The ability to undergo experience-dependent plasticity in the neocortex is often limited to early development, but also to particular cortical loci and specific experience. In layers II-IV of the barrel cortex, plasticity evoked by removing all but one vibrissae (univibrissa rearing) does not have a time limit except for layer IV barrels, where it can only be induced during the first postnatal week. In contrast, deprivation of every second vibrissa (chessboard deprivation) removes time limits for plasticity. The mechanism permitting plasticity in response to chessboard deprivation and halting it in reply to univibrissa rearing is unknown. Condensation of chondroitin sulfate proteoglycans into perineuronal nets and an increase in intracortical inhibition mediated by parvalbumin-containing interneurons are implicated in closing the critical period for ocular dominance plasticity. These factors could also be involved in setting up the critical period in barrels in a way that depends on a particular sensory experience. We therefore examined changes in density of parvalbumin-containing cells and perineuronal nets during development of mouse barrel cortex and after brief univibrissa and chessboard experience in adolescence. We observed a progressive increase in the density of the two markers across cortical layers between postnatal day 10 and 20, which was especially pronounced in the barrels. Univibrissa rearing, but not chessboard deprivation, increased the density of perineuronal nets and parvalbumin-containing cells in the deprived barrels, but only those that immediately neighbour the undeprived barrel. These data suggest the involvement of both tested factors in closing the critical period in barrels in an experience-dependent manner.

BackgroundIt has been postulated that exercise-induced activation of brain-derived neurotrophic factor (BDNF) may account for improvement of stepping ability in animals after complete spinal cord transection. As we have shown previously, treadmill locomotor exercise leads to up-regulation of BDNF protein and mRNA in the entire neuronal network of intact spinal cord. The questions arise: (i) how the treadmill locomotor training, supplemented with tail stimulation, affects the expression of molecular correlates of synaptic plasticity in spinal rats, and (ii) if a response is related to BDNF protein level and distribution.We investigated the effect of training in rats spinalized at low thoracic segments on the level and distribution of BDNF immunoreactivity (IR) in ventral quadrants of the lumbar segments, in conjunction with markers of presynaptic terminals, synaptophysin and synaptic zinc.ResultsTraining improved hindlimb stepping in spinal animals evaluated with modified Basso-Beattie-Bresnahan scale. Grades of spinal trained animals ranged between 5 and 11, whereas those of spinal were between 2 and 4. Functional improvement was associated with changes in presynaptic markers and BDNF distribution. Six weeks after transection, synaptophysin IR was reduced by 18% around the large neurons of lamina IX and training elevated its expression by over 30%. The level of synaptic zinc staining in the ventral horn was unaltered, whereas in ventral funiculi it was decreased by 26% postlesion and tended to normalize after the training. Overall BDNF IR levels in the ventral horn, which were higher by 22% postlesion, were unchanged after the training. However, training modified distribution of BDNF in the processes with its predominance in the longer and thicker ones. It also caused selective up-regulation of BDNF in two classes of cells (soma ranging between 100-400 μm2 and over 1000 μm2) of the ventrolateral and laterodorsal motor nuclei.ConclusionOur results show that it is not BDNF deficit that determines lack of functional improvement in spinal animals. They indicate selectivity of up-regulation of BDNF in distinct subpopulations of cells in the motor nuclei which leads to changes of innervation targeting motoneurons, tuned up by locomotor activity as indicated by a region-specific increase of presynaptic markers.

Glutamate receptors (GluRs) provide the major excitatory input to cortical neurons. Four main subtypes of GluRs are distinguished, namely, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate, and metabotropic receptors. All of them have been implicated in neuronal plasticity, and this paper reviews data that may be pertinent to the role played by GluRs in neocortical plasticity both in adult animals as well as during postnatal development. Emphasis is given to receptor distribution analyzed by various means, such as physiological responses, ligand binding as revealed by receptor autoradiography, and expression of receptor subunits at both mRNA and protein (immunoreactivity) levels. Possible mechanisms of involvement of GluRs in plastic changes on cortical neuron response are reviewed, and data on up- and downregulation of GluRs in neocortical plasticity are summarized. Functional studies involving either activation or blocking, and effects of such manipulation on cortical plasticity are discussed.

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Three vesicular glutamate transporters have been identified in mammals. Two of them, VGLUT1 and VGLUT2, define the glutamatergic phenotype and their distribution in the brain is almost complementary. In the present study we examined the distribution and expression levels of these two VGLUTs during postnatal development of the mouse barrel cortex. We also investigated changes in the localization of VGLUT1 and VGLUT2 within particular compartments of the barrel field (barrels/septa) during its development. We found differences in the time course of developmental expression, with VGLUT1 peaking around P14, while VGLUT2 increased gradually until adulthood. Over the examined period (P3 - adult) both transporters had stronger expression in the barrel interiors, and in this compartment VGLUT2 dominated, whereas in the inter-barrel septa VGLUT1 dominated over VGLUT2. Furthermore, we found that some nerve terminals in the barrel cortex coexpressed both transporters until adulthood. Colocalization was observed within the barrels, but not within the septa.