olfactory Bulb. When a drop of sucrose solution touches its antennae or mouthpart (proboscis), a bee reflexively extends its proboscis to consume the sucrose (proboscis extension reflex; PER). After sucrose consumption, the PER will last 50 sec or more, with the probability of PER declining over that time. If an odor is presented before the sucrose reward over several trials, the insect will associate the odor with the sucrose so that subsequent presentation of the same odor will be sufficient to trigger the PER. We have found that reversing the order of the stimuli (sucrose then 15 sec later odor) leads to interruption of ongoing PER by the odor. In this protocol, a sucrose solution is presented to both the antennae and the proboscis. In groups of bees for which an odor was presented 15s after the sucrose, the retraction of the PER was accelerated when compared to another group for which no odor was presented. We refer to this as ‘olfactory interference’. This olfactory interference is consistent with a previous report that presenting sucrose 15s before an odor produces conditioned inhibition to that odor (i.e. subsequent associative learning between this odor and sucrose in slowed). We are now investigating the roles of AL neurotransmitter and neuromodulatory pathways -histamine, GABA-A and GABA-B and octopamine- in olfactory interference. Blocking histaminergic inhibition prevented the interference of the odor with the PER. On the other hand, histamine itself had odor- and concentration-dependent effects. Second, we are currently using calcium imaging to measure in vivo the odor-specific activation pattern within the AL before and after a sucrose presentation. Finally, we designed a realistic mathematical model describing the activation dynamics of AL neurons according to two parameters: connectivity between the various types of neurons and temporal relationship between olfactory and gustatory (i.e. sucrose) input. The versatile architecture of this model allowed test of various hypotheses. In particular, the results of the stimulations were consistent with the experimental observations obtained with behavioral pharmacology and calcium imaging. Disclosures:  M. Dacher , None; F. Locatelli, None; B.H. Smith, None. Support: NIH (NCRR grant RR014166) NIH (NIDCD grant DC007997)