Differential expression of c-fos in subtypes of GABAergic cells following sensory stimulation in the cat primary visual cortex

Recent immunocytochemical stainings on cat visual cortex, visually stimulated for 1 h, showed a strong induction of Fos expression in cortical neurons. We initiated immunocytochemical double staining experiments with different cytochemical markers to investigate the neurochemical and morphological character of these activated neurons showing Fos induction after sensory stimulation. Double staining with Fos and glutamic acid decarboxylase (GAD) demonstrated the presence of Fos in the nuclei of GABAergic neurons of the primary visual cortex. To further subdivide this Fos/GABAergic cell population we investigated whether Fos colocalized with parvalbumin, calbindin or calretinin. Colocalization of Fos with these calcium-binding proteins delineated distinct neuronal subclasses of Fos-immunoreactive neurons in supra- and infragranular layers of cat area 17. Quantitative analysis of the proportion of immunoreactive local circuit neurons revealed that 35% of the GABAergic neurons showed Fos induction in supragranular layers, whereas in infragranular layers a mere 10% of the GABAergic cells revealed Fos expression. Fos coexisted in about 24% of the calbindin-immunopositive cells within supra- and infragranular layers, but only a minority of the parvalbumin and the calretinin neuronal subgroups were immunopositive for Fos in the corresponding layers of area 17. These findings suggest that visual stimulation induces Fos expression in distinct subsets of inhibitory neurons in cat primary visual cortex.     

A neurochemical signature of visual recovery after extrastriate cortical damage in the adult cat

In adult cats, damage to the extrastriate visual cortex on the banks of the lateral suprasylvian (LS) sulcus causes severe deficits in motion perception that can recover as a result of intensive direction discrimination training. The fact that recovery is restricted to trained visual field locations suggests that the neural circuitry of early visual cortical areas, with their tighter retinotopy, may play an important role in attaining perceptual improvements after damage to higher level visual cortex. The present study tests this hypothesis by comparing the manner in which excitatory and inhibitory components of the supragranular circuitry in an early visual cortical area (area 18) are affected by LS lesions and postlesion training. First, the proportion of LS-projecting pyramidal cells as well as calbindin- and parvalbumin-positive interneurons expressing each of the four AMPA receptor subunits was estimated in layers II and III of area 18 in intact animals. The degree to which LS lesions and visual retraining altered these expression patterns was then assessed. Both LS-projecting pyramidal cells and inhibitory interneurons exhibited long-term, differential reductions in the expression of glutamate receptor (GluR)1, -2, -2/3, and -4 following LS lesions. Intensive visual training post lesion restored normal AMPAR subunit expression in all three cell-types examined. Furthermore, for LS-projecting and calbindin-positive neurons, this restoration occurred only in portions of the ipsi-lesional area 18 representing trained visual field locations. This supports our hypothesis that stimulation of early visual cortical areas-in this case, area 18-by training is an important factor in restoring visual perception after permanent damage to LS cortex.     

Inhibitory networks in epilepsy-associated gangliogliomas and in the perilesional epileptic cortex

Developmental glioneuronal lesions, such as gangliogliomas (GG) are increasingly recognized causes of chronic pharmaco-resistant epilepsy. It has been postulated that chronic epilepsy in patients with malformations of cortical development is associated with dysfunction of the inhibitory GABA-ergic system. We aimed to identify the subtypes of interneurons present within GG specimens and the expression and cellular distribution patterns of GABA receptors (GABAR) and GABA transporter 1 (GAT1). The expression of the various components of the GABA-ergic system were also analyzed in the perilesional cortex. We investigated the expression of parvalbumin, calbindin, calretinin, GABA(A)R (a1 subunit)(,) GABA(B) (R1 and R2) and GAT-1 using immunocytochemistry in 30 specimens of GG obtained during epilepsy surgery, including 10 cases with sufficient amount of perilesional cortex. Immunocytochemistry for calbindin (CB), calretinin (CR) and parvalbumin (PV) demonstrate the presence of inhibitory neurons of different subtypes within the GG specimens. Calcium-binding protein-positive interneurons represent a small fraction of the total neuronal population. Both GABA(A)R and GABA(B)R (R1 and R2) subtypes were detected within the neuronal component of GG specimens. In addition, GABA(B)R2 immunoreactivity (IR) was observed in glial cells. GG specimens displayed also expression of GAT-1 IR. Compared to normal cortex, the density of PV- and CB-immunoreactive interneurons was reduced in the perilesional cortex of GG patients, whereas CR-labeling was similar to that observed in normal cortex. GAT-1 IR was also significantly reduced in the perilesional specimens. The cellular distribution of components of the GABA-ergic system in GG, together with the perilesional changes suggest that alterations of the GABA-ergic system may contribute to the complex abnormal functional network of these highly epileptogenic developmental lesions.     

Visual activity is required to maintain the phenotype of supragranular NPY neurons in rat area 17

Visual activity governs the functional maturation of the mammalian visual cortex. We report here, that visual experience is required for stabilizing the phenotype of a subset of cortical interneurons. Neurons expressing neuropeptide Y mRNA (NPY neurons) display a transiently higher expression in the early postnatal visual areas 18a and 17 that is followed by a phenotype restriction during the second postnatal month: about 50% of the NPY neurons in supragranular and infragranular layers of area 18a, and in infragranular layers of area 17 gradually stop the NPY expression. In contrast, the expression remains unchanged in supragranular layers of area 17. Dark rearing rats from birth to up to 100 days does neither prevent the developmental onset of NPY mRNA expression, nor does it prevent the phenotype restriction from occurring. In contrast, in dark reared animals NPY neurons in supragranular layers of area 17 now also undergo a phenotype restriction. Returning animals to light after variable periods of darkness results in an upregulation of NPY mRNA expression selectively in neurons in supragranular layers of area 17. These neurons acquire a constitutive expression during the second postnatal month. This suggests that the phenotypic specification of a distinct subset of cortical interneurons is regulated by visual experience which thus influences on the maturation of the neurochemical architecture of area 17.     

Development of subpopulations of GABAergic neurons in cat visual cortical areas.

The development of GABAergic interneurons in feline striate area and extrastriate areas was tracked by single and double labeling immunohistochemistry using antibodies to GABA and to molecular markers which identify subpopulations of GABAergic neurons in adult mammalian neocortex; i.e., neuropeptide Y, somatostatin, and the calcium-binding proteins parvalbumin and calbindin. The density of GABA-ir neurons was relatively constant during development and among visual areas. By contrast, most of the GABA-subpopulations increased in the cortex of visual areas during postnatal development, and thus the proportion of GABA-ir neurons which also expressed another molecular marker increased during development. By the end of the first postnatal month, the neurotransmitter phenotypes of the neocortical GABAergic neurons are mature.     

Distribution and morphological characterization of phosphate-activated glutaminase-immunoreactive neurons in cat visual cortex

Phosphate-activated glutaminase (PAG) is the major enzyme involved in the synthesis of the excitatory neurotransmitter glutamate in cortical neurons of the mammalian cerebral cortex. In this study, the distribution and morphology of glutamatergic neurons in cat visual cortex was monitored through immunocytochemistry for PAG. We first determined the specificity of the anti-rat brain PAG polyclonal antibody for cat brain PAG. We then examined the laminar expression profile and the phenotype of PAG-immunopositive neurons in area 17 and 18 of cat visual cortex. Neuronal cell bodies with moderate to intense PAG immunoreactivity were distributed throughout cortical layers II-VI and near the border with the white matter of both visual areas. The largest and most intensely labeled cells were mainly restricted to cortical layers III and V. Careful examination of the typology of PAG-immunoreactive cells based on the size and shape of the cell body together with the dendritic pattern indicated that the vast majority of these cells were pyramidal neurons. However, PAG immunoreactivity was also observed in a paucity of non-pyramidal neurons in cortical layers IV and VI of both visual areas. To further characterize the PAG-immunopositive neuronal population we performed double-stainings between PAG and three calcium-binding proteins, parvalbumin, calbindin and calretinin, to determine whether GABAergic non-pyramidal cells can express PAG, and neurofilament protein, a marker for a subset of pyramidal neurons in mammalian neocortex. We here present PAG as a neurochemical marker to map excitatory cortical neurons that use the amino acid glutamate as their neurotransmitter in cat visual cortex.     

Decrease in parvalbumin-expressing neurons in the hippocampus and increased phencyclidine-induced locomotor activity in the rat methylazoxymethanol (MAM) model of schizophrenia

Treatment of rats with methylazoxymethanol (MAM) on gestational day (GD)17 disrupts corticolimbic development in the offspring (MAM-GD17 rats) and leads to abnormalities in adult MAM-GD17 rats resembling those described in schizophrenic patients. The underlying changes in specific cortical and limbic cell populations remain to be characterised. In schizophrenia, decreases in inhibitory gamma-aminobutyric acid (GABA)-containing interneurons that express the calcium-binding protein parvalbumin have been reported in the prefrontal cortex and hippocampus. In this study we analysed the expression of parvalbumin (PV), calretinin (CR) and calbindin (CB) in the prefrontal cortex and hippocampus of MAM-GD17 rats. Exposure in utero to MAM led to a significant decrease in the number of neurons expressing PV in the hippocampus, but not the prefrontal cortex. Neurons expressing CR or CB were not affected in either structure. The neurochemical changes in MAM-GD17 rats were accompagnied by increased hyperlocomotion after administration of phencyclidine (PCP), analogous to the hypersensitivity of schizophrenic patients to PCP. Therefore, the developmental MAM-GD17 model reproduces key neurochemical and behavioural features that reflect cortical and subcortical dysfunction in schizophrenia, and could be a useful tool in the development of new antipsychotic drugs.     

Connections of the multiple visual cortical areas with the lateral posterior-pulvinar complex and adjacent thalamic nuclei in the cat

The present report describes the patterns of cat thalamocortical interconnections for each of the 13 retinotopically ordered visual areas and additional visual areas for which no retinotopy has yet emerged. Small injections (75 nl) of a mixture of horseradish peroxidase and [3H]leucine were made through a recording pipette at cortical injection sites identified by retinotopic mapping. The patterns of thalamic label show that the lateral posterior-pulvinar complex of the cat is divided into three distinct functional zones, each of which contains a representation of the visual hemifield and shows unique afferent and efferent connectivity patterns. The pulvinar nucleus projects to areas 19, 20a, 20b, 21a, 21b, 5, 7, the splenial visual area, and the cingulate gyrus. The lateral division of the lateral posterior nucleus projects to areas 17, 18, 19, 20a, 20b, 21a, 21b, and the anterior medial (AMLS), posterior medial (PMLS), and ventral (VLS) lateral suprasylvian areas. The medial division of the lateral posterior nucleus projects to areas AMLS, PMLS, VLS, and the anterior lateral (ALLS), posterior lateral (PLLS), dorsal (DLS) lateral suprasylvian areas, and the posterior suprasylvian areas. In addition, many of these visual areas are also interconnected with subdivisions of the dorsal lateral geniculate nucleus (LGd). Every retinotopically ordered cortical area (except ALLS and AMLS) is reciprocally interconnected with the parvocellular C layers of the LGd. The medial intralaminar nucleus of the LGd projects to areas 17, 18, 19, AMLS, and PMLS. Finally, each cortical area (except area 17) receives a projection from thalamic intralaminar nuclei. These results help to define the pathways by which visual information gains access to the vast system of extrastriate cortex in the cat.     

Functional plasticity in extrastriate visual cortex following neonatal visual cortex damage and monocular enucleation

Neonatal lesions of primary visual cortex (areas 17, 18 and 19; VC) in cats lead to significant changes in the organization of visual pathways, including severe retrograde degeneration of retinal ganglion cells of the X/beta class. Cells in posteromedial lateral suprasylvian (PMLS) cortex display plasticity in that they develop normal receptive-field properties despite these changes, but they do not acquire the response properties of striate neurons that were damaged (e.g., high spatial-frequency tuning, low contrast threshold). One possibility is that the loss of X-pathway information, which is thought to underlie striate cortical properties in normal animals, precludes the acquisition of these responses by cells in remaining brain areas following neonatal VC damage. Previously, we have shown that monocular enucleation at the time of VC lesion prevents the X-/beta-cell loss in the remaining eye. The purpose of the present study was to determine whether this sparing of retinal X-cells leads to the development of striate-like response properties in PMLS cortex. We recorded the responses of PMLS neurons to visual stimuli to assess spatial-frequency tuning, spatial resolution, and contrast threshold. Results indicated that some PMLS cells in animals with a neonatal VC lesion and monocular enucleation displayed a preference for higher spatial frequencies, had higher spatial resolution, and had lower contrast thresholds than PMLS cells in cats with VC lesion alone. Taken together, these results suggest that preserving X-pathway input during this critical period leads to the addition of some X-like properties to PMLS visual responses.     

Cortical and brainstem neurons containing calcium-binding proteins in a murine model of Duchenne's muscular dystrophy: selective changes in the sensorimotor cortex

In the muscular dystrophic (mdx) mouse, which is characterized by deficient dystrophin expression and provides a model of Duchenne's muscular dystrophy, we previously demonstrated marked central nervous system alterations and in particular a quantitative reduction of corticospinal and rubrospinal neurons and pathologic changes of these cells. Prompted by these findings and in view of the relations between calcium ions and dystrophin, we analyzed with immunohistochemistry the neurons containing the calcium-binding proteins parvalbumin, calbindin D28k, and calretinin in cortical areas and brainstem nuclei of mdx mice. In the sensorimotor cortex, parvalbumin-positive and calbindin-positive neurons, which represent a subset of cortical interneurons, were significantly more numerous in mdx mice than in wild-type ones. In addition, the laminar distribution of parvalbumin-positive neurons in the motor and somatosensory cortical areas of mdx mice was altered with respect to wild-type animals. No alterations in the number and distribution were found in the parvalbumin- or calbindin-expressing cell populations of the visual and anterior cingulate cortices of mdx mice. The pattern of calretinin immunoreactivity was normal in all investigated cortical areas. The cell populations containing either calcium-binding protein were similar in brainstem nuclei of mdx and wild-type mice. The present findings demonstrated selective changes of subsets of interneurons in the motor and somatosensory cortical areas of mdx mice. Therefore, the data showed that, in the cortices of these mutant animals, the previously demonstrated pathologic changes of corticospinal cell populations are accompanied by marked alterations in the local circuitry.     

Neurochemical gradients along monkey sensory cortical pathways: calbindin-immunoreactive pyramidal neurons in layers II and III

We examined the distribution of neurons containing immunoreactivity for three calcium-binding proteins, calbindin, parvalbumin and calretinin, as well as nonphosphorylated neurofilament protein, in cortical areas along the ventral and dorsal cortical visual pathways, and in ventrally-directed somatosensory and auditory cortical pathways. Calbindin-immunoreactive pyramidal neurons showed the most prominent regional differences. They were largely restricted to layers II and III and their number monotonically increased from the primary sensory areas to the anteroventral areas along the ventral visual pathway and along the ventrally-directed somatosensory and auditory pathways. The number of calbindin-immunoreactive pyramidal neurons in layers II and III also increased along the dorsal visual pathway, but the number in the last recognized stage of the dorsal visual pathway (area 7a) was significantly smaller than that at the corresponding stage in the ventral visual pathway (TE). The number of calbindin-immunoreactive pyramidal neurons was highest in layers II and III of areas 35/36, TG, and TF/TH, which represent terminal cortical regions of the pathways. These results show neurochemical differences between cortical areas located at early and late stages along serial corticocortical pathways, as well as confirming differences between pyramidal neurons in the supragranular and infragranular layers.     

Development of inhibitory circuitry in visual and auditory cortex of postnatal ferrets: immunocytochemical localization of calbindin- and parvalbumin-containing neurons

The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is thought to play an important role in activity-dependent stages of brain development. Previous studies have shown that different functional subclasses of cortical GABA-containing neurons can be distinguished by antibodies to the calcium-binding proteins parvalbumin and calbindin. Thus insight into the development of distinct subsets of inhibitory cortical circuits can be gained by studying the development of these calcium-binding protein-containing neurons. Previous studies in several mammalian species have suggested that calcium-binding proteins are upregulated in sensory cortex when thalamocortical afferents arrive. In ferrets, the ingrowth of thalamic axons into cortex occurs well into postnatal development, allowing access to early stages of cortical development and calcium-binding protein expression. We find in ferrets that both parvalbumin- and calbindin-immunoreactivity are present in primary visual and primary auditory cortex long before thalamocortical synapse formation, but that there is a sharp decline in immunoreactivity by postnatal day 20. Day 20 in ferrets corresponds to postnatal day 1 in cats, and thus previous studies in postnatal cats would have missed this early pattern of calcium-binding protein distribution. Another surprising finding is that the proportion of parvalbumin- and calbindin-immunoreactive neurons peaks secondarily late in development, between P60 and adulthood. This result suggests that the parvalbumin- and calbindin-containing subclasses of nonpyramidal neurons remain immature until late in the critical period for cortical plasticity, and that they are positioned to play an important role in experience-dependent modification of cortical circuits.     

Transient Colocalization of Parvalbumin and Calbindin D28k in the Postnatal Cerebral Cortex: Evidence for a Phenotypic Shift in Developing Nonpyramidal Neurons

In the adult rat cerebral cortex the calcium-binding proteins parvalbumin and calbindin D28k are present in essentially non-overlapping populations of GABAergic interneurons. These proteins follow different developmental patterns in the cortex: calbindin D28k-immunoreactive nonpyramidal neurons are abundant until the second postnatal week and decrease markedly thereafter; it is at this time that parvalbumin immunoreactivity develops in cortical nonpyramidal neurons. To determine whether parvalbumin-immunoreactive neurons derive from calbindin D28k-positive cells we used double-immunofluorescence studies for both calcium-binding proteins, together with combined immunocytochemistry for calbindin D28k and in situ hybridization for parvalbumin mRNA during postnatal development. Double-labelled cells were found in all cortical layers between P9 and P21, coinciding with the onset of parvalbumin expression. The percentage of colocalization of the two calcium-binding proteins depended on the age and layer examined. Colocalization reached a peak (80–100%) during the second postnatal week in layers II–IV and VI and decreased thereafter to adult levels by the end of the third postnatal week. Double-labelled neurons were rare in layer V at all ages studied. The present results indicate a phenotypic shift during the development of some cortical interneurons that halts the expression of calbindin D28k while parvalbumin expression starts. These findings agree with lineage analyses reporting that different types of nonpyramidal neuron arise from a common progenitor.     

Cyto- and chemoarchitecture of the cerebral cortex of the Australian echidna (Tachyglossus aculeatus). I. Areal organization

We have examined the topography of the cerebral cortex of the Australian echidna (Tachyglossus aculeatus), using Nissl and myelin staining, immunoreactivity for parvalbumin, calbindin, and nonphosphorylated neurofilament protein (SMI-32 antibody), and histochemistry for acetylcholinesterase (AChE) and NADPH diaphorase. Myelinated fibers terminating in layer IV of the cortex were abundant in the primary sensory cortical areas (areas S1, R, and PV of somatosensory cortex; primary visual cortex) as well as the frontal cortex. Parvalbumin immunoreactivity was particularly intense in the neuropil and somata of somatosensory regions (S1, R, and PV areas) but was poor in motor cortex. Immunoreactivity with the SMI-32 antibody was largely confined to a single sublayer of layer V pyramidal neurons in discrete subregions of the somatosensory, visual, and auditory cortices, as well as a large field in the frontal cortex (Fr1). Surprisingly, SMI-32 neurons were absent from the motor cortex. In AChE preparations, S1, R, V1, and A regions displayed intense reactivity in supragranular layers. Our findings indicate that there is substantial regional differentiation in the expanded frontal cortex of this monotreme. Although we agree with many of the boundaries identified by previous authors in this unusual mammal (Abbie [1940] J. Comp. Neurol. 72:429-467), we present an updated nomenclature for cortical areas that more accurately reflects findings from functional and chemoarchitectural studies.     

Parvalbumin-containing GABAergic interneurons in the rat neostriatum

Antibodies to the intracellular calcium binding protein parvalbumin were shown to label specifically a distinct group of neostriatal GABAergic neurons. These neurons corresponded to the intensely staining subclass of neostriatal GABAergic neurons that have previously been shown to be a class of aspiny interneurons in the neostriatum. The parvalbumin neurons were aspiny neurons with varicose dendrites distributed throughout the neostriatum in a pattern identical to the intensely stained GABA neurons, and both populations of neurons showed increased numbers in the lateral part of the neostriatum. Double labeling of single neurons with both the GABA and parvalbumin antisera showed that all parvalbumin neurons were positive for GABA, but some GABA labelled neurons were not immunoreactive for parvalbumin. These parvalbumin-negative GABAergic neurons were morphologically similar to the spiny projection neurons, which are GABAergic but usually are not so heavily stained. The relationship of the GABA-containing parvalbumin neurons to the striatal mosaic organization was determined by using immunocytochemistry for another calcium binding protein, calbindin D28K, to label the matrix compartment of the striatum. The distribution of parvalbumin-positive neurons relative to the calbindin-positive matrix and calbindin-poor patches was determined by using pairs of adjacent sections stained with the calbindin and parvalbumin antisera. This analysis showed that the somata of the parvalbumin neurons were present in both patch and matrix compartments, and their axons and dendrites crossed the boundaries between compartments. A quantitative analysis of the number of neurons in each compartment revealed that the neurons showed no preferential distribution in either compartment, but instead were present according to the area occupied by that compartment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional influence of areas 17, 18, and 19 on lateral suprasylvian cortex in kittens and adult cats: implications for compensation following early visual cortex damage

The aim of the present study was to investigate the mechanisms of physiological compensation that is seen in the posteromedial lateral suprasylvian (PMLS) cortex of cats that received visual cortex (areas 17, 18, and 19) damage early in life. The strategy was to compare the response properties of PMLS neurons just after visual cortex damage (before any compensation has occurred) with the properties of PMLS neurons in normal cats and cats with long-standing visual cortex damage. Fourteen animals (aged 8 weeks, 18 weeks, 26 weeks, or adult) received a unilateral visual cortex lesion and recordings were made from ipsilateral PMLS cortex within about 24 h. An additional 4 adult cats were studied within either 24 or 3 h of a bilateral visual cortex lesion. Results from these animals were compared with results from normal cats and cats with long-standing visual cortex damage studied previously in this laboratory. At all ages studied, an acute visual cortex lesion reduced the percentage of direction-sensitive cells in PMLS cortex from nearly 80% in normal cats to about 20% after the lesion. In 8- and 18-week-old kittens, nearly all of the remaining PMLS cells responded best to stimulus movement but were not direction sensitive. In 26-week-old and adult cats, the remaining cells were divided between those that responded to movement without a directional preference and those that responded as well to stationary flashed stimuli as to moving stimuli. The presence of receptive-field surround inhibition was not affected significantly by an acute lesion at any age. In addition, few PMLS cells were orientation selective to elongated slits of light in cats with an acute lesion, just as in normal cats. The ocular dominance distributions of PMLS neurons also were normal following an acute visual cortex lesion at all ages studied. These results suggest that the influences of areas 17, 18, and 19 on the response properties of PMLS neurons are the same when the properties first reach maturity as in adult cats. The results also suggest that the mechanisms of physiological compensation for an early visual cortex lesion differ for different response properties. Compensation of direction sensitivity and orientation selectivity (an anomalous property) develops de novo after the early lesion. In contrast, compensation of ocular dominance appears to be due to the maintenance of a preexisting property that is present immediately after the lesion. Thus, plasticity after early visual cortex damage represents multiple developmental changes in the remaining visual pathways.     

Distribution and morphology of area 17 neurons that project to the cat's extrastriate cortex

We used intracellular dye injections in lightly fixed cortical slices to examine the distribution and morphology of area 17 neurons that project to extrastriate cortex. Both the projection to the medial bank of the posterior lateral suprasylvian sulcus (PMLS) and the projection to area 18 arise from a number of different morphological types distributed throughout layers 2-6. The majority are found in the superficial layers and include large, medium, and small pyramidal neurons. Some are also found in the deep layers and they include very large, pyramidal neurons as well as some heretofore undescribed, fusiform neurons. The projection to area 18 contains two types not found in the projection to PMLS: spinous stellate neurons in layer 4 and inverted pyramidal neurons in layer 3. Finding that a variety of morphological types contribute projections to a single cortical area raises the possibility that corticocortical projections, like retinogeniculate and geniculocortical projections, comprise multiple parallel pathways with different physiological properties and patterns of termination. Finding that the projection to area 18 contains morphological types that do not project to PMLS indicates that the projections from area 17 are likely to contribute to the functional specialization of extrastriate visual areas.     

Projections to the visual cortex in the golden hamster.

Retrograde transport of horseradish peroxidase (HRP) was used to determine the origins of afferent connexions to the visual cortex (areas 17, 18a and 18b) in the hamster. The distribution of neurons projecting to the visual cortex from other cortical areas, from the thalamus and from the brainstem was studied using a computer technique for three-dimensional reconstruction. There is a topographically organized projection from the dorsal lateral geniculate nucleus to area 17, but probably to no other of the areas studied. The lateral posterior nucleus of the thalamus (LP) projects to area 18a and weakly to area 17. The lateral nucleus (L) projects to area 18b and also, probably, weakly to area 17. The cortical projections from LP and L are also organized topographically but relatively grossly compared with the geniculo-cortical pathway. There are reciprocal association projections between area 17 and areas 18a and 18b. Areas 18a projects weakly to 18b. The main commissural connexions of the posterior neocortex are between the area 17/18a boundary zones in the two hemispheres, with little between the bodies of area 17. Labelled neurons were found bilaterally in the locus coeruleus, more ipsilaterally than contralaterally, after multiple injections into the visual cortex: single, small injections sometimes resulted in the labelling of a single cell body in the locus coeruleus.     

Cortical areas involved in horizontal OKN in cats: metabolic activity

Cerebral cortex improves optokinetic responses to high target velocities, but the specific cortical areas involved are unknown. Using the 14C-deoxyglucose technique, we compared local rates of cerebral glucose utilization in cats viewing a moving optokinetic nystagmus (OKN) drum (experimental group) with those in cats viewing a stationary OKN drum (control group). In the experimental group, glucose utilization was increased in areas 17 and 18 and in 4 areas in suprasylvian cortex (21a, 21b, PMLS, and VLS). There were no changes in glucose utilization in areas 7, 19, 20a, 20b, ALLS, AMLS, DLS, PLLS, the posterior suprasylvian area, and the splenial visual area. The increases in glucose utilization in areas 17 and 18 were most significant in the granular layers (inner III and IV). In areas 21a, 21b, PMLS, and VLS, the increases in glucose utilization extended from layers II through V. There was also a regional distribution of the increase in glucose utilization within each of these areas in the experimental animals. The increase in glucose utilization did not include the rostral portion of PMLS or the borders between areas PMLS and 21a, and VLS and 21b. In addition, there was a smaller increase in glucose utilization at the borders between areas 17 and 18 than in other portions of these 2 areas. The results indicate that areas 17, 18, 21a, 21b, PMLS, and VLS may be involved in the cortical modulation of horizontal OKN. The laminar distribution of label within the cortical areas corresponds with the distribution of projections from the dorsal lateral geniculate nucleus to areas 17 and 18, and from areas 17 and 18 to PMLS. The regional distribution of the metabolic activity within areas 17, 18, and PMLS coincides with that portion of cortex expected to be excited by either the spatial frequency of the stimulus or the retinalslip velocity (drum velocity minus slow phase eye velocity) occurring during the eye movements.