Basic HTML Version
#P76
POSTER SESSION II:
TRIGEMINAL SYSTEM; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Noradrenergic Modulation of Rhythmic Activity and
Sensory Processing in the Main Olfactory Bulb
Qiang Nai
1
, Hongwei Dong
1
, Christiane Linster
2
, Matthew Ennis
1
1
University of Tennessee Memphis, TN, USA,
2
Cornell University,
Ithaca, NY, USA
Norepinephrine (NE) modulates rhythmic oscillations and sensory
processing in cortical circuits. Here, we investigated NE effects on
the spontaneous and olfactory nerve (ON) evoked activity of
external tufted (ET) and mitral/tufted (M/T) cells in rat and mouse
olfactory bulb slices. Bath application or focal glomeruli puffs of
NE, NE uptake inhibitors or the β receptor agonist isoproterenol
increased the frequency and regularity of rhythmic oscillations
and spiking. These effects persisted in APV-CNQX-gabazine or
calcium channel blockers, but were abolished by TTX. These and
other results indicate that activation of β receptors in the glomeruli
directly increases ET cell excitability and rhythmic bursting and in
turn enhances rhythmic oscillatory activity in M/T cells.
Recordings in normal media showed that low NE concentrations
(<1 µM) enhanced the ON-evoked response magnitude, while
higher concentrations (>3 µM) reversed the facilitation. This
concentration-dependent modulation matches the bidirectional
modulation of granule cell excitability and GABAergic inhibition
of M/T cells (Nai et al., 2009, 2010). Thus, in addition to direct
excitation of ET and M/T cells (Hayar et al., 2000), NE also
modulates ON responses by dynamic regulation of GABAergic
inhibition. NE also increased the temporal precision of ON
responses, reducing onset latency and variability of evoked spikes
at all concentrations tested. NE levels vary with behavioral state
and context. Our findings indicate that varying NE levels enhance
rhythmic oscillations and the temporal precision of ON responses
in a manner that would improve fidelity to the respiratory cycle.
The concentration-dependent modulation of ON response
magnitude by NE may allow for dynamic regulation of odor
response strength as a function of behavioral state.
Acknowledgements: Supported by: DC008702, DC003195.
#P77
POSTER SESSION II:
TRIGEMINAL SYSTEM; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Locus Coeruleus Activation Modulates Stimulus-Driven
and Spontaneous Firing of MOB Granule Cells on Short
and Long Timescales
Heike S. Demmer, Stephen D. Shea
Cold Spring Harbor Laboratory Cold Spring Harbor, NY, USA
Social events such as mate and offspring encounters, imprinting to
maternal odors, and individual recognition increase noradrenaline
(NA) levels in the olfactory bulbs (OB) via input from the
brainstem nucleus locus coeruleus (LC). This surge in NA is
obligatory for certain olfactory memories. In anesthetized male
mice, LC stimulation paired with odor results in a long-lasting,
stimulus-specific habituation of firing in the mitral cells (MC) of
the MOB. This suppression may be achieved by either a feed
forward or a feedback mechanism. For example, inhibition by
periglomerular cells regulates sensory neuron input to MCs. If NA
increases inhibition in the glomerular layer, then the odor
habituation of MCs may result from a presynaptic removal of drive.
Alternatively, GABAergic granule cells (GC) form reciprocal
dendro-dendritic feedback connections with MCs. Thus, NA-
triggered increases in the synaptic output of GCs could actively
suppress MC responses. LC fibers terminate densely at the GCs and
their connections with MCs and sparsely at the glomerular layer,
favoring the latter mechanism. We therefore recorded spike activity
of GCs in vivo in anaesthetized mice using the loose-patch
technique in combination with juxtacellular staining, and we paired
odor- or light-evoked sensory stimulation with LC activation. As
expected, NA-release resulted in short-term suppression of GC
activity. Surprisingly, we found that odor responses in GCs are also
suppressed long-term when paired with LC stimulation. This is
consistent with either a feedforward mechanism of NA plasticity, or
alternatively a model in which the dendro-dendritic synapses
inhibit MCs in a spike independent manner. To resolve this, we are
recording MCs intracellularly in vivo. Acknowledgements: Funded
by an award to SDS from the Klingenstein Foundation.
#P78
POSTER SESSION II:
TRIGEMINAL SYSTEM; TASTE CNS;
NEUROIMAGING; OLFACTION CNS
Anesthesia impacts the spontaneous and odor-induced
oscillatory activities in the mouse olfactory bulb
Claire Martin, Hirac Gurden, Romain Chery
Imagerie et Modélisation en Neurobiologie et Cancérologie
(IMNC), UMR 8165, Universités Paris 7 et 11 Orsay,
F-91405, France
The olfactory bulb (OB) is the first relay of olfactory information
processing in the brain. In this structure, large oscillations are
recorded in the local field potential (LFP) during spontaneous
activity or following odor stimulation. These oscillations have been
shown to rely on a specific feature of the OB network, the
reciprocal dendro-dendritic synapses between excitatory mitral
cells and inhibitory granule cells. While anesthetized animal
recordings have been extensively used to decipher odor
representation at the level of the OB, little is known about the
influence of the anesthetic drugs used to maintain sedation on
temporal dynamics. Anesthesia can be induced by injection of a
cocktail of ketamine combined with one of the two available
agonists at the α2 class of adrenergic receptors, xylazine (low α2
affinity) or medetomidine (high α2 affinity). In this context, the
objective of this work is to compare oscillatory activities of the
LFP in these two different conditions of anesthesia and in the
awake state in the same mouse. We use chronically implanted
electrodes (100µ diameter) in the OB to record the spontaneous and
odor-induced activities: (i) under ketamine/xylazine (ii) under
ketamine/medetomidine (iii) in freely moving animal. Data show
that for the three conditions, odor stimulation elicited a decrease in
number of detected oscillations in the gamma frequency band
together with an increase in the beta band (15-45Hz). We observed
that under anesthesia, the frequency of oscillations was lower in the
beta band and higher in the gamma band compared to awake.
Xylazine tended to increase frequency and power of the
spontaneous but not the odor induced activity. This modulation was
abolished when a constant air flow was delivered to the mice.
To separate the specific effect of the α2 agonists from the
perturbation induced by ketamine, we injected intraperitoneally
xylazine, medetomidine and NaCl successively in the same awake
freely moving mice. We found that α2 agonists decreased
oscillations power in the gamma band, and that xylazine increased
frequency compared to medetomidine. In conclusion, xylazine and
medetomidine differentially impact the temporal dynamics of the
olfactory bulb. Acknowledgements: Agence Nationale de la
Recherche ANR-09-JCJC-0117-01
Abstracts | 53
Abstracts are printed as submitted by the author(s)
P O S T E R P R E S E N T AT I O N S