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Discusses neural connections established in rat visual cortex (VC) and lateral geniculate nucleus (LGN) cultures, isolated in early infancy. The observation of similarities to adult VC indicates that intrinsic mechanisms in VC and LGN may guide the formation of synaptic connections.

Long-term depression (LTD) of synaptic transmission at parallel fiber (PF)-Purkinje cell (PC) synapses plays an important role in cerebellum-related motor coordination and learning. LTD is induced by the conjunction of PF stimulation and climbing fiber (CF) stimulation or somatic PC depolarization, while long-term potentiation (LTP) is induced by PF stimulation alone. Therefore, it is considered that different types of stimulation induce different types of synaptic plasticity. However, we found that a small number of conjunctive stimulations (PF + somatic depolarization of PC) induced LTP, but did not induce LTD of a small size. This LTP was not associated with changes in paired-pulse ratio, suggesting postsynaptic origin. Additionally this LTP was dependent on nitric oxide. This LTP was also induced by a smaller number of physiological conjunctive PF and CF stimuli. These results suggested that a larger number or longer period of conjunctive stimulation is required to induce LTD by overcoming LTP. Ca 2+ transients at the PC dendritic region was measured by calcium imaging during LTD-inducing conjunctive stimulation. Peak amplitude of Ca 2+ transients increased gradually during repetitive conjunctive stimulation. Instantaneous peak amplitude was not different between the early phase and late phase, but the average amplitude was larger in the later phase than in the early phase. These results show that LTD overcomes LTP, and increased Ca 2+ integration or a number of stimulations is required for LTD induction., Competing Interests: Declarations. Ethics Approval: All experiments were approved by the Animal Research Committee of the National Center of Neurology and Psychiatry and in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. Conflict of Interest: The authors declare no competing interests., (© 2024. The Author(s).)

Autism spectrum disorder (ASD) is a multifactorial disorder with characteristic synaptic and gene expression changes. Early intervention during childhood is thought to benefit prognosis. Here, we examined the changes in cortical synaptogenesis, synaptic function, and gene expression from birth to the juvenile stage in a marmoset model of ASD induced by valproic acid (VPA) treatment. Early postnatally, synaptogenesis was reduced in this model, while juvenile-age VPA-treated marmosets showed increased synaptogenesis, similar to observations in human tissue. During infancy, synaptic plasticity transiently increased and was associated with altered vocalization. Synaptogenesis-related genes were downregulated early postnatally. At three months of age, the differentially expressed genes were associated with circuit remodeling, similar to the expression changes observed in humans. In summary, we provide a functional and molecular characterization of a non-human primate model of ASD, highlighting its similarity to features observed in human ASD., (© 2021. The Author(s).)

We present a novel model for timing behavior. This model is based on the firing property of neurons in the superficial layers of the posterior cingulate granular retrosplenial cortex (GRS) and does not require a unit-time clock. Suppose that event B occurs N seconds after event A and triggers behavior C. By our behavioral, physiological and anatomical experiments, we found the following facts. 1) Thalamic input carrying sensory information, A, is provided to the superficial layers of the GRS and delayed by the lateral cascading connection within the layers. 2) Hippocampal input (recall information, B) is provided to the deep layers of the GRS. 3) The GRS neurons show timing behavior that is dependent on the trial cycle. 4) Lesioning the GRS impaired the acquisition of trace fear memory and the production of fear-induced freezing behavior, C. Thus we would propose that neural circuits in the GRS play a crucial role in the animal behaviors requiring time discrimination. The question of whether Hebbian learning occurs at the convergent neurons that integrates thalamic and hippocampal information remains unanswered.

Rodent granular retrosplenial cortex (GRS) has dense connections between the anterior thalamic nuclei (ATN) and hippocampal formation. GRS superficial pyramidal neurons exhibit distinctive late spiking (LS) firing property and form patchy clusters with prominent apical dendritic bundles. The aim of this study was to investigate spatiotemporal dynamics of signal transduction in the GRS induced by ATN afferent stimulation by using fast voltage-sensitive dye imaging in rat brain slices. In coronal slices, layer 1a stimulation, which presumably activated thalamic fibers, evoked propagation of excitatory synaptic signals from layers 2-4 to layers 5-6 in a direction perpendicular to the layer axis, followed by transverse signal propagation within each layer. In the presence of ionotropic glutamate receptor antagonists, inhibitory responses were observed in superficial layers, induced by direct activation of inhibitory interneurons in layer 1. In horizontal slices, excitatory signals in deep layers propagated transversely mainly from posterior to anterior via superficial layers. Cortical inhibitory responses upon layer 1a stimulation in horizontal slices were weaker than those in the coronal slices. Observed differences between coronal and horizontal planes suggest anisotropy of the intracortical circuitry. In conclusion, ATN inputs are processed differently in coronal and horizontal planes of the GRS and then conveyed to other cortical areas. In both planes, GRS superficial layers play an important role in signal propagation, which suggests that superficial neuronal cascade is crucial in the integration of multiple information sources. NEW & NOTEWORTHY Superficial neurons in the rat granular retrosplenial cortex (GRS) show distinctive late-spiking (LS) firing property. However, little is known about spatiotemporal dynamics of signal transduction in the GRS. We demonstrated LS neuron network relaying thalamic inputs to deep layers and anisotropic distribution of inhibition between coronal and horizontal planes. Since deep layers of the GRS receive inputs from the subiculum, GRS circuits may work as an integrator of multiple sources such as sensory and memory information., (Copyright © 2017 the American Physiological Society.)

Background: The brain of the common marmoset (Callithrix jacchus) is becoming a popular non-human primate model in neuroscience research. Because its brain fiber connectivity is still poorly understood, it is necessary to collect and present connection and trajectory data using tracers to establish a marmoset brain connectivity database., New Method: To visualize projections and trajectories of axons, brain section images were reconstructed in 3D by registering them to the corresponding block-face brain images taken during brain sectioning. During preprocessing, autofluorescence of the tissue was reduced by applying independent component analysis to a set of fluorescent images taken using different filters., Results: The method was applied to a marmoset dataset after a tracer had been injected into an auditory belt area to fluorescently label axonal projections. Cortical and subcortical connections were clearly reconstructed in 3D. The registration error was estimated to be smaller than 200 μm. Evaluation tests on ICA-based autofluorescence reduction showed a significant improvement in signal and background separation., Comparison With Existing Methods: Regarding the 3D reconstruction error, the present study shows an accuracy comparable to previous studies using MRI and block-face images. Compared to serial section two-photon tomography, an advantage of the proposed method is that it can be combined with standard histological techniques. The images of differently processed brain sections can be integrated into the original ex vivo brain shape., Conclusions: The proposed method allows creating 3D axonal projection maps overlaid with brain area annotations based on the histological staining results of the same animal., (Copyright © 2017 Elsevier B.V. All rights reserved.)

The rodent granular retrosplenial cortex (GRS) has dense connections with the hippocampal formation and anterior thalamic nuclei. However, functional connectivity within the GRS has not been examined. The aim of this study is to investigate the intracortical circuit of the GRS, including late-spiking (LS) neurons in layers 2 and 3. We conducted extracellular recordings of field potentials from slice preparations of the rat GRS following stimulations of layer 1a and white matter (WM). Current source-density analysis demonstrated that layer 1a stimulation first evoked synaptic current sinks in layer 1 followed by sinks in layers 2-4. These sinks were extinguished by glutamate antagonists. WM stimulation induced long latency synaptic current sinks in layers 2-4 and 6. Thus, signal inputs from the thalamus to layer 1a might be transmitted to layer 5, presumably delayed by LS neurons in layers 2 and 3. According to previous anatomical studies, current sinks in layers 2-4 following WM stimulation were attributed to the horizontal connections of LS neurons. Based on these results we suggest that GRS microcircuitry possibly enables layer 5 neurons to integrate time-delayed thalamic inputs with direct inputs from other brain regions., (Copyright © 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.)

The rodent granular retrosplenial cortex (GRS) is reciprocally connected with the hippocampus. It is part of several networks implicated in spatial learning and memory, and is known to contain head-direction cells. There are, however, few specifics concerning the mechanisms and microcircuitry underlying its involvement in spatial and mnemonic functions. In this report, we set out to characterize intrinsic properties of a distinctive population of small pyramidal neurons in layer 2 of rat GRS. These neurons, as well as those in adjoining layer 3, were found to exhibit a late-spiking (LS) firing property. We established by multiple criteria that the LS property is a consequence of delayed rectifier and A-type potassium channels. These were identified as Kv1.1, Kv1.4 and Kv4.3 by Genechip analysis, in situ hybridization, single-cell reverse transcriptase-polymerase chain reaction, and pharmacological blockade. The LS property might facilitate comparison or integration of synaptic inputs during an interval delay, consistent with the proposed role of the GRS in memory-related processes.

Cadherins, cell adhesion molecules widely expressed in the nervous system, are thought to be involved in synapse formation and function. To explore the role of cadherins in neuronal activity, we performed electrophysiological and morphological analyses of rat hippocampal cultured neurons overexpressing type-II cadherins, such as cadherin-6B and cadherin-7. We found that cadherin-6B increased but cadherin-7 decreased the number of protrusions of dendritic spines, and affected the frequency of miniature excitatory postsynaptic currents. Our results suggest that type-II cadherins may modulate neural activity by regulating neuronal morphology., (2011 Wolters KluwerHealth | Lippincott Williams & Wilkins.)

Using tensile tests, this study investigated differences in the welding strength of casts of cobalt-chromium and gold alloys resulting from changes in the voltage and pulse duration in order to clarify the optimum conditions of laser irradiation for achieving favorable welding strength. Laser irradiation was performed at voltages of 150 V and 170 V with pulse durations of 4, 8, and 12 ms. For cobalt-chromium and gold alloys, it was found that a good welding strength could be achieved using a voltage of 170 V, a pulse duration of 8 ms, and a spot diameter of 0.5 mm. However, when the power density was set higher than this, defects tended to occur, suggesting the need for care when establishing welding conditions.

Background: Since, similarly to humans, songbirds learn their vocalization through imitation during their juvenile stage, they have often been used as model animals to study the mechanisms of human verbal learning. Numerous anatomical and physiological studies have suggested that songbirds have a neural network called 'song system' specialized for vocal learning and production in their brain. However, it still remains unknown what molecular mechanisms regulate their vocal development. It has been suggested that type-II cadherins are involved in synapse formation and function. Previously, we found that type-II cadherin expressions are switched in the robust nucleus of arcopallium from cadherin-7-positive to cadherin-6B-positive during the phase from sensory to sensorimotor learning stage in a songbird, the Bengalese finch. Furthermore, in vitro analysis using cultured rat hippocampal neurons revealed that cadherin-6B enhanced and cadherin-7 suppressed the frequency of miniature excitatory postsynaptic currents via regulating dendritic spine morphology., Methodology/principal Findings: To explore the role of cadherins in vocal development, we performed an in vivo behavioral analysis of cadherin function with lentiviral vectors. Overexpression of cadherin-7 in the juvenile and the adult stages resulted in severe defects in vocal production. In both cases, harmonic sounds typically seen in the adult Bengalese finch songs were particularly affected., Conclusions/significance: Our results suggest that cadherins control vocal production, particularly harmonic sounds, probably by modulating neuronal morphology of the RA nucleus. It appears that the switching of cadherin expressions from sensory to sensorimotor learning stage enhances vocal production ability to make various types of vocalization that is essential for sensorimotor learning in a trial and error manner.

Apical dendritic bundles from pyramidal neurons are a prominent feature of cortical neuropil but with significant area specializations. Here, we investigate mechanisms of bundle formation, focusing on layer (L) 2 bundles in rat granular retrosplenial cortex (GRS), a limbic area implicated in spatial memory. By using microarrays, we first searched for genes highly and specifically expressed in GRS L2 at postnatal day (P) 3 versus GRS L2 at P12 (respectively, before and after bundle formation), versus GRS L5 (at P3), and versus L2 in barrel field cortex (BF) (at P3). Several genes, including neurotrophin-3 (NT-3), were identified as transiently and specifically expressed in GRS L2. Three of these were cloned and confirmed by in situ hybridization. To test that NT-3-mediated events are causally involved in bundle formation, we used in utero electroporation to overexpress NT-3 in other cortical areas. This produced prominent bundles of dendrites originating from L2 neurons in BF, where L2 bundles are normally absent. Intracellular biocytin fills, after physiological recording in vitro, revealed increased dendritic branching in L1 of BF. The controlled ectopic induction of dendritic bundles identifies a new role for NT-3 and a new in vivo model for investigating dendritic bundles and their formation.

Neocortical neuronal circuits are refined by experience during the critical period of early postnatal life. The shift of ocular dominance in the visual cortex following monocular deprivation has been intensively studied to unravel the mechanisms underlying the experience-dependent modification. Synaptic plasticity is considered to be involved in this process. We previously showed in layer 2/3 pyramidal neurons of rat visual cortex that low-frequency stimulation-induced long-term potentiation (LTP) at excitatory synapses, which requires the activation of Ni(2+)-sensitive (R-type or T-type) voltage-gated Ca(2+) channels (VGCCs) for induction, shared a similar age and experience dependence with ocular dominance plasticity. In this study, we examined whether this LTP is involved in ocular dominance plasticity. In visual cortical slices, LTP was blocked by mibefradil, kurtoxin and R-(-)-efonidipine, T-type VGCC blockers, but not by SNX-482, an R-type VGCC blocker, indicating that LTP induction requires T-type VGCC activation. Mibefradil did not affect synaptic transmission even at a dose about 30 times higher than that required for LTP blockade. Therefore, this drug was used to test the effect of T-type VGCC blockade on ocular dominance shift produced by 6 days of monocular deprivation during the critical period using visual evoked potentials (VEPs). Although this monocular deprivation commonly produced both depression of deprived eye responses and potentiation of nondeprived eye responses, only the former change occurred when mibefradil was infused into the visual cortex during monocular deprivation. Mibefradil infusion produced no acute effects on VEPs. These results suggest that T-type VGCC-dependent LTP contributes to the experience-dependent enhancement of visual responses.

Cortical pyramidal neurons alter their responses to input signals depending on behavioral state. We investigated whether changes in somatic inhibition contribute to these alterations. In layer 5 pyramidal neurons of rat visual cortex, repetitive firing from a depolarized membrane potential, which typically occurs during arousal, produced long-lasting depression of somatic inhibition. In contrast, slow membrane oscillations with firing in the depolarized phase, which typically occurs during slow-wave sleep, produced long-lasting potentiation. The depression is mediated by L-type Ca2+ channels and GABA(A) receptor endocytosis, whereas potentiation is mediated by R-type Ca2+ channels and receptor exocytosis. It is likely that the direction of modification is mainly dependent on the ratio of R- and L-type Ca2+ channel activation. Furthermore, somatic inhibition was stronger in slices prepared from rats during slow-wave sleep than arousal. This bidirectional modification of somatic inhibition may alter pyramidal neuron responsiveness in accordance with behavioral state.

Transient synapse formation between thalamic axons and subplate neurons is thought to be important in thalamocortical targeting. Shaking rat Kawasaki (SRK), having reversed cortical layering similarly observed in reeler mouse, provides an interesting model system to test this idea. The spatial and temporal pattern of excitation was investigated using optical recording with voltage-sensitive dyes in thalamocortical slice preparations from SRK. At postnatal day 0 (P0), a strong optical response was elicited within the superplate of the SRK in the cell layer corresponding to subplate in wild-type (WT) rats. By P3, this response rapidly descended into deep cortical layers comprised of layer IV cells, as identified with 5-bromo-2'-deoxyuridine birthdating at embryonic day 17. During the first 3 postnatal days, both the subplate and cortical plate responses were present, but by P7, the subplate response was abolished. Tracing individual axons in SRK revealed that at P0-P3, a large number of thalamocortical axons reach the superplate, and by P7-P10, the ascending axons develop side branches into the lower or middle cortical layers. Synaptic currents were also demonstrated in WT subplate cells and in SRK superficial cortical cells using whole-cell recording. These currents were elicited monosynaptically, because partial AMPA current blockade did not modify the latencies. These results suggest that the general developmental pattern of synapse formation between thalamic axons and subplate (superplate) neurons in WT and SRK is very similar, and individual thalamic arbors in cortex are considerably remodeled during early postnatal development to find layer IV equivalent neurons.

We have shown that some neural activity is required for the maintenance of long-term potentiation (LTP) at visual cortical inhibitory synapses. We tested whether this was also the case in N-methyl-d-aspartate (NMDA) receptor-independent LTP of excitatory connections in layer 2/3 cells of developing rat visual cortex. This LTP occurred after 2-Hz stimulation was applied for 15 min and always persisted for several hours while test stimulation was continued at 0.1 Hz. When test stimulation was stopped for 1 h after LTP induction, only one-third of the LTP instances disappeared, but most did disappear under a pharmacological suppression of spontaneous firing, indicating that LTP maintenance requires either evoked or spontaneous activities. LTP was totally abolished by a temporary blockade of action potentials with lidocaine or the removal of extracellular Ca(2+) after LTP induction, but it persisted under a voltage clamp of postsynaptic cells or after a temporary blockade of postsynaptic activity with the glutamate receptor antagonist kynurenate, suggesting that LTP maintenance requires presynaptic, but not postsynaptic, firing and Ca(2+) entry. More than one-half of the LTP instances were abolished after a pharmacological blockade of P-type Ca(2+) channels, whereas it persisted after either L-type or Ni(2+)-sensitive Ca(2+) channel blockades. These results show that the maintenance of NMDA receptor-independent excitatory LTP requires presynaptic firing and Ca(2+) channel activation as inhibitory LTP, although the necessary level of firing and Ca(2+) entry seems lower for the former than the latter and the Ca(2+) channel types involved are only partly the same.

The phosphodiesterase inhibitor, ibudilast, has many effects on lymphocytes, endothelial cells, and glial cells. We examined the neuroprotective role of ibudilast in neuron and microglia co-cultures. Ibudilast significantly suppressed neuronal cell death induced by the activation of microglia with lipopolysaccharide (LPS) and interferon (IFN)-gamma. To examine the mechanisms by which ibudilast exerts a neuroprotective role against the activation of microglia, we examined the production of inflammatory and anti-inflammatory mediators and trophic factors following ibudilast treatment. In a dose-dependent manner, ibudilast suppressed the production of nitric oxide (NO), reactive oxygen species, interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha and enhanced the production of the inhibitory cytokine, IL-10, and additional neurotrophic factors, including nerve growth factor (NGF), glia-derived neurotrophic factor (GDNF), and neurotrophin (NT)-4 in activated microglia. Thus, ibudilast-mediated neuroprotection was primarily due to the inhibition of inflammatory mediators and the upregulation of neurotrophic factor. In the CA1 region of hippocampal slices, long-term potentiation (LTP) induced by high frequency stimulation (HFS) could be inhibited with LPS and interferon-gamma stimulation. Ibudilast returned this LTP inhibition to the levels observed in controls. These results suggest that ibudilast may be a useful neuroprotective and anti-dementia agent counteracting neurotoxicity in activated microglia.

We analysed the laminar distribution of transmembrane currents from embryonic (E) day 17 until adulthood after selective thalamic stimulation in slices of rat forebrain to study the development of functional thalamocortical and cortico-cortical connections. At E18 to birth a short-latency current sink was observed in the subplate and layer 6, which was decreased, but not fully abolished in a cobalt containing solution or after the application of glutamate receptor blockers (APV and DNQX). This indicated that embryonic thalamic axons were capable of conducting action potentials to the cortex and some of them had already formed functional synapses there. Between birth and P3, when thalamic axons were completing their upward growth, a sink gradually appeared more superficially in the dense cortical plate and synchronously, a current source aroused in layer 5. Both sinks and sources completely disappeared after blocking synaptic transmission. The adult-like distribution of CSDs became apparent after P7. The component in layer 6 cannot be blocked completely after this age suggesting antidromic activation. This study demonstrated that cells of the lowest layers of the cortex received functional thalamic input before birth and that thalamocortical axons formed synapses with more superficial cells as they grew into the cortical plate.

High-frequency activation of excitatory synapses produces long-term depression (LTD) at inhibitory synapses in rat visual cortex. The LTD generation mechanism was studied by recording inhibitory postsynaptic potentials from layer V cells in response to layer IV stimulation under pharmacological blockade of excitatory synaptic transmission. LTD occurred after depolarizing current pulses applied to postsynaptic cells elicited repetitive firing. LTD induction was facilitated by a bath application of an L-type Ca(2+) channel activator, 1,4-Dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl) phenyl]-3-pyridinecarboxylic acid, methyl ester (BAY K 8644), while it was prevented by either the bath application of L-type Ca(2+) channel blocker nifedipine or postsynaptic loading of Ca(2+) chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N',N',-tetraaceticacid (BAPTA). These results suggest that LTD induction is at least partly mediated by Ca(2+) entry through L-type Ca(2+) channels in association with postsynaptic action potentials.

To examine whether the surface reaction layer of titanium castings can be reduced by lowering the mold temperature during casting, we cast titanium at three mold temperatures, including an ultra-low temperature produced by cooling the mold with liquid nitrogen, then measured the tensile strength and elongation of the castings. The titanium was cast using a centrifugal casting machine, and the molds were incinerated according to the manufacturers' instructions. Castings were then made with the molds at 200 degrees C, 600 degrees C, and an ultra-low temperature (-196 degrees C). The castability of titanium cast in the mold at the ultra-low temperature was good. The Vickers hardness near the surface layer of castings decreased as the mold temperature decreased.

Multiple forms of synaptic potentiation have been described, but their involvement in development versus learning is unknown. To address this, we examined whether long-term potentiation (LTP) in visual cortex requires protein or RNA synthesis using slice preparations. Theta-burst stimulation of white matter induced two distinct types of LTP in layer 4. A slowly developing LTP, preferentially induced in juveniles, was blocked by protein and RNA synthesis inhibitors and was L-type calcium channel dependent. A quickly developing LTP, induced in juveniles and adults, was independent of macromolecular synthesis and required N-methyl-D-aspartate receptor activation. Thus, slow LTP might account for developmental plasticity in visual cortex including the activity-dependent refinement of neural circuitry while fast LTP might underlie the changes in synaptic strength that may participate in visual learning and memory.

The development of neural connections between transplanted lateral geniculate nucleus (LGN) and host visual cortex (VC) was studied in slice preparations obtained from rat brain in which a fetal (embryonic day 15-17) rat LGN was transplanted to the white matter underlying the VC of a neonate rat (postnatal day 0-1). Placing a fluorescent dye (DiI) in the transplant of the fixed slices revealed that retrogradely labeled cortical cells projecting to the transplant were broadly distributed through layers II to VI at 1 week after transplantation. Three weeks after transplantation, these cells were virtually confined to layer VI. Likewise, anterograde labeling showed that cells in the transplant sent axons up to layer I with a few branches at 1 week after transplantation, while the axons were found to terminate at layer IV with many arborizations at 3 weeks after transplantation. These observations were supported by electrophysiological studies. Analysis of the antidromic responses of the cortical cells to stimulation of the transplant showed that the efferent cells projecting to the transplant were broadly distributed in layers II-VI at 1 week after transplantation, while they were virtually restricted to layer VI at 3 weeks after transplantation. Current source-density analysis of the field potentials and intracellular analysis of the synaptic potentials in the cortical cells demonstrated that geniculocortical connections were broadly established in layers II-VI at 1 week after transplantation, and were localized to layer IV and VI at 3 weeks after transplantation. These results suggest that the development of neural connections between transplanted LGN and host VC is characterized by an initial broad distribution of afferent and efferent connections without laminar specificity, and by later selection of appropriate connections to yield lamina-specific connections comparable to those in normal adult VC.

The formation of specific neural connections in the cerebral cortex was studied using organotypic coculture preparations composed of subcortical and cortical regions. Morphological and electrophysiological analysis indicated that several cortical efferent and afferent connections, such as the corticothalamic, thalamocortical, corticocortical, and corticotectal connections, were established in the cocultures with essentially the same laminar specificity as that found in the adult cerebral cortex, but without specificity of sensory modality. This suggests the existence of a cell-cell recognition system between cortical or subcortical neurons and their final targets. This interaction produces lamina-specific connections, but is probably insufficient for the formation of the modality-specific connections.

The neural circuitry in the visual cortex is characterized by two basic types of organization. One is a laminar organization determining the extrinsic and intrinsic neural connections of cortical cells according to their cortical depth, and the other is a columnar organization where cortical cells are arranged perpendicularly according to their response selectivities. It is known that the columnar organization comprises the postnatal structures dependent on the visual experience, while the laminar organization comprises the prenatal structures unmodified by visual experience. We have investigated the interplay between the pre- and postnatal mechanisms using various in vitro preparations, including visual cortical slices, and transplant and co-culture preparations. It was shown in lateral geniculate and visual cortex transplants and co-cultures including the visual cortex lateral geniculate nucleus that all laminar structures are expressed in these preparations according to the prenatal mechanisms. It was also shown in slice preparations that the details of these circuitries are plastic and modifiable by the visual input, although their basic framework is determined prenatally.