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Volume 17, Number 7,
Issue of April 1, 1997
pp. 2348-2354
Copyright ©1997 Society for Neuroscience
Nucleus-Specific Chloride Homeostasis in Rat Thalamus
Received Dec. 17, 1996; revised Jan. 17, 1997; accepted Jan. 22, 1997.
Daniel Ulrich and
John R. Huguenard
Department of Neurology and Neurological Sciences, Stanford
University School of Medicine, Stanford, California 94305
Synchronous thalamic network activity occurring during slow wave
sleep and paroxysmal discharges critically depends on the ability of
thalamocortical relay cells and inhibitory neurons of the nucleus
reticularis thalami (nRt) to fire bursts of action potentials.
Inhibitory synaptic potentials (IPSPs) originating from nRt cells are
crucial in deinactivating T-channels and thus promoting burst firing in
relay cells, but the functional role of intra-nRt IPSPs is less well
understood. A major factor that regulates the net effects of IPSP
generation is the chloride equilibrium potential
(ECl). Here we applied the perforated
patch-clamp technique, using the cation-selective ionophore gramicidin
to assess the reversal potential of chloride in nRt and relay cells in
brain slices. We found that the reversal potential of GABA-induced
membrane currents (EGABA) was
significantly more hyperpolarized in relay ( 81 ± 2.6 mV), as compared with nRt cells (71 ± 2.5 mV).
EGABA was not significantly different from
the reversal potential of evoked IPSCs
(EIPSC; 82 ± 4.4 mV) in relay cells.
In both relay and reticular neurons the chloride gradient was collapsed
partially by the chloride cation cotransport blocker furosemide,
suggesting an active chloride extrusion mechanism in thalamic neurons.
Given the relatively hyperpolarized resting potentials (approximately 70 mV) reported for nRt and relay cells during in
vitro thalamic oscillations, we conclude that under these
conditions GABAA IPSPs lead to significant
hyperpolarization in relay cells. By contrast, intra-nRt inhibition
essentially would be shunting, i.e., would produce minimal membrane
polarization but still could reduce the amplitude of excitatory
events.
Key words:
GABA;
IPSP;
somatosensory;
nRt;
perforated patch;
inhibition;
chloride transport
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