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Anatomical evidence for a mechanism of lateral inhibition in the rat thalamus
Author(s) -
Pinault Didier,
Deschênes Martin
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00362.x
Subject(s) - biocytin , neuroscience , thalamic reticular nucleus , thalamus , axon , gabaergic , biology , glutamatergic , reticular connective tissue , bursting , neuron , anatomy , electrophysiology , glutamate receptor , inhibitory postsynaptic potential , biochemistry , receptor
The aim of this study was to determine whether or not thalamic reticular nucleus (Rt) neurons form synaptic connections with the thalamocortical (TC) neurons from which they receive synaptic contacts. Therefore, we examined, in adult rats, the relationships between single TC and Rt neurons, which had been marked simultaneously with an anterograde/retrograde tracer (biocytin or Neurobiotin), using the extracellular or juxtacellular technique. (i) From 30 successful extracellular microapplications of marker into the Rt, 22 gave retrogradely marked TC somatodendritic arbors at the fringe of or clear outside the anterogradely darkly stained Rt axon terminal fields. Following biocytin application into the thalamus, few cells were retrogradely stained in the Rt at the periphery of the anterogradely labelled axon terminal field. (ii) The juxtacellular filling of a single Rt cell was accompanied by the back‐filling of a single TC neuron ( n = 4 pairs), which presumably formed synaptic contacts with the former cell. The somatodendritic complex of the back‐filled TC neuron was located outside the Rt cell's axonal arbor. These anatomical data provide clear evidence that Rt and thalamic neurons predominantly form between themselves open rather than closed loop connections. Because TC neurons make glutamatergic synapses onto Rt cells, which are GABAergic, and are the first elements synaptically activated by prethalamic afferents into the TC‐Rt network, the present results strongly support the hypothesis that Rt neurons principally generate a mechanism of lateral inhibition in the thalamus.