Organization of reciprocal connections between the perigeniculate nucleus and dorsal lateral geniculate nucleus in the cat: A transneuronal transport study

Cells of the cat's perigeniculate nucleus (PGN), part of the visual sector of the thalamic reticular nucleus (TRN), provide GABAergic inhibition to the A and A1 layers of the dorsal lateral geniculate nucleus (LGNd) and, therefore, may control information flow from the retina to the cortex. Previous electrophysiological experiments suggested that the PGN may be subdivided on the basis of ocular dominance thus reflecting the afferent and efferent projections with lamina A and A1 of the LGNd. The present study utilized the ability of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to be transported transneuronally following intraocular injections in four cats to examine whether there is any anatomical evidence for eye specific layers within the PGN. Sections were processed with tetramethylbenzidine. Light WGA-HRP transneuronal labeling of LGNd collaterals and somata were seen in the PGN and very light labeling (but not somata) was seen in the TRN. Neither the cells of the PGN projecting to the LGNd nor the LGNd relay collaterals within the PGN were clearly organized into nonoverlapping laminae related to the eye specific layers of the LGNd. However, parts of the PGN immediately adjacent to the LGNd appear devoid of connections with lamina A1 thus creating a thin monocular segment for the contralateral eye.

Acetylcholine excites GABAergic neurons of the ferret perigeniculate nucleus through nicotinic receptors

1. The actions of acetylcholine (ACh) on the GABAergic neurons of the perigeniculate nucleus (PGN) were investigated with the use of extra- and intracellular recording techniques in spontaneously spindling ferret thalamic slices maintained in vitro. 2. Local application of ACh to PGN neurons resulted in rapid depolarization followed by a longer lasting hyperpolarization. Neither of these responses were abolished by blockade of synaptic transmission with tetrodotoxin (TTX) nor with low Ca2+ and elevated Mg2+ solution, indicating that they are direct postsynaptic actions of ACh on PGN cells. Functionally, the rapid depolarizing response could activate both single spike activity, as well as low-threshold Ca2+ spike-mediated bursts. 3. The fast depolarizing response to ACh was selectively blocked by application of the nicotinic antagonist hexamethonium, whereas the slow hyperpolarizing response to ACh was selectively blocked by application of the muscarinic antagonist (-)scopolamine. Application of both hexamethonium and (-)scopolamine blocked the modulation of PGN action-potential firing by ACh. 4. Local application of the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) resulted in a depolarizing response and an increase in membrane conductance, whereas application of the muscarinic agonist DL-muscarine chloride resulted in a hyperpolarizing response and an increase in membrane conductance. When applied to spontaneously spindling PGN cells, both DMPP and DL-muscarine blocked the occurrence of spindle oscillations. However, only DMPP was associated with depolarization and the generation of single spike activity. 5. These results indicate that the GABAergic cells of the PGN possess postsynaptic nicotinic as well as muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative immunogold evidence for enrichment of glutamate but not aspartate in synaptic terminals of retino-geniculate, geniculo-cortical, and cortico-geniculate axons in the cat

A postembedding immunogold procedure was used on thin sections of the dorsal lateral geniculate nucleus (LGN) and perigeniculate nucleus (PGN) of the cat to estimate qualitatively and quantitatively, at the electron-microscopic (EM) level, the intensity of glutamate or aspartate immunoreactivities on identifiable synaptic terminals and other profiles of the neuropil. On sections incubated with a glutamate antibody, terminals of retinal and cortical axons in the LGN, and of collaterals of geniculo-cortical axons in the PGN, contain significantly higher density of immunogold particles than GABAergic terminals, glial cells, dendrites, and cytoplasm of geniculate cells. By contrast, in sections incubated with an aspartate antibody, terminals of retino-geniculate, cortico-geniculate, and geniculo-cortical axons did not show a selective enrichment of immunoreactivity, but instead the density of immunogold particles was generally low in the different profiles of the neuropil, with the exception of nucleoli. These results suggest that glutamate, but not aspartate, is a neurotransmitter candidate in the retino-geniculo-cortical pathways.

Brain-stem modulation of the response properties of cells in the cat's perigeniculate nucleus

Transmission through the lateral geniculate nucleus is facilitated following activation of the cholinergic input from the brain stem, which is thought to reflect activity patterns seen during arousal. One of the underlying mechanisms is the suppression of inhibitory circuits local to the lateral geniculate nucleus. However, evidence exists that some visually driven inhibitory inputs to geniculate relay cells may be preserved or even enhanced under conditions of arousal, and during electrical activation of the parabrachial region of the brain stem. We have therefore reexamined the effect of brain-stem activation on the visual responses of one group of local inhibitory inputs to geniculate relay cells, those emanating from the adjacent perigeniculate nucleus. We recorded single perigeniculate cells in anesthetized, paralyzed cats. Axons innervating the lateral geniculate and perigeniculate nuclei from the parabrachial region of the brain stem were electrically activated, and the effect of this activation was assessed on both spontaneous and visually evoked responses. Visual stimulation consisted of sinusoidally modulated sine–wave gratings of varying spatial and temporal frequency. For the great majority of perigeniculate cells (32 of 40), brain-stem activation inhibited spontaneous activity, while one cell was excited, three showed a mixed effect and four were unaffected. Nevertheless, the responses of most cells (30 of 40) were facilitated when brain-stem activation was paired with certain spatio-temporal patterns of visual stimulation. Spatial tuning curves were constructed for 17 cells and temporal tuning curves for 14, before and during parabrachial activation. The responses of any one cell could be facilitated, unchanged, or suppressed, depending on the visual stimulus used. In some cases, this substantially modified the cell’s spatial and temporal tuning properties. We conclude that activation of the brain stem disinhibits geniculate relay cells in the absence of visual stimulation, but it has the potential to enhance either the magnitude or specificity of visually driven inhibition arising from the perigeniculate nucleus.