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J Skangiel-Kramska

Publications and source records attributed to J Skangiel-Kramska.

At least 19 recordsLinked to original sources
PubMed2001

Differential response of synaptic zinc levels to sensory deprivation in the barrel cortex of young and adult mice.

The distribution of synaptic zinc after short-term (up to 48 h) tactile deprivation of vibrissae was investigated in the barrel cortex of mice using histochemical staining. In adult mice, 12 h after trimming selected rows of vibrissae, an increase in zinc staining in the deprived barrels was observed. This increase was still present 48 h after trimming. These results indicate that the level of synaptic zinc is rapidly regulated by neuronal activity in adult mice. In young (8-day-old) mice, the short-term deprivation did not alter zinc staining and only chronic sensory deprivation produced an increase in zinc staining. However, after long-term deprivation no changes were found in adult mice. These results suggest that different mechanisms might be involved in functional reorganization of zinc containing terminals in young and fully mature cerebral cortex.

Afferent Pathways↗
PubMed2001

Deprivation and denervation differentially affect zinc-containing circuitries in the barrel cortex of mice.

In the neocortex, a population of glutamatergic synapses contains chelatable zinc that is released upon depolarization. The present study compares the effect of chronic tactile deprivation and vibrissectomy performed at different postnatal ages on the synaptic zinc distribution in the mouse barrel cortex. We found that a chronic unilateral tactile deprivation resulted in an increase of synaptic zinc in deprived barrels. Distribution and intensity of zinc staining in non-deprived barrels resembled the control situation. The increase of zinc staining was observed if chronic deprivation started in early postnatal life or in adolescent mice but not in 70-day-old animals. This suggests that a critical period exists for plasticity of zinc containing terminals in the barrel cortex. The alteration of zinc staining was localized to not only the thalamorecipient layers IV but also layer II/III, and upper layer V. Neonatal denervation of selected vibrissal rows resulted in rearrangement of synaptic zinc distribution following cytoarchitectonic alterations in the barrel field. However, no changes in the intensity of zinc staining were observed. Vibrissectomy performed after the critical period for barrel formation did not affect either the distribution or intensity of zinc staining. It appears that the integrity of vibrissa-barrel pathway is necessary to induce activity-dependent alterations in synaptic zinc.

Afferent Pathways↗
PubMed2000

Differences between rats and rabbits in NMDA receptor-mediated calcium signalling in hippocampal neurones.

In vivo microdialysis combined with the measurement of (45)Ca(2+) efflux from prelabelled hippocampus demonstrated a pronounced N-methyl-D-aspartate (NMDA)-evoked (45)Ca(2+) release to the dialysate in the rat dentate gyrus (DG) and CA1, whereas in rabbit a slight release of (45)Ca(2+) was observed only in the DG. In vitro, we noticed that the NMDA-evoked increase in Fura-2 detected intracellular Ca(2+) concentration in synaptoneurosomes from the rat, but not from the rabbit hippocampus, was strongly inhibited by the ryanodine receptor (RyR) antagonists dantrolene and ryanodine. To establish the mechanism of these differences, we characterised their possible dependence on the expression of RyR and their co-localisation with the calcium binding protein calbindin D(28k). A pronounced expression of [(3)H]ryanodine binding sites in the rat DG, which is only slight in the CA1, was demonstrated whereas in rabbit they were only found in the DG. The pattern of expression of calbindin D(28k) immunoreactivity and RyR in the rat and rabbit hippocampus was similar. These results suggest that the functional role of RyR in the generation of the NMDA receptor-mediated intracellular Ca(2+) signalling in the rabbit hippocampal neurones is marginal when compared to the rat. These differences reflect a diverse expression of RyR in both species. The corresponding differences in calbindin D(28k) immunoreactivity are most probably secondary in nature.

Animals↗
PubMed2000

Phosphorylated MAP-1B isoforms in the developing mouse barrel cortex.

Developmental expression of two phosphorylation modes of microtubule-associated protein 1B (MAP-1B) has been studied in the barrel cortex of mice at postnatal days (P)5, P12, P21 and P90 using immunocytochemistry with antibodies 125 and 150 that recognize phosphorylation modes II and I, respectively. The antibody 125 immunoreactive processes, identified as dendrites, are not yet detectable at P5; they are already present at P12 and become more evident at P21. In the barrel cortex of P90 animals the antibody 125 immunopositive dendrites are still present, although they are much less pronounced. The antibody 150 punctate immunostaining seen at P5 is not detectable at P12. At P21, however, thin immunopositive fibres appear, implicating a re-expression of the microtubule-associated protein 1B phosphorylation mode I in a portion of axons. The antibody 150 immunopositive axons are no longer present in the P90 barrel cortex. The re-expression of the MAP-1B phosphorylation mode I, which is a juvenile isoform characteristic for growing axons, may imply induction of mechanisms providing mouse barrel cortex neurons with the potency for plastic changes at a terminal stage of synaptogenesis.

Animals↗
PubMed1999

Deafferentation induced changes in GAD67 and GluR2 mRNA expression in mouse somatosensory cortex.

Partial vibrissectomy in adult mice induces body map plasticity in SI barrel cortex. To examine if the disturbed balance of cortical activation affects the excitatory and inhibitory neurotransmitter systems, we studied glutamic acid decarboxylase (GAD 67) and AMPA receptor subunit GluR2 mRNA expression in the barrel cortex. At varying times post-vibrissectomy, sparing row C of whiskers on one side of the snout, the brains were processed for in situ hybridization using specific [(35)S]oligonucleotides to detect the laminar localization of GAD67 and GluR2 mRNAs. Three and seven days after vibrissectomy, the expression of GAD67 was decreased in the deafferented cortex, while 30 days post-lesion, no effects were observed. At 3 days post-lesion, an ipsilateral decrease in GAD67 mRNA expression was also observed. No decreases in GluR2 transcripts were found in the deafferented cortex, but an increased expression was observed in the representation of the spared row C of whiskers 3 days after vibrissectomy. Seven and 30 days post lesion no changes in GluR2 expression were found. These data indicate that in the barrel cortex, peripheral deafferentation transiently regulates GAD67 and GluR2 expression at the transcriptional level. We suggest that this may be a manifestation of adaptive processes.

Afferent Pathways↗
PubMed1998

Development of laminar distributions of kainate receptors in the somatosensory cortex of mice.

Kainate receptors were present at birth in the murine somatosensory cortex as revealed by quantitative in vitro autoradiography. During the first five postnatal days [3H]kainate binding rapidly increased and the maximum density in layer IV was reached at P12. The adult laminar pattern of receptor binding distribution was established by the third postnatal week with the heaviest labeling of infragranular layers. The sharp increase of kainate receptor during the first postnatal week coincides with the critical period for cytoarchitectonic plasticity of the barrels and establishment of functional thalamo-cortical connections in the barrel field.

Animals↗
PubMed1997

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.

Animals↗
PubMed1997

Glutamate receptors in cortical plasticity: molecular and cellular biology.

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.

Animals↗
PubMed1996

Transient increase of AMPA and NMDA receptor binding in the barrel cortex of mice after tactile stimulation.

The effects of sensory stimulation and sensory conditioning upon [3H]MK-801 [(+)-5-methyl-10,11-dihydro- 5H-dibenzo[a,d]cyclohepten-5, 10-imine] binding to N-methyl- d-aspartate (NMDA) receptor sites and [3H]AMPA (alpha-amino-3-hydroxy-5-methylisoxasole-4-propionic acid) binding to AMPA receptor sites were examined in the primary somatosensory (SI) cortex of mice. Following short-lasting unilateral tactile stimulation of a selected row of vibrissae, and tactile stimulation paired with noxious stimulus (the pairing procedure was found to alter cortical representation of vibrissae), in vitro receptor binding autoradiography was performed on the sections of the barrel cortex of mice. One hour after the end of tactile stimulation or training procedure there was an increase of [3H]MK-801 and [3H]AMPA binding in the corresponding row of barrels in layer IV of the SI cortex of adult mice. These effects disappeared 24 h after the end of each experimental procedure. The results suggest that both subtypes of glutamate receptors are regulated in an activity-dependent way and that sensory stimulation transiently modifies local cortical processing.

Afferent Pathways↗
PubMed1996

Subchronic intraventricular infusion of quinolinic acid produces working memory impairment--a model of progressive excitotoxicity.

It has been proposed by Yamada et al. [Neurosci. Lett. 118: 128-131 (1990); J. Pharmacobiodyn. 14: 351-355 (1991)] that subchronic i.c.v. infusion of the NMDA receptor agonist quinolinic acid may serve as a model for some aspects of neurodegenerative dementia. In the present study, quinolinic acid (9 mM) was infused i.c.v. by ALZET osmotic minipumps for 2 weeks. This treatment produced a short-term working memory deficit in the T-maze (alternation) but no change in reversal learning in the same test. The working memory deficit in the T-maze was progressive i.e. seen after 14, but not 3 days of infusion and persisted for at least for 3 weeks after the termination of the infusion. Histological examination revealed a modest decrease in the number of cells in the nucleus basalis magnocellularis but not in the striatum, entorhinal cortex, or hippocampus. However, in most of the structures studied, morphological changes such as swollen somata and irregular shape were observed indicative of alterations in neuronal function. Autoradiography in the hippocampus revealed a decrease in [3H]hemicholinium and [3H]quinuclidinyl benzilate (QNB) binding to choline uptake sites and muscarinic receptors respectively. Surprisingly no change was observed in [3H]MK-801 binding to NMDA receptor channels in the hippocampus and cortex. The subchronic infusion of quinolinic acid may serve as a model of progressive deterioration of cognitive functions.

Alzheimer Disease↗
PubMed1996

Dendritic pattern in mouse barrel field after a neonatal vibrissal follicles removal: MAP-2 immunohistochemistry.

A distribution of dendrites was studied in mouse barrel field after a neonatal unilateral partial lesion of vibrissal follicles using anti-MAP-2 immunohistochemistry. The effect of a neonatal vibrissal follicles removal was studied in adult mice: barrels corresponding to intact follicles were enlarged whereas those representing removed follicles had not developed. MAP-2 immunopositive profiles were considered to be dendritic clusters and their packing density (a number per unit area) was calculated in an enlarged barrel and compared to a control barrel in a contralateral hemisphere. A decrease in the packing density of large dendritic clusters (area over 10 microns 2), presumably arising from layer V, was observed in an enlarged barrel in comparison to its control counterpart. This result may indicate a rearrangement of a dendritic pattern in mouse barrel field after a selective neonatal lesion of vibrissal follicles.

Animals↗
PubMed1995

Partial blocking of NMDA receptors restricts plastic changes in adult mouse barrel cortex.

Changes of cortical body maps can be evoked in brains of adult animals by injury to sensory nerves. We investigated changes of functional representation of row C of mystacial vibrissae in the barrel cortex of mice. Plastic changes of cortical representations were mapped with 2-deoxyglucose autoradiography. Seven days after lesions of all vibrissae except row C, cortical representation of the spared row increased in width by 60%. Partial blocking of N-methyl-D-aspartate (NMDA) receptors by subdural implants of thin sheets of Elvax impregnated with DL-2-amino-5-phosphonovaleric acid (APV) prevented development of the increase of row C representation. Low level of NMDA receptor blocking did not affect significantly the basal level of 2DG uptake and stimulus evoked uptake but prevented the plastic change of the body map.

Animals↗
PubMed1995

NMDA receptors in mouse barrel cortex during normal development and following vibrissectomy.

The development of N-methyl-D-aspartate (NMDA) receptors and the effects of vibrissectomy upon [3H]MK-801 binding were examined in the barrel cortex of mice. Autoradiographic studies showed that initially very low binding of [3H]MK-801 sharply increased during the second postnatal week reaching the adult level by the end of the third week. Scatchard analysis performed on cortical membrane preparations indicated that this rise of [3H]MK-801 labelling was due to an increase in the number of binding sites and a decrease of Kd at postnatal day 15 and 28. The interlaminar differences of labelling were registered from postnatal day 8. Changes of interlaminar distribution were found during the second and third postnatal weeks. In adult barrel cortex the highest binding was found in supragranular layers. In layer IV of the cortex, the pattern of binding resembled the pattern of barrels. Unilateral denervation of vibrissae performed in neonatal and adult mice did not alter the intensity of [3H]MK-801 labelling or the laminar distribution of binding sites. These results suggest that NMDA receptor binding does not reflect the plastic changes occurring in the barrel cortex.

Analysis of Variance↗
PubMed1995

Sensory conditioning and sensory stimulation do not affect GABAA receptor binding in the barrel field of mice.

The whisker-to-barrel system of adult mice was used in a study on the effects of short-lasting tactile stimulation and sensory conditioning training on GABAA receptor binding in the barrel field of somatosensory cortex. In vitro receptor binding autoradiography was used to examine the pattern and intensity of [3H]muscimol binding to GABAA receptors. A well-defined pattern of GABAA receptors in the barrel field remained unaffected after both procedures used. Also, no differences in intensity of GABAA receptor binding were observed. These results suggest that GABAA receptors are not involved in the plastic changes developing during sensory conditioning training.

Animals↗
PubMed1994

Reduction of GABAA receptor binding of [3H]muscimol in the barrel field of mice after peripheral denervation: transient and long-lasting effects.

The effect of peripheral sensory deprivation upon GABAA receptor binding of [3H]muscimol was investigated in the barrel cortex--cortical representation of mystacial vibrissae of mice--by means of in vitro quantitative autoradiography. Unilateral lesions of all vibrissae or selected rows of whiskers were performed neonatally or in adulthood. [3H]muscimol binding was examined after various survival times up to 60 days. Both types of lesions performed in adult mice resulted in a transient decrease (10-25%) of binding values in the deafferented areas of the barrel field as compared with the unoperated control side. Sixty days after denervation [3H]muscimol binding returned to control values. Similar results were found after neonatal removal of all vibrissae. Neonatal lesion of selected rows of vibrissae, however, resulted in a decrease of [3H]muscimol binding (by about 26%) lasting up to 60 days in corresponding rows of barrels. This last result was accompanied by severe cytoarchitectonic malformation of the barrel field. The results support the hypothesis that a decrease of inhibition plays a facilitatory role in the plastic reorganization of cortical circuitry.

Aging↗
PubMed1993

Development of NMDA receptor-channel complex and L-type calcium channels in mouse hippocampus.

In vitro binding autoradiography was used to examine the pattern and intensity of binding of [3H]glutamate to NMDA receptors, [3H]MK 801 to NMDA receptor associated channels, and [3H]PN-200 110 to L-type calcium channels in the hippocampus of mice aged 3-70 days. The distribution of NMDA receptors and NMDA receptor associated channels was similar but not identical at the tested ages. Beginning with postnatal day 8, high binding levels were confined mostly to the hippocampal strata: the oriens and radiatum (CA1 and CA3 with [3H]MK 801 labeling but only CA1 with NMDA displaced [3H]glutamate labeling), the moleculare (higher labeling with [3H]MK 801 than with NMDA displaced [3H]glutamate binding), and the lucidum. The binding values for NMDA receptor-channel complex rose in the examined period (especially within the second and third week), reaching a plateau at the end of the third postnatal week. Sharp growth of binding within the second and third week of life was about 50% greater with [3H]MK 801 than with NMDA displaced [3H] glutamate labeling. L-type calcium channels were found to be most abundant in the strata: the oriens of the CA3 field, the moleculare, and the lucidum. The time course of binding value changes for the calcium channel was similar to the time course found for the NMDA receptor-channel complex.

Age Factors↗