Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
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