Abstracts - Association for Chemoreception Sciences

#P214 POSTER SESSION V:
HUMAN TASTE PSYCHOPHYSICS;
OLFACTION RECEPTORS; TASTE DEVELOPMENT
Potentiation of Primary Afferent Innervation in the
Rostral Nucleus of the Solitary Tract
Robert M. Bradley, James A. Corson
University of Michigan/ Biologic and Materials Sciences Ann Arbor,
MI, USA
The development of mature primary afferent circuitry results
from a Hebbian-like synaptic strengthening in a number of
sensory systems. This synaptic strengthening is accompanied
by a pruning of non-strengthened inputs resulting in a mature
terminal field anatomy. Gustatory afferents innervating the oral
cavity project to the rostral nucleus of the solitary tract (rNTS),
the terminal fields of which prune between postnatal days 15
and 60 into an adult-like organization. However, it is not known
whether any activity dependent changes in synaptic strength
can be induced during this period that may correspond to the
anatomical remodeling. To investigate the activity-modulated
plasticity of primary afferent inputs to the rNTS, acute
horizontal rNTS slices were prepared from rats of postnatal ages
covering the period of anatomical plasticity. The solitary tract
was stimulated with a concentric bipolar electrode and excitatory
postsynaptic currents (ePSC) were recorded. The ability of
a synapse to be potentiated was investigated by stimulating
the solitary tract at 50 Hz paired with a 5 ms depolarization.
Following this tetanic stimulation increases in ePSC amplitude
and rise slope were observed in each age examined, though only
in a subset of neurons at each age. Interestingly, the probability
of inducing potentiation appears to decrease between postnatal
days 20-25 and subsequently increases from postnatal day 30
onward. Primary afferent potentiation lasted over variable
time scales ranging from 1 to 30 minutes, indicative of either
short-term or long-term potentiation. These results suggest that
subpopulations of primary afferent synapses can be potentiated
throughout development, and the presynaptic nerve and/
or postsynaptic target specificity for this potentiation will the
focus of future studies. Acknowledgements: T32DC000011,
RO1DC000288
#P215 POSTER SESSION V:
HUMAN TASTE PSYCHOPHYSICS;
OLFACTION RECEPTORS; TASTE DEVELOPMENT
Ephrin-B/EphB signaling influences the innervation of
fungiform papillae
David Collins 1 , Natalia Hoshino 1 , Elizabeth M Runge 1 , Son Ton 1 ,
Omar Diaz 1 , Jessica Decker 1 , Mark Henkemeyer 2 , M William Rochlin 1
1
Loyola U Chicago/Biology Chicago, IL, USA, 2 UT Southwestern/
Developmental Biology Medical Center/ Dallas, TX, USA
Geniculate ganglion axons innervate fungiform taste buds
whereas the trigeminal ganglion neurites innervate the adjacent
non-taste epithelium. Owing to the proximity of their terminal
fields, non-diffusible repellents are likely to have a role in
preventing incorrect targeting. Eph receptors and ephrins are
cell-attached receptor/ligands capable of triggering contactdependent
repulsion or stabilization. An antibody that detects
EphB1, B2, and B3 stains both geniculate and trigeminal axons
throughout embryonic development. Anti-ephrin-B1 and antiephrin-B2
labeled the dorsal lingual epithelium uniformly at
E17, when axons first penetrate the papilla epithelium in rat.
In ephrin-B2 lacZ mice, label was also observed throughout the
dorsal epithelium but only from E16.5, well after initial invasion
of axons into the epithelium (E14.5). However, in ephrin-B1
lacZ mice, only fungiform papilla epithelium was labeled, and
this labeling was observed at E14.5. Mice lacking EphB1 and
EphB2 exhibited normal levels of gustatory innervation at
E13.5, but less innervation than controls by E17.5, suggesting
that ephrin-B/EphB forward signaling may have a stabilizing
influence on gustatory afferents in vivo. In vitro, substratum
stripes prepared from high concentrations of ephrin-B2-Fc (40
ug/ml) repel neurites from both the geniculate and trigeminal
ganglia, and this did not depend on which neurotrophin
was used to promote growth. Stripes prepared from lower
concentrations of ephrin-B2-Fc (4 ug/ml) were not repellent;
indeed, coverglasses coated uniformly with 4 ug/ml ephrin-B2
mildly promoted trigeminal neurite outgrowth length, depending
on the stage and neurotrophin. We are currently analyzing
the effects of ephrin-B1 on geniculate and trigeminal neurites.
Acknowledgements: 1R15DC010910-01
#P216 POSTER SESSION V:
HUMAN TASTE PSYCHOPHYSICS;
OLFACTION RECEPTORS; TASTE DEVELOPMENT
Glial Contributions to the Formation of the Solitary Tract and
the Rostral Nucleus of the Solitary Tract
Sara L Corson, Robert M Bradley, Charlotte M Mistretta
University of Michigan School of Dentistry Department of Biologic and
Materials Sciences Ann Arbor, MI, USA
The solitary tract (ST) consists of afferent fibers that originate in
the oral cavity and project to the rostral nucleus of the solitary
tract (rNST), the site of the first synaptic relay in transmitting
taste-related information to higher brain areas. We are interested
in the regulatory elements that direct ST formation and rNST
development. Glia represent approximately half of the cells
in the CNS and play roles in neuron guidance and synapse
development and function. However, the time course of glial
development and the role of glia in the gustatory brainstem are
unknown. We surveyed the expression of glial and neuronal
markers in the pre- and post-natal developing rat ST and rNST
to characterize their contribution to the development of the
gustatory brainstem. We examined the expression of neuronal
markers, including calbindin and NeuN, and glial markers,
including glial fibrillary acidic protein (GFAP), myelin basic
protein (MBP) and brain lipid binding protein (BLBP), in
conjunction with P2X2, a marker of gustatory nerve terminal
fields, in the developing ST and rNST. We found persistent but
dynamic expression of calbindin, GFAP and BLBP throughout
pre- and post-natal development. In particular, GFAP expression
shifts from more fibrillary to more astrocyte-like labeling in the
POSTER PRESENTATIONS
Abstracts are printed as submitted by the author(s).
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