Neurons In Lateral Geniculate Nucleus Research Articles

Excitatory actions of synaptically released catecholamines in the rat lateral geniculate nucleus

The gating properties of thalamic relay neurons are influenced by the actions of a variety of neuromodulators in concert with the intrinsic properties of these relay neurons. In this study, we have investigated the consequences of synaptically released catecholamines on the excitability of neurons in the rat dorsal lateral geniculate nucleus. Tetanic stimulation of the optic tract, in which catecholamine fibers also course near or through, produced a strong depolarization that consisted of a fast and slow component. The fast excitatory postsynaptic potential was attenuated by ionotropic glutamate receptor antagonists and further unmasked the slow excitatory postsynaptic potential. The amplitude of the slow excitatory postsynaptic potential was dependent on the frequency and intensity of the tetanic stimulation. The α1-adrenergic receptor antagonist, prazosin, and the D1-like dopamine receptor antagonist, SCH23390, attenuated the slow excitatory postsynaptic potential; however, the slow excitatory postsynaptic potential was unaltered by metabotropic glutamate, cholinergic, α2-adrenergic, and β-adrenergic receptor antagonists. On the other hand, tetanic stimulation of the optic radiations (corticothalamic axons) evoked a slow excitatory postsynaptic potential that was completely attenuated by metabotropic glutamate receptor antagonists. Our results suggest that tetanic stimulation of catecholamine fibers within the optic tract produces synaptic release of norepinephrine and dopamine that in turn activates both α 1-adrenergic and D1-like dopamine receptors leading to a robust membrane depolarization. By altering the excitability of relay neurons, ascending activating systems may modulate the efficacy of information transfer through the thalamus.

Novelty-induced correlation between visual neurons and the hippocampal theta rhythm in sleep and wakefulness

Various rhythms have been shown to affect sensory processing such as the waking–sleep cycle and the hippocampal theta waves. Changes in the firing of visual lateral geniculate nucleus neurons have been reported to be dependent on the animal's behavioral state. The lateral geniculate extracellular neuronal firing and hippocampal field activity were recorded in chronically implanted animals to analyze the relationship during quiet wakefulness and sleep associated with stimulation shifts that may introduce novelty. During wakefulness, a change in light flash stimulation pattern (stimuli frequency shift, stimuli on and off) caused an increment in the theta band power in 100% of the cases and a phase-locking of the spikes in 53% of the recorded neurons. During slow wave sleep, there were no consistent changes in the theta power notwithstanding 13% of the neurons exhibited phase-locking, i.e., novelty may induce changes in the temporal correlation of visual neuronal activity with the hippocampal theta rhythm in sleep. The present results suggest that visual processing in slow wave sleep exists, while auditory information and learning were reported during slow wave sleep in animals and newborn humans. The changes in the theta power as well as in the neuronal phase-locking amount indicate that in slow wave sleep, the ability of the hippocampus to detect/process novelty, although present, may be decreased. This is consistent with the noticeable decrease in awareness of the environment during sleep.

Chronic morphine exposure induces degradation of receptive field properties of LGN cells in cats1

To investigate the effect of chronic morphine exposure on the receptive field properties of lateral geniculate nucleus (LGN) neurons in cats. Cats were injected with morphine (10 mg/kg) or saline twice daily, for 10 d. Subsequently, extracellular single-unit recording techniques were used to examine the sensitivity of LGN neurons to visual stimuli in chronic morphine-treated and saline-treated cats. Compared with saline-treated cats (as controls), LGN neurons in morphine-treated cats had decreased signal-to-noise ratios (1.9 vs 3.1), and orientation and direction sensitivity (0.103 vs 0.135 and 0.074 vs 0.10, respectively), accompanied by significant increases in spontaneous (27.4 vs 17.5) and evoked activity (preferred: 42.2 vs 38.1; average: 28.1 vs 22.3). Chronic morphine exposure can lead to the functional degradation of LGN neurons in cats, which might result from the effects of chronic morphine exposure on inhibitory neurotransmission.

Spatial coding and response redundancy in parallel visual pathways of the marmoset Callithrix jacchus

Many neurons in the primary visual cortex (area V1) show pronounced selectivity for the orientation and spatial frequency of visual stimuli, whereas most neurons in subcortical afferent streams show little selectivity for these stimulus attributes. It has been suggested that this transformation is a functional sign of increased coding efficiency, whereby the redundancy (or overlap in response properties) is reduced at consecutive levels of visual processing. Here we compared experimentally the response redundancy in area V1 with that in the three main dorsal thalamic afferent streams, the parvocellular (PC), koniocellular (KC), and magnocellular (MC) divisions of the dorsal lateral geniculate nucleus (LGN) in marmosets. The spatial frequency and orientation tuning of single cells in the LGN and area V1 were measured, using luminance contrast sine-wave gratings. A joint spatial frequency-orientation response selectivity profile was calculated for each cell. Response redundancy for each population was estimated by cross-multiplication of the joint selectivity profiles for pairs of cells. We show that when estimated in this way, redundancy in LGN neurons is approximately double that of neurons in cortical area V1. However, there are differences between LGN subdivisions, such that the KC pathway has a spatial representation that lies between the redundant code of the PC and MC pathways and the more efficient sparse spatial code of area V1.

Thalamocortical Connections in the Pond Turtle Pseudemys scripta elegans

Thalamocortical connections are a neuroanatomical feature shared among vertebrates, although the extent and organization of these connections vary among species. From an evolutionary standpoint, reptiles represent early stages of the pattern of connectivity between the thalamus and cortex, and elucidation of these pathways may help to reveal the biological significance of these projections. The present tract tracing study was performed to examine the organization of thalamocortical projections in the pond turtle, Pseudemys scripta elegans. All experiments were carried out using in vitro brain preparations. Injections of neurobiotin into the medial cortex resulted in labeled neurons in the ipsilateral dorsomedial anterior nucleus of the thalamus, those in the dorsomedial cortex labeled neurons in the dorsolateral anterior nucleus, and injections into the dorsal cortex resulted in labeled neurons in the dorsal lateral geniculate nucleus of the thalamus. Injections of neurobiotin into these thalamic nuclei confirmed the projections to the cortex. Finally, neurobiotin injections primarily into the medial cortex resulted in bilateral label of axons and terminals in the suprapeduncular nucleus of the hypothalamus. The results of the neurobiotin injections revealed a topographic pattern of thalamocortical connections such that medial cortical regions connect with medial thalamic nuclei and lateral cortical regions connect with lateral nuclei. These findings suggest that the presence of functionally segregated thalamocortical projections is a conserved feature of brain organization among amniotes. Moreover, this work describes a descending pathway linking cortical regions with the red nucleus via the hypothalamus thereby providing indirect cortical control of the reptilian rubrospinal system.

Zinc accumulation after target loss: an early event in retrograde degeneration of thalamic neurons

Accumulation of cytoplasmic zinc is linked with a cascade of events leading to neuronal death. In many in vivo models of zinc-induced cell death, toxic concentrations of synaptically released zinc enter vulnerable neurons via neurotransmitter- or voltage-gated ion channels. In vitro studies demonstrate, in addition, that zinc can be liberated from intracellular stores following oxidative stress and contribute to cell death processes, including apoptosis. Here we describe accumulation of intracellular zinc in an in vivo model of cell death in the absence of presynaptic zinc release. We focused on the lateral geniculate nucleus (LGN) because LGN neurons undergo apoptosis when separated from their target, the primary visual cortex (V1), and the LGN is mostly devoid of zinc-containing presynaptic terminals. Infant and adult rats and adult mice received unilateral ablation of V1, either by aspiration or kainate injection. One to 14 days later, brain sections were stained with selenium autometallography or fluorescently labeled to localize zinc, or stained immunochemically for activated caspase-3. V1 lesions led to zinc accumulation in LGN neurons in infant and adult subjects. Zinc-containing neurons were evident 1-3 days after aspiration lesions, depending on age, but not until 14 days after kainate injection. Zinc accumulation was followed rapidly by immunostaining for activated caspase-3. Our data indicate that like neurotrauma and excitotoxicity, target deprivation leads to accumulation of zinc in apoptotic neurons. Moreover, zinc accumulation in vivo can occur in the absence of presynaptic zinc release. Together these findings suggest that accumulation of intracellular zinc is a ubiquitous component of the cell death cascade in neurons.

Influence of Ca2+-binding proteins and the cytoskeleton on Ca2+-dependent inactivation of high-voltage activated Ca2+ currents in thalamocortical relay neurons

Ca2+-dependent inactivation (CDI) of high-voltage activated (HVA) Ca2+ channels was investigated in acutely isolated and identified thalamocortical relay neurons of the dorsal lateral geniculate nucleus (dLGN) by combining electrophysiological and immunological techniques. The influence of Ca2+-binding proteins, calmodulin and the cytoskeleton on CDI was monitored using double-pulse protocols (a constant post-pulse applied shortly after the end of conditioning pre-pulses of increasing magnitude). Under control conditions the degree of inactivation (34+/-9%) revealed a U-shaped and a sigmoid dependency of the post-pulse current amplitude on pre-pulse voltage and charge influx, respectively. In contrast to a high concentration (5.5 mM) of EGTA (31+/-3%), a low concentration (3 microM) of parvalbumin (20+/-2%) and calbindin(D28K) (24+/-4%) significantly reduced CDI. Subtype-specific Ca2+ channel blockers indicated that L-type, but not N-type Ca2+ channels are governed by CDI and modulated by Ca2+-binding proteins. These results point to the possibility that activity-dependent changes in the intracellular Ca2+-binding capacity can influence CDI substantially. Furthermore, calmodulin antagonists (phenoxybenzamine, 22+/-2%; calmodulin binding domain, 17+/-1%) and cytoskeleton stabilizers (taxol, 23+/-5%; phalloidin, 15+/-3%) reduced CDI. Taken together, these findings indicate the concurrent occurrence of different CDI mechanisms in a specific neuronal cell type, thereby supporting an integrated model of this feedback mechanism and adding further to the elucidation of the role of HVA Ca2+ channels in thalamic physiology.

Distinct properties of stimulus-evoked bursts in the lateral geniculate nucleus.

Neurons in the lateral geniculate nucleus (LGN) of the thalamus produce spikes that can be classified as burst spikes and tonic spikes. Although burst spikes are generally associated with states of sleep and drowsiness, bursts may also play an important role in sensory processing. This study explores the stimulus properties that evoke burst and tonic spikes and examines the reliability of LGN neurons to produce visually driven bursts. Using reverse-correlation techniques, we show that the receptive fields of burst spikes are similar to, but significantly different from, the receptive fields of tonic spikes. Compared with tonic spikes, burst spikes (1) occur with a shorter latency between stimulus and response, (2) have a greater dependence on stimuli with transitions from suppressive to preferred states, and (3) prefer stimuli that provide increased drive to the receptive field center and even greater increased drive to the receptive field surround. These differences are not attributable to the long interspike interval that precedes burst spikes, because tonic spikes with similar preceding interspike intervals also differ from burst spikes in both the spatial and temporal domains. Finally, measures of reliability are significantly greater for burst spikes than for tonic spikes with similar preceding interspike intervals. These results demonstrate that thalamic bursts contribute to sensory processing and can reliably provide the cortex with information that is similar to, but distinct from, that of tonic spikes.

Modulatory effects mediated by metabotropic glutamate receptor 5 on lateral geniculate nucleus relay cells

Glutamate is thought to be the excitatory neurotransmitter in the lateral geniculate nucleus (LGN) of the cat, mediating visual transmission from the retina via ionotropic receptors of both D,L-alpha-amino-3-hydroxy-5-alpha-methyl-4-isoxazolepropionate and N-methyl-D-aspartate subtypes. Moreover, glutamate also exerts an important modulatory influence on LGN cells, where metabotropic glutamate receptors (mGluRs) seem to play a crucial role. Here we show in anesthetized adult cats that iontophoretic application of the specific mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) produced two, distinctly different, effects on LGN neurons. Visual responses to flashing spots and drifting gratings were attenuated (decreased by an average of 59%) in 13 of 23 of the cells but augmented (increased by an average of 60%) in 10 of 23 of the cells. Further, in each case when the specific mGluR5 agonist (R,S)-2-chloro-5-hydroxyphenylglycine was applied, the effects obtained were the opposite to those of MPEP. Data obtained in a second group of experiments to determine a possible interaction between mGluR5 blockade by MPEP and glutamate ionotropic receptors show that, in the majority of neurons (11 of 15, 73%), the MPEP-mediated effects seem to be independent of N-methyl-D-aspartate and D,L-alpha-amino-3-hydroxy-5-alpha-methyl-4-isoxazolepropionate receptor activity. Our results demonstrate a physiological role for mGluR5 in controlling retinal input and show, in vivo, a more intricate scenario than previously suggested, highlighting the complexity of metabotropic receptor interactions with excitatory and inhibitory elements in the thalamus.

The effect of feedback inhibition on throughput properties of the dorsal lateral geniculate nucleus

The effect of feedback inhibition from thalamic reticular cells on retinogeniculate transmission by thalamocortical neurons of the dorsal lateral geniculate nucleus is analyzed using a minimal integrate-and-fire-or-burst network model. Potassium leakage conductances control the neuromodulatory state of the network and eliminate rhythmic bursting in the presence of spontaneous input. During oscillatory full-field stimulation, feedback inhibition from thalamic reticular neurons leads to thalamocortical relay neuron burst responses. Depending on average input rate, contrast level, and temporal frequency of modulation, the response of the aroused network may or may not be phase-locked to the visual stimulus.

Photostimulation alters c-Fos expression in the dorsal raphe nucleus

Retinal afferents to the dorsal raphe nucleus (DRN) have been described in a number of species, including Mongolian gerbils, but functional correlates of this optic pathway are unknown at present. To determine whether temporally modulated photostimulation can affect c-Fos expression in the gerbil DRN, quantitative analysis of c-Fos-immunoreactive (c-Fos-ir) neurons was conducted following 60-min exposure to pulsed (2 Hz) photostimulation at selected times over the 12:12 h light/dark cycle. For comparison, c-Fos expression was also analyzed in the subnuclei of the lateral geniculate complex and in the suprachiasmatic nucleus (SCN). In the DRN, a substantial reduction was observed in the number of c-Fos immunoreactive (c-Fos-ir) neurons during the light period and early dark period in photostimulated vs. control animals. Similar results were obtained in the intergeniculate leaflet (IGL) and ventral lateral geniculate (VLG). However, no significant changes were observed in the number of c-Fos-ir neurons in the dorsal lateral geniculate nucleus or suprachiasmatic nucleus (SCN) following photostimulation, except for an increase in the middle of the dark period. These findings indicate that photic stimulation can lead to a suppression or down-regulation of c-Fos expression in the DRN that is probably mediated via the direct retinal pathway to the DRN in this species. The similarity between c-Fos expression profiles in the DRN and IGL/VGL suggest that efferent projections from the DRN may modulate c-Fos expression to visual stimulation in these subnuclei of the lateral geniculate complex.

Morphological identification of ganglion cells expressing the α subunit of type II calmodulin‐dependent protein kinase in the macaque retina

Expression of the alpha subunit of type II calmodulin-dependent protein kinase (alphaCamKII) distinguishes the koniocellular neurons of the primate lateral geniculate nucleus (LGN) from the primary parvo- and magnocellular neurons, but whether the same neurochemical signature distinguishes the retinal ganglion cells providing them input is not known. We find that, in the retina, alphaCamKII expression also differentiates two primary groups of ganglion cell, both characterized by broad, sparsely branching dendritic trees and cell bodies intermediate in size between the parvo- and magnocellular-projecting ganglion cells. Cells in the first group have three or four primary dendrites, a thick axon, and a rounded cell body and likely are made up of multiple types. In contrast, ganglion cells in the second group demonstrate a highly regular morphology, with strictly two primary dendrites and a thinner axon emanating from a smaller, elliptical cell body. This cell resembles the "large sparse" ganglion cell identified by others in retrograde labeling from the LGN and represents about 2% of all ganglion cells. In the optic nerve, alphaCamKII+ axons are also intermediate in size and form a bimodal distribution, correlating with the axonal sizes of the two groups of ganglion cell. For the LGN, we describe a group of alphaCamKII+ axon terminals with morphology consistent with terminals from retinal ganglion cells. These terminals form long, filamentous contacts with alphaCamKII+ relay cells and increase in frequency from the dorsal to the ventral koniocellular regions. Our results indicate that ganglion cells expressing alphaCamKII represent multiple projections to the brain, at least one of which provides input to one or more koniocellular regions of the LGN.

BDNF down-regulates the caspase 3 pathway in injured geniculo-cortical neurones

Visual cortex ablation in newborn rats causes a rapid and almost complete degeneration of neurones in the dorsal lateral geniculate nucleus (dLGN), as a consequence of the axotomy of geniculo-cortical fibres. Death of dLGN neurones occurs by apoptosis and is partially prevented (approximately 50%) by intraocular delivery of brain-derived neurotrophic factor (BDNF). Here we investigated the molecular mechanisms of BDNF-mediated neuroprotection. We found that exogenous administration of BDNF partially decreases (approximately 50%) the up-regulation of apoptotic proteins (phosphorylated c-Jun, cytochrome C and cleaved caspase 3), that occurs in dLGN neurones following visual cortex ablation at postnatal day 7. These results demonstrate that the neuroprotective action of BDNF on axotomised dLGN neurones involves the partial blockade of well-characterised apoptotic pathways.

Profound Contrast Adaptation Early in the Visual Pathway

Summary has investigated slow contrast adaptation in the primate retina, and that found substantially less adaptation than Prior exposure to a moving grating of high contrast led to a substantial and persistent reduction in the in the salamander. We describe here new observations that sharply clarify the picture in the primate visual pathcontrast sensitivity of neurons in the lateral geniculate nucleus (LGN) of macaque. This slow contrast adapta- way and have major implications for psychophysical studies: neurons in magnocellular LGN (M cells), but tion was potent in all magnocellular (M) cells but essentially absent in parvocellular (P) cells and neurons not those in parvocellular LGN (P cells), show strong contrast adaptation that originates in the retina. that received input from S cones. Simultaneous recordings of M cells and the potentials of ganglion cells driving them showed that adaptation originated in gan- Results glion cells. As expected from the spatiotemporal tuning of M cells, adaptation was broadly tuned for spatial Aftereffects of Adaptation to High-Contrast Stimuli frequency and lacked orientation selectivity. Adapta- We studied the responses of single neurons in LGN tion could be induced by high temporal frequencies of anesthetized macaque before, during, and through to which cortical neurons do not respond, but not by recovery from adaptation to contrast modulation of diflow temporal frequencies that can strongly adapt cor- ferent stimuli. Our initial experiments were prompted tical neurons. Our observations confirm that contrast by observations in ganglion cells (Baccus and Meister,

The derivation of direction selectivity in the striate cortex.

In the central visual pathway of binocular animals, the property of directional selectivity (DS) is first exhibited in striate cortex. In this study, we sought to determine the neural circuitry underlying the transformation from non-DS neurons to DS cortical cells. In a well established model, DS receptive fields (RFs) are derived from the sum of two non-DS inputs with 90 degrees (quadrature) spatiotemporal phase differences. We explored possible input sources for this model, which include non-DS simple cells and lateral geniculate nucleus (LGN) neurons, by examination of spatiotemporal RFs of single cells and of pairs of cells. We find that distributions of non-DS simple RFs do not match the temporal predictions of the quadrature model because of a lack of long-latency responses. The long-latency inputs could potentially arise from lagged LGN afferents. However, analysis of cell pairs indicates that DS cells receive cortical input from non-DS simple cells for both short- and long-latency components, with temporal phase differences typically <90 degrees. Furthermore, the distribution of minimum phase differences needed to generate DS cells overlaps that exhibited by non-DS simple cells. Considered together, these results are consistent with a linear model whereby DS simple cells are formed from simple-cell inputs, with temporal phase differences often less than quadrature.

GABA C receptor mediated inhibition in acutely isolated neurons of the rat dorsal lateral geniculate nucleus

In the dorsal lateral geniculate nucleus (dLGN), GABA C receptors seems to be specifically expressed by local GABAergic interneurons. Although the presence of GABA C receptors has been demonstrated, a quantitative estimation of their contribution to inhibition in dLGN is lacking. Because the amount of inhibition mediated by these receptors might reflect their functional importance we performed whole-cell patch clamp recordings from dLGN cells acutely dissociated from brain slices. We focally applied the GABA receptor agonist muscimol and quantified effects mediated through either GABA C or GABA A receptors. Because their basic dendritic morphology was preserved, we tried to morphologically differentiate between thalamocortical cells and local interneurons. In the majority of multipolar cells, representing thalamocortical projection neurons, the specific GABA A receptor antagonist bicuculline completely blocked muscimol induced currents. In contrast, in most of the bipolar cells, representing interneurons, bicuculline blocked only 70–80% of the muscimol induced currents. The remaining currents were blocked by co-application of TPMPA, a specific GABA C receptor antagonist, or picrotoxin, an unspecific GABA A and GABA C receptor blocker. The latter neurons were also sensitive to the selective GABA C receptor agonist cis-aminocrotonic acid. These results indicate that in those dLGN neurons that express GABA C receptors, these receptors contribute considerably to GABAergic inhibitory inputs.

Quantitative age-related changes in dorsal lateral geniculate nucleus relay neurons of the rat.

An ultrastructural and quantitative study of the age-related changes occurring in the relay neurons of the dorsal lateral geniculate nucleus (dLGN) was carried out using male Wistar rats aged 3, 18, 24, and 28 months. Morphometric techniques were used to obtain data regarding cellular activity including soma, nuclear, and nucleolar size. Volume fractions for rough endoplasmic reticulum (RER), mitochondria, and lipofuscin, as well as numbers and sizes of mitochondria and dense bodies (DB) was also calculated. Among the few alterations found in the perikaryon, we can highlight the redistribution and fragmentation of RER and an increase and progressive aggregation of lipofuscin. Quantitative data show a significant decrease in the volume of the soma (-42.77%) and the nucleus (-33.66%), and in the volume fraction of the RER (-18.81%) and mitochondria (-10.16%). A significant increase in lipofuscin (+213.29%), and variations in size and number of mitochondria and dense bodies were also found. Some histophysiological considerations about the findings are discussed. The findings lead to the conclusion that a relative degree of morphological stability is exhibited by relay neurons, although the quantitative data show evident intracellular changes, especially from 24 to 28 months. These changes suggest that accompanying physiological alterations may occur, with putative effects on visual function during ageing.

Influence of contrast on orientation and temporal frequency tuning in ferret primary visual cortex.

Neurons in primary visual cortex are highly sensitive to the contrast, orientation, and temporal frequency of a visual stimulus. These three stimulus properties can be varied independently of one another, raising the question of how they interact to influence neuronal responses. We recorded from individual neurons in ferret primary visual cortex to determine the influence of stimulus contrast on orientation tuning, temporal-frequency tuning, and latency to visual response. Results show that orientation-tuning bandwidth is not affected by contrast level. Thus neurons in ferret visual cortex display contrast-invariant orientation tuning. Stimulus contrast does, however, influence the structure of orientation-tuning curves as measures of circular variance vary inversely with contrast for both simple and complex cells. This change in circular variance depends, in part, on a contrast-dependent change in the ratio of null to preferred orientation responses. Stimulus contrast also has an influence on the temporal-frequency tuning of cortical neurons. Both simple and complex cells display a contrast-dependent rightward shift in their temporal frequency-tuning curves that results in an increase in the highest temporal frequency needed to produce a half-maximum response (TF(50)). Results show that the degree of the contrast-dependent increase in TF(50) is similar for cortical neurons and neurons in the lateral geniculate nucleus (LGN) and indicate that subcortical mechanisms likely play a major role in establishing the degree of effect displayed by downstream neurons. Finally, results show that LGN and cortical neurons experience a contrast-dependent phase advance in their visual response. This phase advance is most pronounced for cortical neurons indicating a role for both subcortical and cortical mechanisms.

Postnatal development of the noradrenergic system in the dorsal lateral geniculate nucleus of the rat

The noradrenergic innervation of the developing dorsal lateral geniculate nucleus of the rat was examined with light and electron microscopic immunocytochemistry. At birth, few, relatively thick, noradrenergic fibers innervated the nucleus. Their density was steadily increased and they became thinner, tortuous, and varicose with the progression of age. Only a minority (11–15%) of labeled varicosities made synaptic contacts. Most of these synapses were symmetrical and on dendritic shafts. The present findings demonstrate the establishment of the anatomical relationships between noradrenergic afferents and neurons of the dorsal lateral geniculate nucleus during development and may help to understand the role of noradrenaline in the processing of visual information.

Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System

Proliferation and survival of different cell types is thought to be modulated by cell interactions during development that achieve numerical and functional balance. We tested the precision of coregulation of numbers of neurons, glial cells, and endothelial cells in the dorsal lateral geniculate nucleus (LGN) in 58 isogenic strains of mice. We acquired matched counts of retinal ganglion cells (RGCs) in these strains and tested the precision of numerical matching between retina and LGN. Cells were counted using unbiased counting protocols and tissue from the Mouse Brain Library (www.mbl.org). Classification criteria were assessed using immunohistochemical criteria. The LGN contains an average of 17,000 neurons, 12,000 glial cells, and 10,000 endothelial cells. Variation around these means is typically twofold, and cell ratios vary widely. Strain differences in LGN volume correlate moderately well with glial cell number (r = 0.69) and less well with RGC number (r = 0.35) and with LGN neuron number (r = 0.32). Populations of LGN neurons and glial cells correlate only modestly (r = 0.44; p < 0.01). The single most surprising and unequivocal finding was the lack of any detectable correlation between populations of LGN neurons and RGCs, a correlation of merely 0.01 across 56 strains. In contrast, RGC number correlates significantly with LGN glial cell number, a surprising twist on the numerical matching hypothesis (r = 0.33; p < 0.01). We conclude that numbers of these two functionally coupled neuron populations are modulated over a wide range by independent genetic and developmental mechanisms.