Basic HTML Version
Abstracts | 25
Abstracts are printed as submitted by the author(s)
act independently to modify specific parameters of the OB
response. For example, only the phasic component of the VSDi
response was impaired by high frequency sniffing. Similarly, odor-
evoked response latency could be shortened only by increasing
flow rate. These results show that sniffing variations confer an
important degree of adaptability to the olfactory system. This
probably helps, as suggested by others, in improving olfactory
capabilities by allowing the optimization of the deposition of odor
molecules through the olfactory epithelium. We address this
question in one of our current projects.
#50
SYMPOSIUM: THE ROLE OF RESPIRATION IN
OLFACTORY & FLAVOR PROCESSING
Active sampling and gain control in olfaction: how sniffing
does and does not shape odor representations in the early
olfactory pathway
Matt Wachowiak
1, 2
, Tristan Cenier
1, 2
, John McGann
2
,
Yusuke Tsuno
2
1
University of Utah Department of Physiology and Brain Institute
Salt Lake City, UT, USA,
2
Boston University Department of Biology
Boston, MA, USA
Active odor sampling is associated with a repertoire of sniffing
strategies involving changes in multiple parameters of respiration,
including the amplitude and duration of an individual sniff and the
frequency of sniffs in a bout. Our laboratory has investigated how
such variations in sampling shape the responses of olfactory
receptor neurons (ORNs) and olfactory bulb (OB) neurons.
We earlier reported that sniff frequency affects the magnitude,
or gain, of ORN input to the OB and, more modestly, the gain of
mitral/tufted cell output from the OB. Here we focus on the effect
of sniff amplitude - as defined by peak intranasal airflow generated
by inhalation - on ORN inputs. In particular we tested the
longstanding hypothesis that sniff amplitude can shape ORN inputs
in a manner determined by an odorant’s sorption onto the olfactory
epithelium. This hypothesis predicts that ORN responses will be
differentially correlated depending on the sorption properties of the
sampled odorant. If true, animals may differentially modulate sniff
magnitude in order to optimally sample different odorants. We
tested this hypothesis — for the first time in awake rodents — by
imaging from ORNs and monitoring intranasal airflow. We found
that ORN responses were poorly correlated with sniff flowrate and
that this correlation was weak for both high and low-sorption
odorants (mean r²=0.04). We also tested whether rats modulated
sniff flowrate depending on odorant sorption properties during an
odor discrimination task, and found little evidence for such
modulation. These results suggest that sniff strength has
surprisingly little effect on ORN response amplitudes; instead,
sniff frequency may be the most effective bottom-up mechanism
for gain control of olfactory inputs during active sensing.
Acknowledgements: NIDCD
#51
SYMPOSIUM: THE ROLE OF RESPIRATION IN
OLFACTORY & FLAVOR PROCESSING
Respiration drives network activity and modulates synaptic
and circuit processing of lateral inhibition in the olfactory bulb
Matthew E Phillips
1,2
, Robert NS Sachdev
3
, David C Willhite
2
,
Gordon M Shepherd
2
1
Yale University, Department of Physics New Haven, CT, USA,
2
Yale University School of Medicine, Department of Neurobiology
New Haven, CT, USA,
3
Yale University School of Medicine,
Department of Neurobiology, Kavli Institute for Neuroscience
New Haven, CT, USA
Respiration produces rhythmic activity in the entire olfactory
system, driving neurons in the olfactory epithelium, bulb (OB) and
cortex. The rhythmic nature of this activity is believed to be a
critical component of sensory processing. OB projection neurons,
mitral and tufted cells, exhibit both spiking and subthreshold
membrane potential oscillations rhythmically coupled to
respiration. The network and synaptic mechanisms that produce
respiration-coupled activity, and the effects of respiration on lateral
inhibition, a major component of sensory processing in OB circuits,
are not known. Is respiration-coupled activity in mitral and tufted
cells produced by sensory synaptic inputs from nasal airflow alone,
cortico-bulbar feedback, or intrinsic membrane properties of the
projection neurons? Does respiration facilitate or modulate the
activity of inhibitory lateral circuits in the OB? Here, in vivo
intracellular recordings from identified mitral and tufted cells in
anesthetized rats demonstrate that nasal airflow provides excitatory
synaptic inputs to both cell types and drives respiration-coupled
spiking. Lateral inhibition — inhibitory post-synaptic potentials
evoked by intrabulbar microstimulation — was modulated by
respiration. In individual mitral and tufted cells inhibition was
larger at specific respiratory phases, but was not uniformly larger
during a particular respiratory phase in either cell type. Removing
nasal airflow abolished respiration-coupled spiking in both cell
types and nearly eliminated spiking in mitral, but not tufted, cells.
In the absence of nasal airflow, lateral inhibition was weaker in
mitral cells and less modulated in tufted cells. Thus, respiration
drives distinct network activities that functionally modulate sensory
processing in the OB. Acknowledgements: NIH/NIDCD:
DC000086, F31DC009921, and 5T32NS007224
O R A L A B S T R A C T S