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Biomedical subjects

S Głazewski

Publications and source records attributed to S Głazewski.

7 recordsLinked to original sources

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↗

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↗

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↗

Functional plasticity and neurotransmitter receptor binding in the vibrissal barrel cortex.

A form of activity dependent, functional plasticity can be induced in the barrel cortex by sensory deprivation without damage to the sensory receptors. Changes of cortical representation of a spared C3 vibrissa, when all other whiskers were plucked out, were mapped with 2-deoxyglucose autoradiography in mice and rats after a short-lasting deprivation. An increase in the volume of cortical column activated by the spared vibrissa was found already after one week of deprivation. We have found previously that if deprivation is commenced immediately after birth, the changes in cortical representation of the spared whisker appeared in the third week of life. In search of a possible reason for the delayed expression of functional plasticity in neonatal animals we examined the developmental curves of neurotransmitter receptor binding for several transmitters though to be involved in plastic processes of the cerebral cortex. We found that the beta noradrenergic and muscarinic cholinergic receptor binding increased rapidly at the end of the second postnatal week and subsequently remained high. By contrast, the metabotropic glutamate receptor binding decreased during the first month of postnatal development. The AMPA receptors binding values rose during the first two weeks of life, and then decreased. Together with our previous data on the development of NMDA and GABAa receptor and voltage dependent calcium channel binding, the results suggest that slow development of functional plasticity in neonatal animals may be due to low levels of receptors of several neurotransmitters implicated in brain plasticity.

Animals↗

Cholinergic markers in the plasticity of murine barrel field.

Cholinergic muscarinic receptor binding and acetylcholinesterase (AChE) histochemistry were studied in the barrel cortex of adult, vibrissae deprived and vibrissae denervated mice. In the control barrel field muscarinic receptors labeled with [3H]quinuclidinyl benzilate ([3H]QNB) showed a higher density in the granular cortex and a higher accumulation of label in the barrels. AChE staining revealed a punctuated pattern corresponding to the barrels in the upper part of layer IV and a reverse-image pattern of staining showing only the walls of barrels in the lower part of layer IV. Neonatal denervation of rows of vibrissae lowered both binding of [3H]QNB to the tissue in the shrunken rows and AChE activity in the denervated rows of barrels. Deprivation and late denervation produced no effects on either pattern, or intensity, of [3H]QNB labeling and AChE staining. These observations suggest that the changes in cholinergic markers are related to the altered morphological structure and not to the abnormal functioning of the barrel cortex which received reduced sensory input from the vibrissae.

Acetylcholinesterase↗

Effect of various aminoglycoside antibiotics on glucose formation in isolated rabbit kidney-cortex tubules.

The effect of six aminoglycoside antibiotics on the rate of gluconeogenesis was studied in isolated rabbit kidney-cortex tubules incubated with various substrates. All antibiotics studied did not affect glucose formation from both malate and 2-oxoglutarate. The rank order of the drug-induced inhibition of glucose formation from lactate, pyruvate and propionate was the following: neomycin = gentamicin greater than tobramycin greater than kanamycin = amikacin greater than streptomycin. This in principle corresponds to their ability to diminish pyruvate carboxylation in isolated kidney-cortex mitochondria, as well as to their known nephrotoxic potential observed in vivo. Aminoglycoside antibiotics decreased the respiration of tubule suspension incubated with various substrates. However, the rank order of the inhibition by antibiotics of oxygen uptake was different from that observed for gluconeogenesis, suggesting that the rate of energy generation does not limit glucose formation under conditions studied.

Aminoglycosides↗