We used whole-cell patch recording to study 102 local interneurons in the r
at dorsal lateral geniculate nucleus in vitro. Input impedance with this te
chnique (607.0 +/- 222.4 M Omega) was far larger than that measured with sh
arp electrode techniques, suggesting that interneurons may be more electrot
onically compact than previously believed. Consistent and robust burst firi
ng was observed in all interneurons when a slight depolarizing boost was gi
ven from a potential at, or slightly hyperpolarized from, resting membrane
potential. These bursts had some similarities to the low-threshold spike de
scribed previously in other thalamic neuron types. The bursting responses w
ere blocked by Ni+, suggesting that the low-threshold calcium current I-T,
responsible for the low-threshold spike, was also involved in interneuron b
urst firing. Compared to the low-threshold spike of thalamocortical cells,
however, the interneuron bursts were of relatively long duration and low in
traburst frequency. The requirement for a depolarizing boost to elicit the
burst is consistent with previous reports of a depolarizing shift of the I-
T activation curve of interneurons relative to thalamocortical cells, a fin
ding we confirmed using voltage-clamp. Voltage-clamp study also revealed an
additional long-lasting current that could be tentatively identified as th
e calcium activated non-selective cation current, I-CAN, based on reversal
potential and on pharmacological characteristics. Computer simulation of th
e interneuron burst demonstrated that its particular morphology is likely d
ue to the interaction of I-T and I-CAN. In the slice, bursts could also be
elicited by stimulation of the optic tract, suggesting that they may occur
in response to natural stimulation. Synaptically triggered bursts were only
partially blocked by Ni+, but could then be completely blocked by further
addition of (+/-)-2-amino-5-phosphonopentanoic acid. The existence of robus
t bursts in this cell type suggests an additional role for interneurons in
sculpting sensory responses by feedforward inhibition of thalamocortical ce
lls.
The low-threshold spike is a mechanism whereby activity in a neuron is depe
ndent on a prior lack of activity in that same neuron. Understanding of the
low-threshold spike in the other major neuron types of the thalamus has br
ought many new insights into how thalamic oscillations might be involved in
sleep and epilepsy. Our description of this phenomenon in the interneurons
of the thalamus suggests that these network oscillations might be even mor
e complicated than previously believed. (C) 1999 IBPO. Published by Elsevie
r Science Ltd.