GABAergic Neurons in Mammalian Thalamus: A Marker of Thalamic Complexity?

Metabotropic Glutamate Receptors Differentially Regulate GABAergic Inhibition in Thalamus

“…This decreased sIPSC activity could result from reduced output of F1 (axon terminals) and/or F2 (presynaptic dendrites) terminals, independent of action potential discharge of either interneurons or TRN neurons. To address this issue, we obtained recording from relay neurons in the VB thalamic nucleus, a structure containing very few interneurons and thus consists of virtually only F1 terminal innervation from TRN neurons (Ottersen and Storm-Mathisen, 1984;Arcelli et al, 1997). In VB neurons, mGluR 2,3 agonists produced a robust suppression of sIPSC activity similar to dLGN relay neurons.…”

“…Unfortunately, we cannot distinguish between F1 or F2 type terminals, because both terminal types are present in the rodent dLGN, so we next tested the actions of APDC in a thalamic nucleus that contain very few interneurons. The VB thalamic nucleus contains very few GABAergic interneurons, so this nucleus receives almost exclusive F1 terminal innervation that arises from TRN neurons (Ottersen and StormMathisen, 1984;Arcelli et al, 1997). In the presence of TTX (1 M), APDC (50 M) significantly suppressed sIPSC activity by 61 Ϯ 20% in VB relay neurons (Fig.…”

Visual thalamocortical circuits in parvalbumin-deficient mice

“…Although clear morphological differences were reported among relay cells, TC cells are not PV-ir and an analysis of their electrophysiological properties did not reveal any additional distinguishing characteristics (Krahe et al, 2011). The remaining neurons of mouse dLGN are PV-ir GABAergic interneurons, whose density may be as low as 10-20% (Arcelli et al, 1997;Jaubert-Miazza et al, 2005) as recently confirmed by the analysis of the ultrastructure of synaptic profiles (Bickford et al, 2010). Excitatory projections from dLGN to the visual cortex send collaterals to the visual sector of the reticular thalamic nucleus (RTN) (Rafols and Valverde, 1973;Baldauf, 2010).…”

Dendritic HCN2 Channels Constrain Glutamate-Driven Excitability in Reticular Thalamic Neurons

“…The increased excitability attributable to HCN channel blockade in GABAergic RTN neurons should presumably increase the fre- quency of sIPSCs in VB neurons because the RTN is the sole source of GABA release in the rodent VB (Arcelli et al, 1997); thus, we examined effects of ZD7288 on the frequency of large-amplitude (Ͼ100 pA) sIPSCs in VB neurons. ZD7288 (1 M) nominally increased sIPSC frequency (traces not shown) and, at 5 M, markedly increased the occurrence of large sIPSCs (Fig.…”

“…5). Because the RTN is the sole source of GABAergic input to the VB in rodents (Arcelli et al, 1997), an increase in large sIPSC frequency indicates that there is an increase in spike firing in the RTN. Consistent with those observations, intracellular perfusion of ZD7288 increased intrinsic excitability in HCN2 ϩ/ϩ, but not Ϫ/Ϫ, neurons (Fig.…”