Neuroanatomy, Nucleus Lateral Geniculate


The lateral geniculate nucleus (LGN) belongs to the category of sensory projection nuclei of the thalamus and plays an essential role in normal visual processing. The lateral geniculate nucleus has broadly distributed connectivity projecting to various regions of the extrastriate cortex and receiving input from the same as well as from hindbrain and other midbrain structures. It is located in the posteroventral region of the thalamic nuclei, immediately abutting the pulvinar and posterior to the inferior choroidal point of the choroid plexus. The nucleus' name is from its lateral position relative to the medial geniculate nucleus and the sharp bend (Latin geniculum, "joint") of its laminae.

Structure and Function

The basis of the structure of the lateral geniculate nucleus is mostly in terms of its three distinct cell types: magnocellular (M), parvocellular (P), and koniocellular (K). P and M cells are arranged in six different layers (four dorsal P layers and two ventral M layers), with retinal ganglion signals from the ipsilateral eye synapsing on layers 2, 3, and 5, and signals from the contralateral eye synapsing on layers 1, 4, and 6. M cells in the LGN receive input from the large-field, motion-sensitive Y-type retinal ganglion cells, while P cells receive input from the small-field, color-sensitive X-type retinal ganglion cells. Koniocellular cells project into regions ventral to each of the P and M laminae.

The lateral geniculate nucleus is also the point of origin for the optic radiations (Meyer's loop, central bundle, and Baum’s loop) that project via the internal capsule to the primary visual cortex (V1), primarily synapsing onto spiny stellate neurons in layers 4C-alpha and 4C-beta. Analysis of LGN-dependent fMRI activity in non-V1 extrastriate cortex suggests that the LGN also projects to regions further downstream in the visual pathway (e.g., V2-5).[1] While the LGN receives substantial input from the retinal ganglia, it receives far greater innervation from higher-order regions, such as modulatory feedback from layer 6 of V1 and the thalamic reticular nucleus.[2] It also receives varying degrees of modulatory activity from the raphe nuclei (serotonergic),[3] pedunculopontine and laterodorsal tegmental nuclei (cholinergic),[4] and locus coeruleus (noradrenergic).[5]

The extracellular matrix of the lateral geniculate nucleus is characterized by a decreased presence of the traditional aggrecan-based matrix phenotype, perineuronal nets. It instead displays a high density of axonal coats, a related structure with a more localized matrix at dendrites, suggesting a different organizational strategy possibly specialized for rapid sensory processing.[6][7]

The lateral geniculate nucleus also contains a distinct section between its dorsal and ventral regions known as the intergeniculate leaflet (IGL). The IGL projects to the suprachiasmatic nuclei of the hypothalamus via the geniculohypothalamic tract and to the pineal gland via the geniculopineal tract, implicating the LGN in the modulation of circadian/diurnal rhythms.[8][9][10]

Historically, the lateral geniculate nucleus was highlighted for its role as little more than a signal repeater, following the early conclusions of Glees and LeGros Clark, who argued that "... the geniculate cells probably serve the single function of a relay between the retinal fibers and the visual cortex."[11] However, subsequent research has suggested a more complex account of LGN function, including attentional modulation, temporal decorrelation, and binocular facilitation or suppression via monocular gain modulation.[12][13][14][15] Furthermore, some research has suggested that a subpopulation of K cells in the LGN demonstrate selective sensitivity to stimulus orientation similar to V1 cells.[16]


Early development of the lateral geniculate nucleus characteristically demonstrates heightened retinogeniculate synaptogenesis (as early as 13 weeks of gestation) followed by the subsequent development of corticogeniculate connectivity. However, the structural development of retinogeniculate projections (without synapse formation) occurs as early as 7 weeks.[17] A critical period of increased cell metabolism and synapse development occurs at 15 to 20 weeks.[18] By the end of this period, retinogeniculate projections to the LGN have developed eye-specific segregation.[19] The development of the LGN’s laminar structure occurs at approximately 22 to 25 weeks, beginning with the ventral aspect (the magnocellular layers).[20] The later lamination of the LGN suggests that this process is a function of retinal activity. This concept receives further support from the finding in animal studies that interrupting retinogeniculate segregation severely disrupts the development of LGN's laminar organization.[21]

Blood Supply and Lymphatics

The posterior cerebral artery supplies the lateral geniculate nucleus from the lateral posterior choroidal branch and by the internal carotid artery from its anterior choroidal branch.[22]


Evidence from multiple sources suggests that oculomotor-induced signals to the lateral geniculate nucleus are used to suppress retinal signals during saccades and facilitate the same signals immediately thereafter.[23]

Physiologic Variants

Structural variation in the lateral geniculate nucleus can occur via divergent development of or subsequent damage to upstream structures in the visual pathway. Strabismic amblyopia, the permanent reduction of visual acuity due to abnormal development in the eyes’ alignment, is associated with a significant decrease in LGN gray matter density despite normal development other major neural regions in the visual pathway.[24] Damage to the optic nerve due to primary open-angle glaucoma can similarly induce atrophy in the LGN commensurate with the degree of condition severity.[25][26] Some animal research also suggests that a lack of input from the visual cortical regions can induce cell death sharing many features of apoptosis.[27]

Surgical Considerations

Resection of intraventricular meningiomas may pose a higher risk of postoperative ischemia to the lateral geniculate nucleus due to the proximity of the choroidal arteries, the supply of which may integrate into the tumor.[28]

Clinical Significance

Lesions in the lateral geniculate nucleus, such as those caused by arteriovenous malformations, can produce contralateral homonymous hemianopias and quadrantanopias indicating specific affected laminar subregions with special vulnerability to the macular region given its disproportionate representational region.[29] Given the location of the LGN in the visual pathway and the dual, differential blood supply to the medial and lateral portions of the nucleus, it is possible to determine the specific arterial cause of such a lesion based on the presenting visual field defect.[22] Due to downstream projections to the suprachiasmatic nucleus, the insult of the LGN may also disrupt the effects of stimuli that generally modulate circadian rhythm.[30]

The lateral geniculate nucleus is among the numerous thalamic nuclei that show substantial alterations in individuals with spinocerebellar ataxia type 2 (and possibly type 3), including astrocytosis, loss of neuronal bodies, and increased levels of lipofuscin.[31][32]

For individuals diagnosed with blindsight due to a lesion of the primary visual cortex, the LGN plays an essential role in mediating visually relevant information that is below the level of conscious awareness.[1]

(Click Image to Enlarge)
Lateral geniculate nucleus
Lateral geniculate nucleus
Image courtesy S Bhimji MD


7/24/2023 11:35:12 PM



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