Article Figures & Data
Figures
- Figure 1.
Intrageniculate axonal collaterals arising from lateral geniculate nucleus relay neurons. Ai, A digital image of a biocytin-filled lateral geniculate nucleus relay neuron with associated axon (arrow). Aii, Higher magnification of outlined area in Ai shows that the main axon gives rise to axon collateral (arrowhead). B, Different relay neuron with main axon that gives rise to axon collaterals in lateral geniculate nucleus. Bi, Low-power photomicrograph of relay neuron and its main axon (arrow). Bii, Increased magnification of main axon with two identified axon collaterals (outlined areas). Biii,Biv, Details of the two collaterals (arrowheads) outlined in Bii.
- Figure 2.
Intralaminar interneurons from lateral geniculate nucleus. A, B, Left panels show location of two interneurons studied in the geniculate lamina. The dendritic trees of the cells were always perpendicular to the long axis of lamina A1 (Lam. A1). A, B, Right panels show higher magnification of interneurons. Note the small soma size and complicated dendritic architecture typical for this class of neurons.
- Figure 3.
ACPD increases synaptic activity in a TTX-dependent manner. A, Digital image of typical lateral geniculate nucleus interneuron. Note the extensive dendritic architecture and thin axon-like dendrites. Right, Intracellular recording from neuron on left indicating membrane response to current injection. Note the depolarizing sag in response to hyperpolarizing current pulses, as well as the lack of burst discharge after offset of the hyperpolarizing current steps. Depolarizing current only evokes tonic action potential discharge. B, The mGluR agonist ACPD (125 μm) produces a robust increase in spontaneous baseline activity. Bottom, Same recording at a faster time base. In control conditions, there is little spontaneous activity (1); however, after ACPD application, there is a robust increase in spontaneous depolarizations (2). Right, After bath application of TTX (1μm), ACPD no longer produces any obvious changes in baseline activity. Note the lack of apparent effect at the faster time base (1 vs 2). C, In a current-clamp recording from a relay neuron, ACPD produces a robust depolarization that evokes action potential discharge (spikes truncated). The repolarization of the membrane potential during spike discharge is because of a manual clamping of the membrane potential to resting level. The time course of action potential discharge is similar to that of the increased activity recorded in interneurons (cf. interneuron recording from B at same time calibration).
- Figure 4.
ACPD increases spontaneous EPSPs in interneurons. A, In a recording from geniculate interneuron, excitatory spontaneous activity was isolated by antagonizing GABA receptors with SR-95531 (20 μm) and CGP35348 (200 μm). Under these conditions, application of ACPD (250 μm) produced a robust increase in spontaneous membrane depolarizations. This increased activity could produce spike discharge (truncated), depending on the resting membrane potential of the neuron. B, After the addition of the non-NMDA glutamate receptor antagonist DNQX (30 μm), ACPD produced no apparent change in baseline activity, indicating that the depolarizations were likely EPSPs. C, After washout of DNQX, the ACPD-mediated increase in spontaneous EPSPs was similar to that observed in A. D, Synaptic activity was then attenuated by TTX (1 μm), and, once again, the ACPD-mediated increase in spontaneous EPSP activity was completely attenuated.
