Differential synaptic vesicle protein expression in the barrel field of developing cortex

The distribution of four proteins associated with synaptic vesicles, SV2, synaptophysin, synapsin I, and rab3a, was investigated during postnatal development of the posteromedial barrel subfield (PMBSF) in the rat somatosensory cortex. A distinct progression in the appearance of the different synaptic vesicle proteins within the PMBSF was observed. SV2, synapsin I, and synaptophysin revealed the organization of the barrel field in the neonate. This early demarcation of the cortical representation of the vibrissal array coincides with the earliest known age for the emergence of the cytoarchitectonic organization of this region. In contrast, rab3a did not delimit the barrels until the end of the 1st postnatal week, coincident with the known onset of adult-like physiological activity and the loss of plasticity in afferents to this region. In addition, the appearance of the different synaptic vesicle proteins occurred earlier within the PMBSF than in the adjacent extra-barrel regions of the cortex. These results show that the molecular differentiation of synaptic fields across the cortex is not a homogeneous and synchronous process in terms of synaptic vesicle protein expression. Because these proteins act together in mature synapses to ensure the regulated release of neurotransmitters, our results suggest that this temporo-spatial asynchrony may underlie different potentials for synaptic activity and thus contribute to the development of cortical maps. © 1996 Wiley-Liss, Inc.     

Distribution of a Brain-specific Proteoglycan, Neurocan, and the Corresponding mRNA During the Formation of Barrels in the Rat Somatosensory Cortex

Neurocan is a developmentally regulated chondroitin sulphate proteoglycan in the rat brain. In the present study, spatiotemporal patterns of expression of neurocan and the corresponding mRNA were examined in the developing cortical barrel field of the rat brain by using a monoclonal antibody that was highly specific to neurocan and a riboprobe for a portion of the mRNA. Immunohistochemical analysis revealed that neurocan was distributed throughout the cerebral cortex during early postnatal development but was excluded from the centres of cortical barrels at the time of entry and arborization of thalamocortical axons. At this developmental stage, expression of neurocan mRNA was shown by in situ hybridization to be down-regulated in the barrel centres. When a row of whisker follicles was laser-cauterized on postnatal day 1, the pattern of expression of neurocan was disturbed in the row of barrels that corresponded to the lesioned whisker follicles in the contralateral somatosensory cortex. From these observations, it appears that neuronal stimuli through early thalamocortical fibres from the sensory periphery cause reduced expression of neurocan mRNA in neurocan-producing cells in the presumptive barrel centres. Our findings also suggest that the pattern of distribution of neurocan in early postnatal barrel fields may be due mainly to the down-regulation of expression of neurocan mRNA.     

Effects of monoamine oxidase A inhibition on barrel formation in the mouse somatosensory cortex: Determination of a sensitive developmental period

Genetic inactivation of monoamine oxidase A (MAOA) in C3H/HeJ mice causes a complete absence of barrels in the somatosensory cortex, and similar alterations are caused by pharmacological inhibition of MAOA in wild type mice. To determine when and how MAOA inhibition affects the development of the barrel field, the MAOA inhibitor clorgyline was administered to mice of the outbred strain OF1 for various time periods between embryonic day 15 (E15) and postnatal day 7 (P7), and the barrel fields were analyzed with cytochrome oxidase and Nissl stains in P10 and adult mice. High-pressure liquid chromatography measures of brain serotonin (5-HT) showed three- to eightfold increases during the periods of clorgyline administration. Perinatal mortality was increased and weight gain was slowed between P3 and P6. Clorgyline treatments from E15 to P7 or from P0 to P7 disrupted the formation of barrels in the anterior snout representation and in parts of the posteromedial barrel subfield (PMBSF). Treatments from P0 to P4 caused similar although less severe barrel field alterations. Clorgyline treatments only during embryonic life or starting on P4 caused no detectable abnormalities. In cases with barrel field alterations, a rostral-to-caudal gradient of changes was noted: Rostral barrels of the PMBSF were most frequently fused and displayed an increased size tangentially. Thus, MAOA inhibition resulting in increased brain levels of 5-HT affects barrel development during the entire first postnatal week, with a sensitive period between P0 and P4. The rostral-to-caudal gradient of changes in the barrel field parallels known developmental gradients in the sensory periphery and in the maturation thalamocortical afferents. The observed barrel fusions could correspond to a default in the initial segregation of thalamic fibers or to a continued, exuberant growth of these fibers that overrides the tangential domain that is normally devoted to individual whiskers. J. Comp. Neurol. 393:169–184, 1998. © 1998 Wiley-Liss, Inc.     

Bilateral whisker trimming during early postnatal life impairs dendritic spine development in the mouse somatosensory barrel cortex

The rodent somatosensory barrel cortex is an ideal model for studying the impact of sensory experience on developing brain circuitry. To examine whether and how interference with sensory perception in the early postnatal period can affect the development of synaptic networks in this system, we took advantage of a transgenic mouse strain expressing the yellow fluorescent protein in layer 5B pyramidal neurons of the somatosensory cortex. By using ex vivo confocal imaging, we first demonstrate a cortical‐layer‐specific increase in the number of dendritic spines during postnatal development on apical dendritic shafts of these cells extending up to cortical layer 1. Next, by performing bilateral whisker trimming at distinct developmental stages, we show that disruption of sensory perception before postnatal day 20 impairs dendritic spine development in apical dendritic segments within layers 1 and 2/3 but not in layer 4. The whisker trimming‐induced decrease in dendritic spine density during this period is accompanied by a highly significant decrease in dendritic spine head diameter. Finally, we also show that these whisker trimming‐induced morphological alterations of dendritic spines during the early postnatal period are no longer detectable in adult animals. Altogether, these findings further emphasize the important role of sensory activity in synaptic network assembly in the developing barrel cortex. They also support an as yet unidentified structural mechanism that might contribute to the layer‐ and cell‐type‐specific physiological effects of whisker trimming during the early postnatal period. J. Comp. Neurol. 518:1711–1723, 2010. © 2009 Wiley‐Liss, Inc.     

Lectins demarcate the barrel subfield in the somatosensory cortex of the early postnatal mouse

Plant lectins were used to examine the disposition of glycosylated molecules in vibratome sections through the barrel subfield of mouse somatosensory cortex at selected times during postnatal development. The peroxidase conjugates of peanut agglutinin (PNA, specific for N-acetylgalactosamine), concanavalin A (specific for mannose), and wheat germ agglutinin (specific for N-acetylglucosamine and N-acetylneuraminic acid) were used to study lectin binding in aldehyde-fixed tissue sections of cortex. Following peroxidase cytochemistry and light microscopy, it was found that all three lectins bound in the region of the barrel subfield as early as postnatal day 3 (day of birth = postnatal day 1). The lectins bound to the prospective sides and/or septae of individual barrels in preference to the prospective hollows. This lectin demarcation of the barrel field occurred prior to the detection of this region with cresyl violet staining and was still demonstrable on postnatal day 6, when the individual barrels became discernible with cresyl violet. This suggests that the lectin binding material is present before the barrel field becomes a fully formed and organized region. A decrease in lectin affinity for binding sites in these tissue sections occurs during postnatal development (Cooper and Steindler: Soc. Neurosci. (Abstr.) 10: 43a, '84) and this study demonstrates that lectins do not delineate the barrel field of more mature animals (2-3 months old), whereas barrels can be detected with cresyl violet at this time. A preliminary electron microscope analysis of the postnatal day 6 somatosensory cortex demonstrates that the lectin PNA binds to elements of the forming neuropil and also to Golgi apparatus intermediate saccules in neuronal cells. The prospective barrel field can be detected with lectins during a critical period in development in which alterations can occur in the barrel field in response to peripheral deprivation (Jeanmonod et al: Neuroscience 6:1503-35, '81) and therefore we suggest that the glycans visualized with lectin-peroxidase conjugates denote possible candidates for molecules involved in shaping barrel structure.     

Abnormal glial and glycoconjugate dispositions in the somatosensory cortical barrel field of the early postnatal reeler mutant mouse

During early postnatal development in reeler mutant mice, lectin binding delineates prospective abnormal barrels as they will appear in the adult mutant somatosensory cortex. Glial fibers also may be more condensed within fascicles in developing reeler barrels. These fibers also appear to be misaligned, coursing predominantly in the tangential plane within the abnormal reeler barrel sides as opposed to having a radial orientation as seen in normal mouse barrels. The thalamic barreloid complex, however, reveals a disposition of glycoconjugates that is completely normal in reeler. Thus, there are anomalies in glia and associated glycoconjugates during mainly cortical development in the reeler mutant mouse that might be related to the primary action of the abnormal gene.     

The ontogeny of the distribution of callosal projection neurons in the rat parietal cortex

The ontogeny of callosal projection neurons in the rat parietal cortex was examined using the retrograde and anterograde transport of horseradish peroxidase (HRP), as well as Golgi and Nissl stains. From postnatal day 0 (PND 0) to early PND 4, the callosal projection neurons are distributed as two continuous horizontal bands of cells which extend throughout the subplate in layers Va and Vc-upper VIa. Neurons within the cortical plate (CP), however, do not transport HRP from a contralateral injection site until PND 3 to early PND 4, when a few cells at the lower CP border are generally labeled. However, by late on PND 4, and more consistently by PND 5, several changes in the distribution of callosal projection neurons take place. First, cells at all levels of the CP become labeled in a sequential fashion, from the lower border upward. Second, gaps, or areas devoid of HRP, become apparent in layer IV of the barrel field area. Third, in the cortical areas containing the gaps, as well as in other areas which are destined not to be callosally connected in the adult, there is a noticeable decrease in the number of cells labeled with HRP. This decrease continues through PND 15 and possibly into adulthood. The foregoing developmental events are compared to cortical maturation as seen in both Golgi- and Nissl-stained material. By PND 15, the basic adult pattern of callosal projection neurons is established. The neurons reside mainly in layers III and Va, with fewer in layers II and Vc-upper VIa, and fewer still in the other cortical layers. They are aligned in vertical arrays in discrete areas of the cortex.     

Spatiotemporal distribution of proteoglycans in the developing rat's barrel field and the effects of early deafferentation

The isolectin Vicia villosa B(4) (VV) selectively recognizes N-acetyl-galactosamine-terminal glycoconjugates that form perineuronal nets (PNNs) around a subset of neurons in the cerebral cortex. PNNs are thought to participate in the guidance of incoming thalamic axons and in the posterior stabilization and maintenance of synaptic contacts. Here we examine the spatial and temporal distribution of biotinylated VV in tangential sections through layer IV of the posteromedial barrel subfield in the primary somatosensory cortex (PMBSF) of rats ranging from postnatal day (P)3 to P60, which underwent unilateral deafferentation of whiskers at birth. In the afferented hemisphere, labeling first appears at P5, with a diffuse distribution, probably associated with neuropil, inside PMBSF barrels. VV distribution remains diffuse during the following week, and declines around P17. From P24 onward, however, proteoglycans form PNNs around cell bodies preferentially localized in septal regions of the PMBSF. In the contralateral, deafferented PMBSF the diffuse labeling also appears on P5, but first develops into elongated, homogeneous stripes, which disappear after P24, leaving only scattered cell bodies along layer IV. Our results indicate that proteoglycans appear simultaneous to barrel formation in the developing rat while segregation of PNNs to septal cells might be driven by afferent activity.     

Distribution of synaptic zinc in the developing mouse somatosensory barrel cortex

Histochemical localization of synaptic zinc was examined in the somatosensory (SI) barrel cortex of mouse. The laminar distribution and distribution within the barrel field were described. At postnatal day 3 (P3) and 5 (P5), very faint and uniform zinc staining was present in the lower part of the subplate. At P6, subtle laminar variations emerged. At P8, these variations were clearly observed. Intense zinc staining was found in layers I, II, III, and V. Layers IV and VI showed a weaker staining. From this postnatal age to adult, uneven patchy distribution of synaptic zinc in layer IV could be distinguished in coronal sections. In tangential sections through layer IV, zinc staining showed a barrel-like pattern due to a higher zinc concentration in septa and the surrounding cortex. Barrel sides revealed a lower zinc concentration compared with the barrel hollow. With brain maturation, the zinc staining increased more intensely outside the barrel field, thus producing a progressively higher contrast between the barrel field and adjacent cortical regions. The differences in zinc staining between the barrel side and barrel hollow diminished with age but were still visible at P70. The changes in synaptic zinc distribution probably reflect the process of synaptic maturation of glutamatergic terminals projecting to the SI cortex. The time course of postnatal changes in terminal zinc distribution suggests that synaptic zinc is not involved in the mechanisms of barrel formation. J. Comp. Neurol. 386:652–660, 1997. © 1997 Wiley-Liss, Inc.     

Effects of prenatal alcohol exposure on the development of the vibrissal somatosensory cortical barrel network

We have previously shown that the serotonin (5-HT) and its thalamocortical afferents are compromised by prenatal alcohol exposure (PAE). The development of the sensory cortical barrels is regulated by 5-HT-rich thalamocortical afferents. Therefore, it is hypothesized that PAE will deleteriously affect the postnatal development of the cortical barrel formations. On embryonic day (E)7, C57BL/6 mice were grouped into: Alcohol (Alc), Pair-fed (PF), or Chow, and maintained on diet until E18. On postnatal day 7, cortices were stained with 5-HT for thalamocortical fibers, and a NeuN for identification of mature neurons. The area of the posterior medial barrel subfield (PMBSF), was measured as well as the number of NeuN+ neurons within the barrel patches. Though brain weight and brain volume were similar among the three groups, a significant reduction was seen in total area of the PMBSF, and in the average individual barrel area in the Alc group as compared to Chow. Furthermore, the volumes of the B, but not C row barrels were significantly reduced. Barrels were found missing in layer IV, specifically in the posterior aspects of the A, B, and straddler row in the Alc group. Cell counts demonstrated a nearly 50% reduction in NeuN+ neuron number in both rows. This reduction in size of the PMBSF and fewer neurons within these sensory barreloids may underlie a change in the development of the discriminatory sensitivity of the whiskers and serves as an excellent model for the study of a compromised sensory modality following PAE.     

Cell type specific impact of cannabinoid receptor signaling in somatosensory barrel map formation in mice

Endocannabinoids and their receptors are highly abundant in the developing cerebral cortex and play major roles in early developmental processes, for example, neuronal proliferation, migration, and axonal guidance as well as postnatal plasticity. To investigate the role of the cannabinoid type 1 receptor (CB1) in the formation of sensory maps in the cerebral cortex, the topographic representation of the whiskers in the primary somatosensory cortex (barrel field) of adult mice with different cell type specific genetic deletion of CB1 was studied. A constitutive absence of CB1 (CB1-KO) significantly decreased the total area of the somatosensory cortical map, affecting barrel, and septal areas. Cell specific CB1 deletion in dorsal telencephalic glutamatergic neurons only (Glu-CB1-KO) or in both glutamatergic and forebrain GABAergic neurons (Glu/GABA-CB1-KO) resulted in an increased septa area in the barrel field map. No significant modifications in area parameters could be observed in GABA-CB1-KO mice. These data demonstrate that CB1 signaling especially in cortical glutamatergic neurons is essential for the development of topographic maps in the cerebral cortex.     

Monoaminergic afferents to cortex modulate structural plasticity in the barrelfield of the mouse

Electrolytic lesions of the follicles of a set of mystacial vibrissae, and their innervation, of the mouse placed during the early postnatal period result in a modification in appearance of the corresponding and of adjacent barrels in the somatosensory cortex of the adult animal. These changes can be evoked during the first 6 days of postnatal life — the so-called critical period. The pattern of these modifications varies with the age of the animal at which the lesion was placed. In order to evaluate the contribution of the monoaminergic cortical input to this type of plasticity, the noradrenergic and/or serotonergic afferents to the cerebral cortex of newborn mice were destroyed by systemic administration of various selective neurotoxic drugs (6-hydroxydopamine, 5,7-dihydroxytryptamine, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine). The animals were then subjected, on postnatal day 3 (P3; PO = day of birth), to a lesion of the follicles of the large, caudal mystacial vibrissae of row C. Control animals were injected with vehicle solution only but had the same follicles lesioned. Compared with animals with intact monoaminergic afferents, those treated with neurotoxins showed a different changed barrel pattern, i.e. one that corresponded to a pattern normally obtained after a lesion placed at an earlier stage of development, i.e. at P2 or P1. Thus, monoaminergic depletion of the cortex results in a retardation of the maturation of the parietal cortex as defined by its plastic response to peripheral nerve injury. Interestingly, a peripheral lesion at P4 yields barrel patterns in monoamine deprived mice similar to those in controls, as if monoamines at that stage play no longer a role in this form of brain plasticity.     

Cortical modules in the posteromedial barrel subfield (Sml) of the mouse

An antibody to MAP2 was used on sections through the posteromedial barrel subfield (PMBSF) of primary somatosensory cortex to reveal the distributions of cell bodies and dendrites. It was found that apical dendrites of layer VI neurons form irregular bundles or sheets that break up in layer IV, where most of these dendrites form their terminal tufts. In contrast, the apical dendrites of layer V pyramidal neurons form clusters that ascend into layer II/III where they are joined by apical dendrites of the superficial pyramidal neurons. In layer IV the clusters of the layer V apical dendrites are more concentrated in barrel walls than in hollows. Thus, in layer IV the average center to center spacing between the clusters is about 25 m?m in the barrel hollows, and about 22 m?m in the barrel walls. In part, this differential distribution of the apical dendritic clusters is brought about because the apical dendrites of layer V pyramids beneath the periphery of the barrel hollows arc towards the barrel walls as they pass from layer V into layer IV. Based on previous analyses of the three-dimensional organization of the primary visual areas in the monkey, cat, and rat, it has been proposed that neurons in these cortices are organized into modules that are centered on the clusters of apical dendrites belonging to layer V pyramidal neurons. Mouse PMBSF cortex is composed of similar pyramidal cell modules and the organization of neurons in these modules is similar to that in visual cortex. This suggests that the pyramidal cell modules are fundamental neuronal units that exist throughout the cerebral cortex, and implies that the various functional areas of the cortex in different species are organized according to a common, basic plan. © 1993 Wiley-Liss, Inc.     

Histogenesis of ferret somatosensory cortex

The ferret has emerged as an important animal model for the study of neocortical development. Although detailed studies of the birthdates of neurons populating the ferret visual cortex are available, the birthdates of neurons that reside in somatosensory cortex have not been determined. The current study used bromodeoxyuridine to establish when neurons inhabiting the somatosensory cortex are generated in the ferret; some animals also received injections of [³H]thymidine. In contrast to reports of neurogenesis in ferret visual cortex, most neurons populating the somatosensory cortex have been generated by birth. Although components of all somatosensory cortical layers have been produced at postnatal day 0, the layers are not distinctly formed but develop over a period of several weeks. A small number of neurons continue to be produced for a few days postnatally. The majority of cells belonging to a given layer are born over a period of approximately 3 days, although the subplate and last (layer 2) generated layer take somewhat longer. Although neurogenesis of the neocortex begins along a similar time line for visual and somatosensory cortex, the neurons populating the visual cortex lag substantially during the generation of layer 4, which takes more than 1 week for ferret visual cortex. Layer formation in ferret somatosensory cortex follows many established principles of cortical neurogenesis, such as the well-known inside-out development of cortical layers and the rostro-to-caudal progression of cell birth. In comparison with the development of ferret visual cortex, however, the generation of the somatosensory cortex occurs remarkably early and may reflect distinct differences in mechanisms of development between the two sensory areas. J. Comp. Neurol. 387:179–193, 1997. © 1997 Wiley-Liss, Inc.     

Differential effects of methylmercury intoxication in the rat's barrel field as evidenced by NADPH diaphorase histochemistry

In the present study, we investigated the effects of mercury intoxication on the structure of the posteromedial barrel subfield (PMBSF) in the primary somatosensory cortex (SI) of adult rats, as revealed by histochemical reactivity to the enzyme NADPH diaphorase (NADPH-d). Enzymatic reactivity in the neuropil inside barrels was drastically reduced in intoxicated animals, suggesting that the synthesis and/or transport of the nitric oxide synthase enzyme can be altered in acute mercury intoxication. However, the cell bodies and dendrites of barrel neurons, also strongly reactive to the enzyme, were spared from the mercury's deleterious effects.     

Distribution of GABA(B) receptor protein in somatosensory cortex and thalamus of adult rats and during postnatal development

In the present study we report the immunolocalisation of gamma-aminobutyric acid (GABA)(B) receptors within the cerebral somatosensory cortex (S1) and thalamus of adult and young (1-22 postnatal days) rats. The antibody used recognises a peptide in the carboxy-terminal domain and therefore did not distinguish between the different isoforms GABA(B)1a or GABA(B)1b. The results showed that GABA(B) receptor protein was widely distributed in the brain of both adult and young rats, with different degrees of labelling in separate cerebral nuclei. Antibody labelling was localised both on cells and the neuropil. In the cerebral cortex of adult animals the highest immunolabelling was evident in layers V and VIb, although immunoreactivity was also present in the superficial layers. The strongest signal was evident in the medial habenula.The thalamus showed labelling in the reticular, ventrobasal and geniculate nuclei. In the first postnatal days GABA(B) expression was evident in the cortical cells of layer V, VIb and in the cortical plate. The pattern of labelling in the cerebral cortex of young rats became indistinguishable from that of adult rats by day 12. In the thalamus, the main difference compared to the adult pattern was observed in the mediodorsal nucleus which, in early development, showed a high immunosignal, however, by postnatal day 22 the immunoreactivity decreased with only some scattered cells labelled in the adult brain.     

Acute whisker removal reduces neuronal activity in barrels of mouse SmL cortex

The autoradiographic 2-deoxy-D glucose (2-DG) method has been used to map relative changes in metabolic activity in the CNS during various functional states (Plum et al., '76). Here we describe the application of the 2-DG method to assay regional activity in the posteromedial barrel subfield (PMBSF) region of the mouse SmI cortex after acute removal of mystacial vibrissae. One day prior to isotope injection, various combinations of vibrissae (e.g., all vibrissae, row-C only, rows-B and -D only) were plucked from adult male Swiss Webster mice under anesthetic. The next day, 5 muCi of 14C-2-DG were injected into a tail vein, and the mice were allowed to actively explore an empty cage for 45 minutes. The animals were then sacrificed, the brains quickly removed, frozen, and sectioned either parallel or perpendicular to the pia at 80 mum in a cryostat. The sections were mounted, dried on coverslips, and were used to expose X-ray film, after which the sections were stained with thionin and the X-ray film developed. The tissue sections and matching autoradiograms were compared directly from photomicrographs of each. The autoradiograms showed areas of higher activity in barrels for which corresponding vibrissae were present and lower activity in barrels for which appropriate vibrissae were missing. In tangential sections from animals with all vibrissae intact, the PMBSF was uniformly and consistently higher in activity than in cases with all vibrissae missing. The removal of row-C or rows-B and -D resulted in strips of decreased activity in the corresponding PMBSF rows. The same patterns of increased or decreased activity were also seen in sections normal to the pia, but the changes in activity, while greatest in layer IV, extended through all layers of the cortex. Finally, in a number of the autoradiograms, density patterns could be recognized which later were shown to relate directly to sides of individual barrels. The results indicate: (1) Acute removal of the peripheral vibrissal hairs is sufficient to deprive the related contralateral cortical barrel neurons of normal activity. Thus in the mouse somatosensory system it may be possible to determine the relative importance of sensory deprivation and neonatal peripheral lesions in normal cortical development. (2) The barrels are part of a functional cortical columnar organization similar to that in other sensory systems. And, (3) the 14C-2-DG-X-ray technique is sufficiently sensitive to reveal parts of individual barrels in autoradiograms and thus, with some modification, may be suitable for the study of small populations of neurons.     

gamma-Aminobutyric acid (GABA) immunoreactivity in mouse and rat first somatosensory (SI) cortex: description and comparison

The location and morphological characteristics of gamma-aminobutyric acid (GABA)-immunopositive cells and their processes were studied in rat and mouse first somatosensory (SI) cortex (including 'barrels') in layer IV, and layers above (I-III), and below (V and VI). In coronal sections of SI cortex of both species GABA-immunopositive cells and punctate profiles were found in each of layers I-VI. The cells were of various sizes; the largest, located in layers III and V of each species, resemble the large basket cells seen in Golgi-impregnated material. Most of the immunopositive cells were multipolar and circular or ellipsoidal in shape, but occasionally bipolar cells with fusiform perikarya were also seen. In coronal sections, immunopositive cells did not form a characteristic pattern. GABA-immunopositive cells were observed to be most numerous in the supragranular layers whereas GABA-positive punctate profiles were more numerous in layer IV. In tangential sections from layer IV of SI cortex of both species, GABA-immunopositive cells, processes and punctate profiles were visible throughout the entire barrel field. The pattern of distribution of immunopositive cells was similar (a) in two different morphological groups--i.e. the posteromedial barrel subfield (PMBSF) and the anterolateral barrel subfield (ALBSF) in rat barrel field, and (b) in PMBSF barrels of both rat and mouse (excluding differences due to structural dissimilarities between rat and mouse barrels). GABA-immunopositive neurons were grouped mainly in the barrel side and septum and were visible frequently in small clusters. In barrels of both species GABA-immunopositive cells were of a variety of sizes and ranged in shape from ellipsoidal to circular.     

Critical period-dependent alterations of the transient body image in the rodent cerebral cortex

The present study demonstrates that the boundary patterns of cell surface-associated molecules detected with lectins in the barrel cortex of neonatal rodents are altered, as are the boundary patterns of cortical glia, following perturbation of large vibrissae in the contralateral mystacial face pad. The alterations in the transiently expressed molecular patterns of lectin-receptors provide data that are consistent with the idea that the periphery plays a prominent role in the establishment of functional cytoarchitecture in the developing cortex. The data are also consistent, however, with the notion that factors intrinsic to the cerebrum, such as the immature cortical glial cells, are of considerable importance in this respect and a direct or indirect interaction of thalamocortical afferents with glial cells in the somatosensory cortex of the neonate are indicated. It is suggested therefore that a critical period in early barrel development, a time in which the cortical neuronal architecture is malleable in response to altered afferent input, is directly related to the presence of these cellular and molecular boundaries. The transient barrel boundaries, it is argued, are the morphological and molecular substrates that form the physical basis of the critical period.     

Development of cairetinin immunoreactivity in the neocortex of the rat

The prenatal and postnatal development of calretinin (CR)-containing elements in the neocortex of the rat was analyzed using immunohistochemistry. CR immunoreactivity in the cortical anlage appeared early at embryonic day 14 (E14), with CR-positive neurons located in the primitive plexiform layer and in the emerging subplate and marginal zones. At later prenatal and early postnatal stages, these two layers showed the highest CR immunostaining in the cortex, and large numbers of cell bodies and fibers were immunostained. From postnatal day 3 (P3) onwards, CR immunostaining disappeared progressively from the subplate-layer VIb and the marginal zone-layer I, so that very few cells remained stained in these layers in the adult. In the cortical plate and prospective layers VIa to II–III, CR-positive neurons were seen at prenatal stages, their numbers increasing markedly during the first postnatal week. Most neurons showed undifferentiated nonpyramidal shapes, and matured during the second and third postnatal weeks, when the adult pattern of CR immunostaining was achieved. In addition, some pyramidal-like neurons in the infragranular layers and in layer II–III transiently expressed CR during the postnatal period, most notably between P3 and P12. Colocalization experiments performed at P0–P3 with antibodies against the neurotransmitter γ-aminobutyricacid (GABA) showed that most nonpyramidal CR-positive neurons in the derivates of the cortical plate were also GABAergic during development. In contrast, large numbers of CR-containing neurons in the subplate and marginal zone were GABA-negative. The present results show that in addition to recording the early development of a subset of nonpyramidal neurons, CR is transiently expressed in certain GABA-negative populations of the subplate and marginal zone, and most likely in pyramidal neurons. © 1995 Wiley-Liss, Inc.