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Abstracts - Association for Chemoreception Sciences

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#P54 POSTER SESSION II:<br />

OLFACTORY PHYSIOLOGY & CELL BIOLOGY;<br />

TASTE MOLECULAR GENETICS;<br />

CHEMESTHESIS & TRIGEMINAL<br />

Mitral Cell Responses to Sensory Input Under Tonic Inhibition<br />

Zuoyi Shao, Adam C. Puche, Michael T. Shipley<br />

Department of Anatomy & Neurobiology, Program in<br />

Neuroscience, University of Maryland School of Medicine<br />

Baltimore, MD, USA<br />

Olfactory signals are initially processed in glomeruli, where<br />

olfactory nerve (ON) axons <strong>for</strong>m excitatory synapses onto<br />

principal output neurons, mitral/tufted (MT) cells. MT cells are<br />

generally thought to be regulated mainly by inhibition at their<br />

lateral dendrites from GABAergic granule cells (GC). Less is<br />

known about inhibition occurring at their glomerular tuft by<br />

GABAergic periglomerular (PG) cells. We recently reported that<br />

the intrinsic bursting of ET cells results in strong spontaneous<br />

activation of most GABAergic PG cells to produce tonic<br />

presynaptic inhibition of ON terminals (Shao et al 2009). Since<br />

MT cells receive IPSCs from PG cells in response to ON input,<br />

we hypothesized that MT cells may also receive tonic postsynaptic<br />

inhibition. To test this hypothesis we measured spontaneous IPSC<br />

frequency in MT cells be<strong>for</strong>e and after restricted intraglomerular<br />

puff of gabazine (GBZ). GBZ significantly reduced the rate of<br />

sIPSCs and dramatically increased spontaneous spiking in MT<br />

cells. This indicates that tonic inhibition is of glomerular origin<br />

and potently regulates MT cell firing. To determine if tonic<br />

intraglomerular postsynaptic inhibition is due to ET cell drive of<br />

PG cells, we puffed L/T type calcium channel blockers into the<br />

glomerulus to block spontaneous ET cell bursting (Liu and<br />

Shipley 2008). As predicted, this significantly reduced<br />

spontaneous IPSCs in MT cells. These results, taken with our<br />

previous findings show that MT cell responses to ON sensory<br />

input are strongly regulated by tonic pre- and postsynaptic<br />

inhibition mediated by the ET-PG-MT cell circuit. Tonic<br />

intraglomerular pre- and postsynaptic inhibition may operate to<br />

set the gain and offset of the glomerular input-output function.<br />

Acknowledgements: Supported by NIDCD DC005676<br />

#P55 POSTER SESSION II:<br />

OLFACTORY PHYSIOLOGY & CELL BIOLOGY;<br />

TASTE MOLECULAR GENETICS;<br />

CHEMESTHESIS & TRIGEMINAL<br />

Ethanol Reduces Olfactory Bulb Output by Reducing<br />

Excitatory Drive to Mitral/Tufted Cells<br />

Feras Jeradeh-Boursoulian, Abdallah Hayar<br />

Univ. of Arkansas <strong>for</strong> Medical <strong>Sciences</strong> Little Rock, AR, USA<br />

In alcoholics, the smell of ethanol may be an important<br />

determinant of its acceptance because the drug’s rein<strong>for</strong>cing<br />

properties could be associated with its chemosensory attributes.<br />

Moreover, it is possible that chronic alcohol abuse could make<br />

ethanol smell and taste better. While the effects of ethanol have<br />

been extensively investigated in many brain circuits, its effects on<br />

neuronal processing within the olfactory bulb are still unknown.<br />

In this study, we have used extracellular and whole-cell patchclamp<br />

recordings in olfactory bulb slices to determine the acute<br />

effects of ethanol on output neurons of the olfactory bulb. Mitral<br />

and tufted cells appeared to be more responsive to ethanol<br />

application (50-100 mM) than external tufted cells. The most<br />

prominent effect of ethanol was a decrease in the amplitude and<br />

frequency of spontaneous EPSCs. Moreover, olfactory nerveevoked<br />

EPSCs exhibited a decrease in amplitude and electric<br />

charge. These effects of ethanol persisted in the presence of the<br />

GABA-A receptor blocker, gabazine, but were attenuated in the<br />

presence of the NMDA receptor blocker, APV. Extracellular<br />

recordings revealed that ethanol decreased the firing frequency<br />

and the number of spikes per burst in most mitral and tufted cells.<br />

In the olfactory bulb, NMDA receptors have been implicated in<br />

synaptic plasticity, dendro-dendritic inhibition, self-excitation,<br />

and glutamate spillover. The attenuation of NMDA receptor<br />

activity by ethanol is there<strong>for</strong>e expected to reduce neuronal<br />

interactions and as a consequence attenuate olfactory bulb<br />

synchronous output activity in response to odor stimulation.<br />

This study provides insight into the mechanisms by which ethanol<br />

exposure could modulate olfactory bulb neuronal interactions,<br />

which may lead to an alteration in the sensory perception of<br />

ethanol odor. Acknowledgements: PHS grants: DC007123,<br />

DC007876, RR020146.<br />

#P56 POSTER SESSION II:<br />

OLFACTORY PHYSIOLOGY & CELL BIOLOGY;<br />

TASTE MOLECULAR GENETICS;<br />

CHEMESTHESIS & TRIGEMINAL<br />

Lateral interactions in the in vivo olfactory bulb network of<br />

the rat show heterogeneous distance dependences and vary<br />

strongly with respect to respiratory phase<br />

Matthew E Phillips 1,2 , Gordon M Shepherd 1 , David C Willhite 1<br />

1<br />

Yale University School of Medicine, Department of Neurobiology<br />

New Haven, CT, USA, 2 Yale University, Department of Physics<br />

New Haven, CT, USA<br />

The lateral connectivity of inhibitory granule cells in the<br />

mammalian olfactory bulb (OB) was previously shown to be<br />

sparse and distributed using viral tracers (Willhite et al. 2006).<br />

However, electrophysiological evidence of this distribution has<br />

not previously been shown in the in vivo network. To investigate<br />

this possible network organization we per<strong>for</strong>med intracellular<br />

recordings of Mitral cells (MC) in vivo paired with focal electrical<br />

stimulations of the caudal olfactory nerve layer (ONL). This<br />

preparation allows <strong>for</strong> the activation of distant posterior<br />

(hypothetical “surround”) glomeruli while avoiding presynaptic<br />

stimulation of the recorded cell (hypothetical “center”). Evoked<br />

inhibitory post-synaptic potentials (IPSPs) were recorded in MCs<br />

in response to posterior electrical ONL stimulations at varying<br />

distances from the recording location. IPSP amplitudes showed a<br />

heterogeneous distribution as a function of the distance between<br />

the stimulus and recording locations. This result suggests that the<br />

lateral network of the OB is not organized in a classical centersurround,<br />

distance dependent manner. However, there was a<br />

general tendency <strong>for</strong> more distant ONL stimuli to evoke smaller<br />

amplitude IPSPs than proximal stimuli. But, stimulus location<br />

alone could not predict the evoked IPSP amplitude – <strong>for</strong> example,<br />

the distance dependence nature could vary as a function of the<br />

stimulating current. The evoked IPSP amplitudes depended<br />

strongly on when the ONL stimulation was triggered with<br />

respect to the respiratory phase of the freely breathing animal.<br />

Taken together, these results imply that the OB network is highly<br />

distributed – within which there is a weak center-surround<br />

distance dependence as a function of stimulus strength relative to<br />

the respiratory phase.<br />

P O S T E R S<br />

<strong>Abstracts</strong> are printed as submitted by the author(s)<br />

<strong>Abstracts</strong> | 45

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