F. Grenier et al., LEADING ROLE OF THALAMIC OVER CORTICAL-NEURONS DURING POSTINHIBITORY REBOUND EXCITATION, Proceedings of the National Academy of Sciences of the United Statesof America, 95(23), 1998, pp. 13929-13934
The postinhibitory rebound excitation is an intrinsic property of thal
amic and cortical neurons that is implicated in a variety of normal an
d abnormal operations of neuronal networks, such as slow or fast brain
rhythms during different states of vigilance as well as seizures. We
used dual simultaneous intracellular recordings of thalamocortical neu
rons from the ventrolateral nucleus and neurons from the motor cortex,
together with thalamic and cortical field potentials, to investigate
the temporal relations between thalamic and cortical events during the
rebound excitation that follows prolonged periods of stimulus-induced
inhibition. Invariably, the rebound spike-bursts in thalamocortical c
ells occurred before the rebound depolarization in cortical neurons an
d preceded the peak of the depth-negative, rebound field potential in
cortical areas. Also, the inhibitory-rebound sequences were more prono
unced and prolonged in cortical neurons when elicited by thalamic stim
uli, compared with cortical stimuli. The role of thalamocortical loops
in the rebound excitation of cortical neurons was shown further by th
e absence of rebound activity in isolated cortical slabs. However, whe
reas thalamocortical neurons remained hyperpolarized after rebound exc
itation, because of the prolonged spike-bursts in inhibitory thalamic
reticular neurons, the rebound depolarization in cortical neurons was
prolonged, suggesting the role of intracortical excitatory circuits in
this sustained activity. The role of intrathalamic events in triggeri
ng rebound cortical activity should be taken into consideration when a
nalyzing information processes at the cortical level; at each step, co
rticothalamic volleys can set into action thalamic inhibitory neurons,
leading to rebound spike-bursts that are transferred back to the cort
ex, thus modifying cortical activities.