Axons from the temporal portion of each retina travel through the optic nerve, optic chiasm, and ipsilateral optic tract before terminating in the same side of the brain. On the other hand, axons from the nasal portion of each retina pass through the optic nerve, cross to the opposite side in the optic chiasm, and continue through the contralateral optic tract to end in the opposite side of the brain. This arrangement means that objects in the left field of vision are represented in the right side of the brain, and objects in the right field of vision are represented in the left side of the brain.

The main target for vision is the lateral geniculate nucleus (LGN) of the thalamus, where retinal ganglion cell axons can synapse. The LGN has a retinotopic map, with cells aligned along projection lines across its layers to represent specific retinal locations. The LGN receives projections from both eyes, with one magnocellular layer and two parvocellular layers receiving input from retinal ganglion cells. Ganglion cells that code for color project to groups of cells between the major layers in the intralaminar zones. Therefore, the properties of LGN neurons resemble those of retinal ganglion cells, including the classification as P or M cells and the presence of on-center or off-center receptive fields.

In addition to the retina, the LGN also receives input from the visual areas of the cerebral cortex, the thalamic reticular nucleus, and several nuclei of the brainstem reticular formation. The activity of LGN projection neurons is inhibited by interneurons in both the LGN and thalamic reticular nucleus, which utilize GABA as their inhibitory neurotransmitter. Corticofugal pathways and brainstem neurons transmitting signals via monoamine neurotransmitters further influence the activity of LGN neurons, playing a role in filtering visual information and selective attention.

The LGN projects information to the primary visual cortex (striate cortex) through the visual radiations. Fibers from the lower half of the hemiretinas, representing the contralateral upper visual field, project to the lingual gyrus located on the medial surface of the occipital lobe, below the calcarine sulcus. The visual radiation fibers representing the contralateral lower visual field project to the adjacent cuneus gyrus, just above the calcarine sulcus. Together, the portions of these two gyri lining and bordering the calcarine sulcus form the primary visual cortex (Brodmann area 17).
Fig. 8.9 ). Axons from the temporal portion of each retina pass through the optic nerve, the lateral side of the optic chiasm, and the ipsilateral optic tract and terminate ipsilaterally in the brain. Axons from the nasal portion of each retina pass through the optic nerve, cross to the opposite side in the optic chiasm, and then pass through the contralateral optic tract to end in the contralateral side of the brain. As a result of this arrangement, objects in the left field of vision are represented in the right side of the brain, and those in the right field of vision are represented in the left side of the brain.
Retinal ganglion cell axons can synapse in several parts of the brain, but the main target for vision is the lateral geniculate nucleus (LGN) of the thalamus. There is a point-to-point projection from the retina to the LGN. The LGN thus has a retinotopic map. Cells that represent a particular retinal location are aligned along projection lines that can be drawn across the layers of the LGN.
The projection from each eye is distributed to three of the layers of the LGN, one of the magnocellular layers (layers 1 and 2 receive M cell input) and two of the parvocellular layers (layers 3 to 6 receive P cell input). Color-coded ganglion cells project to groups of cells between the major layers, the intralaminar zones. Thus the properties of LGN neurons are very similar to those of retinal ganglion cells. For example, LGN neurons can be classified as P or M cells, and they have on-center or off-center receptive fields.
The LGN also receives input from the visual areas of the cerebral cortex, the thalamic reticular nucleus, and several nuclei of the brainstem reticular formation. The activity of LGN projection neurons is inhibited by interneurons both in the LGN and in the thalamic reticular nucleus. These cells use GABA as their inhibitory neurotransmitter. In addition, the activity of LGN neurons is influenced by corticofugal pathways and by brainstem neurons that transmit signals via monoamine neurotransmitters. These control systems filter visual information and may be important for selective attention.
The LGN projects to the primary visual cortex or striate cortex by way of the visual radiations. The visual radiation fibers carrying information derived from the lower half of the appropriate hemiretinas (and therefore the contralateral upper visual field) project to the lingual gyrus, which lies
Fig.
8.9 ).Forexample,atinylesionintheretinawouldresultinablindspot(scotoma) inthateye,whereasasimilarlesioninthestriatecortexwouldproducecorrespondingscotomasinbotheyes.Interruptionoftheopticnerveononesideproducesblindnessinthateye.Damagetotheopticnervefibersastheycrossintheopticchiasmresultsinlossofvisioninbothtemporalfieldsofvision;thisconditionisknownasbitemporal hemianopsia andoccursbecausethecrossingfibersoriginatefromganglioncellsinthenasalhalvesofeachretina.Alesionoftheentireoptictract,LGN,visualradiation,orvisualcortexononesidecauseshomonymous hemianopsia, whichislossofvisionintheentirecontralateralvisualfield.Partiallesionsresultinpartialvisualfielddefects.Forexample,alesioninthelingualgyruscausesanupperhomonymous quadrantanopsia, whichinthiscaseislossofvisioninthecontralateral,uppervisualfield.
on the medial surface of the occipital lobe, just below the calcarine sulcus. Axons in the visual radiation that represent the contralateral lower visual field project to the adjacent cuneus gyrus, which lies just above the calcarine sulcus. Together, the portions of these two gyri that line and border the calcarine sulcus constitute the primary visual cortex (or Brodmann area 17;
Fig. 8.10