Mean retinal ganglion cell axon diameter varies with location in the human retina.

PURPOSE: We examined retinal ganglion cell (RGC) axon diameters within the human retinal nerve fibre layer in order to provide information about the possible effects of axonal stimulation when a retinal prosthesis includes the nonfoveal regions. METHODS: Five pairs of eyes were obtained from donors aged from 48 to 84 years. Fixation delay ranged from 5 to 22 h. Tissue was processed for electron microscopy. RESULTS: Inferior and/or nasal RGC axons were on average larger than superior and/or temporal axons. The inferior retina contained some very large axons. Foveal axons were on average smaller than nonfoveal axons and had a size distribution that suggested different size groupings not seen in other samples. Peripheral versus central axons within the superior and inferior nasal retinal samples were compared; peripheral axons were significantly larger, unlike the inferior temporal samples or the samples nasal to the optic disc. CONCLUSIONS: Stimulus-current thresholds will change as a retinal prosthesis increases in size and encroaches on the nonfoveal axons. These changes can be anticipated based on mean axon diameter. Knowing in advance the possible outcome of electrical stimulation of the axonal population may help refine prosthetic procedures and patient training.

'Top-down' influences of ipsilateral or contralateral postero-temporal visual cortices on the extra-classical receptive fields of neurons in cat's striate cortex.

In anesthetized and immobilized domestic cats, we have studied the effects of brief reversible inactivation (by cooling to 10 degrees C) of the ipsilateral or contralateral postero-temporal visual (PTV) cortices on: 1) the magnitude of spike-responses of neurons in striate cortex (cytoarchitectonic area 17, area V1) to optimized sine-wave modulated contrast-luminosity gratings confined to the classical receptive fields (CRFs) and 2) the relative strengths of modulation of CRF-induced spike-responses by gratings extending into the extra-classical receptive field (ECRF). Consistent with our previous reports (Bardy et al., 2006; Huang et al., 2007), inactivation of ipsilateral PTV cortex (presumed homologue of primate infero-temporal cortex) resulted in significant reversible changes (almost all substantial reductions) in the magnitude of spike-responses to CRF-confined stimuli in about half of the V1 neurones. Similarly, in half of the present sample, inactivation of ipsilateral PTV cortex resulted in significant reversible changes (in over 70% of cases, reduction) in the relative strength of ECRF modulation of the CRF-induced spike-responses. By contrast, despite the fact that receptive fields of all V1 cells tested were located within 5 degrees of representation of the zero vertical meridian, inactivation of contralateral PTV cortex only rarely resulted in significant (yet invariably small) changes in the magnitude of spike-responses to CRF-confined stimuli or significant (again invariably small) changes in the relative strength of ECRF modulation of spike-responses. Thus, the ipsilateral, but not contralateral, 'higher-order' visual cortical areas make significant contribution not only to the magnitude of CRF-induced spike-responses but also to the relative strengths of ECRF-induced modulation of the spike-responses of V1 neurons. Therefore, the feedback signals originating from the ipsilateral higher-order cortical areas appear to make an important contribution to contextual modulation of responses of neurons in the primary visual cortices.

Does the development of the perigeniculate nucleus support the notion of a hierarchical progression within the visual pathway?

The development of the visual pathway has been extensively studied. However, despite of the importance of the perigeniculate nucleus within this pathway, there is a lack of information concerning its development. The present study examined the dendritic development of perigeniculate nucleus cells using single cell injections in 400-500 microm thick fixed brain slices from kittens of different ages between postnatal day 0 and postnatal day 125. A total of 189 perigeniculate nucleus cells were reconstructed from serial sections for qualitative and quantitative analysis. Cells during the first month were characterized by an abundance of branch points and appendages. There was a significant (P>0.05), albeit variable, increase in the number of branch points and appendages up to about postnatal day 12 after which the numbers were rapidly reduced over the next two weeks. Similarly, appendage numbers significantly increased over the first two weeks until postnatal day 17 and then fell to near adult levels by postnatal day 34. The majority of branch points and appendages occur within 100-200 microm of the soma (10-30% of the dendritic diameter). The data indicate that perigeniculate nucleus dendritic maturation lags shortly behind that of the retina but may precede that of its dorsal thalamic target, the lateral geniculate nucleus. Thus, it may be that the earlier maturation of the perigeniculate nucleus and its inhibitory input is a necessary requirement for the proper development of retinogeniculate and corticothalamic topographic maps within the dorsal lateral geniculate nucleus and perigeniculate nucleus.

Morphology and ultrastructure of rat hippocampal formation after i.c.v. administration of N-acetyl-L-aspartyl-L-glutamate.

N-Acetyl-L-aspartyl-L-glutamate (NAAG) is one of the most abundant neuroactive compounds in the mammalian CNS. Our recent observations have suggested that NAAG administered into rat cerebral ventricles can cause neuronal death by apparently excitotoxic mechanisms that can be antagonized by the N-methyl-D-aspartate-receptor blockers and by ligands of metabotropic glutamate receptor of Group II. Therefore, the principal aim of the present study has been to use quantitative morphology, electron microscopy and terminal deoxynucleotidyl transferase-mediated biotin dUTP nick-end labeling to study a dose- and time-dependence as well as regional distribution of neurodegeneration in hippocampi of rats after the intraventricular infusion of 0.25 micromol NAAG/ventricle and of equimolar doses of L-glutamate (L-GLU) and N-acetyl-L-aspartate (NAA), breakdown products of NAAG. The degenerative changes were observed after the infusion of 0.25 and 1.25 micromol of NAAG/ventricle, but not when a dose of 0.05 micromol of NAAG/ventricle was injected into each lateral cerebral ventricle. With a dose of 0.25 micromol of NAAG/ventricle the number of degenerated neurons reached a maximum on the fourth day after the infusion. The neuronal damage following bilateral administration of 0.25 micromol of NAAG/lateral cerebral ventricle exhibited features of a delayed neuronal degeneration, expressed mainly in the layer of dentate granule neurons. The degeneration was characterized on the basis of ultrastructural appearance and DNA-fragmentation. The morphological changes caused by L-glutamate and NAA were much smaller than those observed after the administration of NAAG and displayed a different pattern of regional distribution. The present findings suggest that NAAG can cause a loss of hippocampal neurons in vivo, apparently resulting from the neurotoxicity of NAAG itself.

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.

Regional distribution and pharmacological characteristics of [3H]N-acetyl-aspartyl-glutamate (NAAG) binding sites in rat brain.

Autoradiographical studies revealed that 10 nM [3H]N-acetyl-aspartyl-glutamate (NAAG) labelled grey matter structures, particularly in the hippocamus, cerebral neocortex, striatum, septal nuclei and the cerebellar cortex. The binding was inhibited by (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)-glycine (DCG IV), an agonist at group II metabotropic glutamate receptors (mGluR II). (RS)-alpha-Methyl-4-tetrazolylphenylglycine (MTPG), (RS)-alpha-cyclopropyl-4-phosphonoglycine (CPPG) and (RS)-alpha-methylserine-O-phosphate monophenyl ester (MSOPPE), all antagonists at mGluR II and mGluR III, also inhibited [3H]NAAG binding. Other inhibitors were (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (ACPD), a broad-spectrum mGluR agonist with preference for groups I and II and the mGluR I agonists/mGluR II antagonists (S)-3-carboxy-4-hydroxyphenylglycine (3,4-CHPG) and (S)-4-carboxy-3-hydroxyphenylglycine (4,3-CHPG). Neither the mGluR I specific agonist (S)-dihydroxyphenylglycine nor any of the ionotropic glutamate receptor ligands such as kainate, AMPA and MK-801 had strong effects (except for the competitive NMDA antagonist CGS 19755, which produced 20-40% inhibition at 100 microM) suggesting that, at low nM concentrations, [3H]NAAG binds predominantly to metabotropic glutamate receptors, particularly those of the mGluR II type. Several studies have indicated that NAAG can interact with mGluR II and the present study supports this notion by demonstrating that sites capable of binding NAAG at low concentrations and displaying pharmacological characteristics of mGluR II exist in the central nervous tissue. Furthermore, the results show that autoradiography of [3H]NAAG binding can be used to quantify the distribution of such sites in distinct brain regions and study their pharmacology at the same time.

Neurotoxicity of NAAG in vivo is sensitive to NMDA antagonists and mGluR II ligands.

N-Acetyl-aspartyl-glutamate (NAAG), an agonist at Group II metabotropic glutamate receptors (mGluR II), also activates the NMDA-type of ionotropic glutamate receptors and, at high micromolar concentrations, has previously been shown to induce neuronal cell death. In the present study we have morphologically quantified the neurotoxic action of intracerebroventricularly administered NAAG on the hippocampal formation and compared it to the action of the selective endogenous NMDA agonist quinolinic acid. Finally, we examined whether the action of NAAG can be modified by NMDA receptor antagonists and mGluR II ligands. NAAG-induced neurodegeneration was found to be less severe than that induced by quinolinate. It was prevented by inhibitors of NMDA receptors and also by an mGluR II agonist (DCG IV) but not by an mGluR II antagonist (EGlu).

Distribution of calbindin, parvalbumin, and calretinin immunoreactivity in the reticular thalamic nucleus of the marmoset: evidence for a medial leaflet of incertal neurons.

The placement of the reticular thalamic nucleus (RTN) between the dorsal thalamus and the cortex and the inhibitory nature of reticulothalamic projections has led to suggestions that it "gates" the flow of sensory information to the cortex. The New World diurnal monkey, the marmoset, Callithrix jacchus is emerging as an important "model primate" for the study of sensory processing. We have examined the distribution of Nissl-stained somata and calbindin, parvalbumin, and calretinin immunoreactivity in the ventral thalamus for comparison with other species. Cells were labeled using standard immunohistochemistry, ExtraAvidin-HRP, and diaminobenzidine reaction products. The RTN is constituted by a largely homogeneous population of parvalbumin immunoreactive cells with respect to size and orientation. Calbindin and calretinin immunoreactive cells were only found along the medial edge of the RTN adjacent to the external medullary lamina of the dorsal thalamus and laterally near the ventral RTN. These cells were considered to be part of the zona incerta (ZI). The marmoset ZI could be subdivided into dorsal and ventral regions on the basis of its immunoreactivity to calcium binding proteins. Both the ZI and nucleus subthalamicus Luysi contained scattered calbindin and calretinin immunoreactive cells with well-defined dendritic processes. These cells were clearly different to cells in the dorsal thalamus. Parvalbumin immunoreactive cells in RTN, ZI, and subthalamic nucleus were on average larger than neurons positive for the other calcium binding proteins. Future studies reporting the afferent and efferent projections to the RTN must view their results in terms of the close apposition of RTN and ZI somata.

Cortical projections from the suprasylvian gyrus to the reticular thalamic nucleus in the cat.

The cat's suprasylvian gyrus was injected iontophoretically with either 4% wheat germ agglutinin-horseradish peroxidase, 4% dextran-fluororuby or 4% dextran-biotin. The locations of labelled fibres, presumed terminals and cell bodies were determined with the aid of a camera lucida attachment and computer aided stereometry. Cells from the crown of the suprasylvian gyrus project to the dorsal-most portion of the rostral half of the reticular nucleus. The region or 'sector' is distinct, albeit with some overlap, from the visual sector of the reticular nucleus defined by projections from adjacent extrastriate visual cortices. The projection from the suprasylvian gyrus to the reticular nucleus has a rough topography such that the caudal areas project to the more caudal aspects of the sector and rostral areas project to the more rostral areas of the reticular nucleus. There is a large degree of overlap of rostrocaudal projections from the suprasylvian gyrus within the sector, however, the projections originating from rostral sites are situated in a more ventral location compared to the projection originating from the caudal suprasylvian gyrus. Analysis of the distribution of biotin labelled presumptive terminals did not support the notion of 'slabs' or regional variation in terminal density across the mediolateral thickness of the reticular nucleus. In addition, a number of presumptive terminals were found within the internal capsule which coincided with the position of retrogradely labelled cells in the internal capsule following thalamic injections and appears to be part of the perireticular nucleus. The results suggest that the reticular nucleus may be segregated into sectors connected with modality specific cortical areas (e.g. striate and extrastriate visual areas) and nonspecific sectors connected with polymodal (e.g. area 7) cortical regions. The reticular nucleus and its connections with the suprasylvian gyrus may form an important link in binding eye movements to sensory integrative process through visuomotor and auditory thalamic connections.

Intraretinal axon diameters of a New World primate, the marmoset (Callithrix jacchus).

PURPOSE: Previously, measurements of retinal ganglion cell axon diameter have been used to make inferences about the physiology and clinical pathology of the visual pathway. However, few of these studies were able to unequivocally relate axon diameter to retinal ganglion cell type and other associated measurements. In this and our previous study we have examined intraretinal axon diameters to determine if differences in axon diameter may help to explain conduction velocity measurements found previously. METHODS: Individual retinal ganglion cells of a New World primate, the common marmoset (Collithrix jacchus) were injected iontophoretically with 2% Lucifer yellow and 4% neurobiotin. Labelled cells were visualized by horseradish peroxidase immunohistochemistry and diaminobenzidine and then retinae were mounted vitreal side up on a glass slide. Cell measurements were made with the aid of a camera lucida attachment and computer-aided morphometry Axons were photographed under x 100 oil immersion and measured at a final magnification of x 4600. RESULTS: A sample of 62 parasol cells, 22 midget cells, 16 hedge cells and 11 small bistratified cells were analysed. Dendritic field diameter of the different cell classes showed only moderate (non-significant) increases with eccentricity. Only the parasol cells demonstrated a significant increase in mean axon diameter with eccentricity. When the parasol class was examined more closely, it was found that only parasol cells of the superior, inferior and temporal retina (SIT group) showed significant positive correlations between different cell parameters (mean axon diameter, soma diameter, dendritic field diameter, eccentricity). Soma and dendritic field diameters of the SIT group were significantly larger than those of the nasal parasol cells. However, mean axon diameters of the SIT cells were not significantly different from nasal parasol cells. Axon diameters of nasal parasol cells were very variable and overlapped those of the midget and hedge cell classes to a large extent. CONCLUSIONS: The present data show that for marmoset parasol cells there may not be a clearly defined distinction between nasal and superior, inferior and temporal parasol cells on the basis of axon size. Of particular interest in the present analysis is the clear separation of superior, inferior and temporal parasol cells and nasal parasol cells when comparing soma and dendritic field diameters which is not reflected in the distribution of axon diameters. We suggest that changes in diameter along the length of an axon, differences between retinal quadrants and the variability between cells may be related to minimization of spatiotemporal dispersion necessary for accurate perception of motion within the visual world.

Projections from striate and extrastriate visual cortices of the cat to the reticular thalamic nucleus.

We have studied the pattern of connectivity of the visual cortical areas 17, 18, 19, 20a, 21a, posteromedial lateral (PMLS), and the posterolateral lateral (PLLS) suprasylvian areas with the reticular thalamic nucleus (RTN) of the cat ventral thalamus. Three cortical areas per hemisphere were injected iontophoretically with either 4% wheat germ agglutinin-horseradish peroxidase, 4% dextran-fluororuby, or 4% dextran-biotin. The visual field representations of the injection sites were determined by reference to previously published visuotopic maps of the cortex. The locations of labelled fibres, presumed terminals and cell bodies were determined with the aid of a camera lucida attachment and computer aided stereometry. In the ventral thalamus, the primary visual cortices (areas 17 and 18) project in a topographic manner to both the perigeniculate nucleus (PGN) and the RTN. By contrast, the "higher" visual cortical areas (areas 19, 21a, 20a, PMLS, and PLLS) project only to the RTN. Our experiments demonstrate the existence of a single, albeit coarse, visuotopic map within the RTN but do not support the notion of separate subregions within the RTN that can be related specifically to a particular visual cortical area. The putative single visuotopic map in the RTN appears to be organised in such a way that the vertical meridians are represented along the rostrocaudal axis of the RTN, whereas the horizontal meridians are mapped within the dorsoventral axis of the nucleus. The upper visual field is represented within regions of the RTN adjacent to the caudal part of the dorsal lateral geniculate nucleus (LGNd), whereas the lower visual field is represented in the parts of the RTN rostral to the LGNd. The map also shows a ventrodorsal shift along the rostrocaudal axis of the RTN such that in the rostral RTN the representation of vertical meridian is placed more ventrally than that in the caudal part of the nucleus.

Intraretinal axon diameter: a single cell analysis in the marmoset (Callithrix jacchus).

We have labelled individual retinal ganglion cells of a New World primate, the common marmoset (Callithrix jacchus) with neurobiotin and then measured axon, soma and dendritic field diameter. A total of 111 cells were analysed (62 parasol cells, 22 midget cells, 16 hedge cells and 11 small bistratified cells). When all retinal ganglion cells were grouped together axon diameter was positively correlated to soma diameter. When analysed according to cell class only midget cells showed a positive correlation between soma size and mean axon diameter. Dendritic field diameter and mean axon diameter of both parasol and midget cells showed significant correlations. Axon diameter is not constant along the intraretinal length of the axon and the rate of change in diameter appears to be related to the cell class and the initial size of the axon. Midget cell axons showed a rapid increase of up to 20% over the first 200 microm in contrast to parasol cell axons which increased more slowly over this distance but then showed a marked increase in diameter of up to 40% over the next 450 microm. However, axon diameter did not remain at these increased diameters but decreased at greater distances from the soma. The degree to which an axon changes its diameter is related to retinal ganglion cell class and the initial size of the axon. We postulate that these variations in intraretinal axon diameter may have a direct influence on conduction velocity and reflect a compensatory mechanism to minimise spatiotemporal dispersion along the visual pathway.

The human fetal retinal nerve fiber layer and optic nerve head: a DiI and DiA tracing study.

The organization of the primate nerve fiber layer and optic nerve head with respect to the positioning of central and peripheral axons remains controversial. Data were obtained from 32 human fetal retinae aged between 15 and 21 weeks of gestation. Crystals of the carbocyanine dyes, DiI or DiA, and fluorescence microscopy were used to identify axonal populations from peripheral retinal ganglion cells. Peripheral ganglion cell axons were scattered throughout the vitreal-scleral depth of the nerve fiber layer. Such a scattered distribution was maintained as the fibers passed through the optic nerve head and along the optic nerve. There was a rough topographic representation within the optic nerve head according to retinal quadrant such that both peripheral and central fibers were mixed within a wedge extending from the periphery to the center of the nerve. There was no indication that the fibers were reorganized in any way as they passed through the optic disc and into the nerve. The present results suggest that any degree of order present within the fiber layer and optic nerve is not an active process but a passive consequence of combining the fascicles of the retinal nerve fiber layer. Optic axons are not instructed to establish a retinotopic order and the effect of guidance cues in reordering fibers, particularly evident prechiasmatically and postchiasmatically, does not appear to be present within the nerve fiber layer or optic nerve head in humans.

Morphological consequences of myelination in the human retina.

Intraretinal myelination of ganglion cell axons occurs in about 1% of humans and when observed ophthalmoscopically, appears as a white or opaque patch within the fiber layer. Previous studies of myelinated retinal tissue have largely been conducted at the light microscopic level. Three retinae with intraretinal myelination and one normal retina were obtained post-mortem and prepared for electron microscopy. The present study showed that myelinated patches in the human retina contained a mixture of unmyelinated and myelinated axons. Within this population of myelinated axons were structures which were abnormal and there were obvious signs of axonal and myelin sheath degeneration within the myelinated patches. Outside these myelin patches the retina appeared normal without signs of degeneration indicating that post-mortem degeneration prior to fixation could not account for all of the degenerative changes observed. The lack of significant numbers of macrophages and lymphocytes indicated that there was no concomitant inflammatory process within the myelin patches. The myelination present within these eyes appeared to be due to the anomalous location of oligodendrocytes. Both unmyelinated and myelinated axons had larger diameter than axons measured within normal areas of the retina or those within the optic nerve.

Retinotopy of the human retinal nerve fibre layer and optic nerve head.

The organisation of the primate nerve fibre layer and optic nerve head with respect to eccentricity or the positioning of central and peripheral axons remains controversial. Crystals of the carbocyanine dyes DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate), or DiA (4-[4-didecylaminostryryl]-N-methylpridiniumiodide) were used to trace retinal ganglion cell axons within the nerve fibre layer, optic nerve head, and optic nerve. The present study demonstrated that peripheral retinal axons were scattered throughout the vitreal-scleral depth of the nerve fibre layer. This scattered distribution was maintained as the fibres passed through the optic nerve head and into the optic nerve. Axons of the arcuate bundles showed a bias towards the scleral portions of the nerve fibre layer and a variable degree of fibre scatter across the nerve fibre layer which was not as evident in labelling from other retinal regions. There was a rough topographic representation within the optic nerve head according to retinal circumference such that both peripheral and central fibres were mixed within a wedge extending from the periphery to the centre of the nerve. Foveal fibres occupied a large proportion of the temporal aspect of the optic nerve head and nerve, whereas fibres from areas temporal to the fovea appeared to be displaced to more superior and inferior regions. Consistent with the scleral bias seen in the retina, arcuate fibres maintained a peripheral position as they passed through the optic nerve head and occupied a more peripheral position in the nerve. The present results suggest that any degree of order present within the optic nerve is not an active process; optic axons are not instructed to establish a retinotopic order within the initial portions of the visual pathway.

Organization of retinal ganglion cell axons in the optic fiber layer and nerve of fetal ferrets.

Previous authors have hypothesized that retinotopic projections may be influenced by 'preordering' of the axons as they grow towards their targets. In some nonmammalian species, axons are reorganized at or near the optic nerve head to establish a retinotopic order. Data are ambiguous concerning the retinotopy of the mammalian retinal nerve fiber layer and whether fibers become reorganized at the optic nerve head. We have examined this question in fetal and newborn ferrets (Mustela putorius furo) by comparing the arrangement of axons in the retinal nerve fiber layer with that in the optic nerve. Dil or DiA crystals were implanted into fixed tissue in the innermost layers of the retinal periphery, or at a location midway between the periphery and the optic nerve head. Fluorescence labelling was examined in 100-200 microns Vibratome sections, or the eyecup and nerve were photooxidized and 1-2 microns longitudinal or transverse sections were examined. Regardless of fetal age, eccentricity or quadrant of the implant site, a segregation of labelled peripheral axons from unlabelled central ones was not detected within the nerve fiber layer. Axons coursed into the nerve head along the margin of their retinal quadrant of origin, often entering the optic nerve as a radial wedge, thus preserving a rough map of retinal circumference. However, peripheral axons were in no way restricted to the peripheral (nor central) portions of the nerve head or nerve, indicating that the optic axons do not establish a map of retinal eccentricity. Our results demonstrate that (1) the nerve fiber layer is retinotopic only with respect to circumferential position and (2) optic axons are not actively reorganized to establish a retinotopic ordering at the nerve head. The present results suggest that any degree of order present within the optic nerve is a passive consequence of combining the fascicles of the retinal nerve fiber layer; optic axons are not instructed to establish, nor constrained to maintain, a retinotopic order within the optic nerve.

Soma and axon diameter distributions and central projections of ferret retinal ganglion cells.

Using a combination of retrograde horseradish peroxidase (HRP) labelling, silver staining, and electron microscopy, we have assessed the relationship between retinal ganglion cell soma size and axon diameter in the adult ferret (Mustela putorius furo). Retinal ganglion cells were labelled following injections of HRP into the lateral geniculate nucleus (LGN), superior colliculus (SC), or LGN+SC. The soma size distributions following LGN, SC, or LGN+SC injections were all unimodal showing considerable overlap between different cell classes. This was confirmed for alpha cells identified on the basis of dendritic filling or from neurofibrillar-stained retinae. Analysis of the soma size and axon diameters of a population of heavily labelled retinal ganglion cells showed a significant correlation between the two. However, the overall distribution of intraretinal axon diameter was bimodal with an extended tail. Analysis of the ganglion cell distributions in the adult ferret indicates that beta cells comprise about 50.5-55%, gamma 42.5-47%, and alpha 2.5% of the ganglion cell population. This implies that the proportion of gamma, beta, alpha cells in both cat and ferret retina is highly conserved despite differences in visual specialization in the two species.

Connections between the reticular nucleus of the thalamus and pulvinar-lateralis posterior complex: a WGA-HRP study.

The present study utilises the capacity of wheat germ agglutinin-conjugated horseradish peroxidase to label both afferent and efferent projections from selected regions of the thalamic reticular nucleus (TRN) to the pulvinar lateralis-posterior complex (Pul-LP) of the cat. Fourteen injections into the TRN located between anterior-posterior levels 8.5 and 4.5 were analysed. The projection of the TRN to the Pul-LP complex is roughly organised in a topographic manner and is not widespread within the thalamus. Anterograde labelling in the Pul-LP extended rostrocaudally with a slight oblique dorsoventral orientation. Projections to the medial LP were predominantly but not exclusively from rostral areas of TRN, while projections to the lateral LP were largely from caudal areas of the TRN. Projections to other areas of the Pul-LP were sparse. The connections between TRN and Pul-LP were reciprocal, although the distribution of labelled cells and anterograde labelling was not completely overlapping. Reciprocal connections with the dorsal lateral geniculate nucleus were largely with the C-laminae and the medial interlaminar nucleus. The results are discussed with reference to the corticothalamic projections and the visuotopy of the Pul-LP.

Photic responses of the lateral geniculate nucleus can be used as a stereotaxic guide for micropipette placement.

Neuroanatomical studies of the cat's thalamus require accurate placement of a micropipette for tracer injections. In order to determine interanimal differences, we describe a simple method which compares the location of the different laminae of the dorsal lateral geniculate nucleus (LGNd) with a stereotaxic atlas. The visual electrophysiological response to a flash was recorded from the LGNd with an enamelled stainless-steel electrode. The response steadily increased in amplitude through the optic radiation, lamina A and lamina A1. Further penetration through the LGNd resulted in the reversal of the recorded potential. The reversal point was lesioned and found to lie between lamina A1 and lamina C. Based on the dorsal level of laminae A, A1 and C as determined by the reversal point, these estimates of LGNd location can be compared with a stereotaxic atlas and corrections made to subsequent placement of micropipettes used for injections in other thalamic structures.

Rostral reticular nucleus of the thalamus sends a patchy projection to the pulvinar lateralis-posterior complex of the cat.

The pulvinar lateralis posterior complex (Pul-LP) and the reticular nucleus of the thalamus (RE) are thought to be involved in visual and attention-related tasks. This report provides data on the anatomical connections between these two nuclei following the analysis of injections of horseradish peroxidase (HRP) + [3H]leucine into the Pul-LP and RE of the cat. Following the retrograde transport of HRP from the Pul-LP, labeled cells were distributed in regions of the RE ventral to the caudate nucleus and adjacent to the stria terminalis between Horsley-Clarke anterior-posterior (AP) coordinates 13.0 and 9.5 and more caudally in areas dorsal and ventral to the lateral geniculate nucleus (LGN) between AP 9.0 and 4.5. The majority of the cell labeling within the RE following injections within the Pul-LP was seen dorsal to the lateral geniculate nucleus around AP 6.5-6.0. Cell labeling was heaviest following injections within the lateral LP in contrast to injections within the Pul which resulted in fewer labeled cells. Autoradiographic analysis of the anterograde transport of leucine showed that the labeled Pul-LP fibers within the RE did not completely coincide with the distribution of HRP-labeled reticular cells from the same injection site. This indicated a lack of strict reciprocity between these two nuclei. In addition, injections of [3H]leucine into dorsomedial areas of the RE near the rostral pole of the LGN resulted in a patchy distribution of label within the Pul-LP which was most prominent as oblique dorsoventral slabs across the thalamus. It was inferred that this distribution was along the borders between different subdivisions within the Pul-LP. The lack of strict reciprocity between the thalamic relay nuclei and the reticular nucleus implies that areas of the Pul-LP may receive inhibition from RE regions which they do not directly influence; this anatomical feature may provide a basis for selective inhibition of thalamic nuclei.