Journal of Neuroscience, Vol 15, 7367-7376, Copyright © 1995 by Society for Neuroscience
Neural network of structures in which GABAB receptors regulate absence seizures in the lethargic (lh/lh) mouse model
DA Hosford, FH Lin, DL Kraemer, Z Cao, Y Wang and JT Wilson Jr
Department of Medicine (Neurology), Duke University, Durham, North Carolina, USA.
In previous work we have shown that GABAB receptors are required for
expression of absence seizures in the lethargic (lh/lh) mouse model; that
lh/lh mice have increased numbers of GABAB binding sites compared to
nonepileptic littermates (designated +/+); and that the magnitude of the
increased number of GABAB receptors in lh/lh mice correlated positively
with the frequency of absence seizures. We performed this study to
delineate the neural network in which GABAB receptors regulate absence
seizures in lh/lh mice. We designed three successive screens which had to
be passed by a candidate neuronal population before it could be considered
a member of the neural network in which GABAB receptors regulate absence
seizures. First, the neuronal populations in lh/lh mice had to have
enriched GABAB binding sites compared to homologous populations in matched
nonepileptic controls; baclofen- displaceable 3H-GABA binding was measured
in autoradiograms for this screen. Second, the candidate populations had to
generate spike-wave discharges (SWDs) during absence seizures in lh/lh
mice; bipolar recording electrodes implanted into candidate neuronal
structures were used in this screen. Third, the candidate populations had
to demonstrate GABAB receptor-mediated regulation of absence seizures in
lh/lh mice; microinjections of a GABAB agonist [(-)-baclofen] and
antagonist (CGP 35348) were used for this screen. In this study we found
that anterior ventral lateral thalamic nucleus (VLa), nucleus reticularis
thalami (NRT), nucleus reuniens (RE) passed all three screens, and hence
are members of the neural network in which GABAB receptors regulate absence
seizures in lh/lh mice.
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