Developmental regulation of intracellular calcium by N-methyl-D-aspartate and noradrenaline in rat visual cortex.
The effects of N-methyl-D-aspartate and noradrenaline on intracellular Ca2+ concentration in slices of rat visual cortex were studied using a fluorescent indicator, Fura-2. Bath application of N-methyl-D-aspartate (1-100 microM) increased intracellular Ca2+ concentration in a dose-dependent manner, especially in layers II/III. Noradrenaline (1-100 microM) also increased intracellular Ca2+ concentration in a dose-dependent manner, especially in layers I and IV. However, the maximum increase in intracellular Ca2+ concentration after 100 microM noradrenaline application was less than half of that after 100 microM N-methyl-D-aspartate application in slices obtained from animals in the sensitive period. The effect of noradrenaline was most prominent in slices of the sensitive period, whereas the N-methyl-D-aspartate-induced intracellular Ca2+ concentration response decreased with age. Additive effects from application of both N-methyl-D-aspartate and noradrenaline on intracellular Ca2+ concentration were found only in the neonatal stage. Pharmacological experiments showed that alpha1-adrenergic receptors play a major role in the noradrenaline-induced intracellular Ca2+ concentration response, although both alpha2- and beta-adrenergic receptors were also partially involved. The release of Ca2+ from intracellular storage underlay the early phase of the noradrenaline-induced intracellular Ca2+ concentration response, while extracellular Ca2+ influxes contributed to the sustained phase. Experiments using a gliotoxin, fluorocitric acid, suggested that the function of glial cells is involved in the noradrenaline-induced increase of intracellular Ca2+ concentration. The larger intracellular Ca2+ concentration response to noradrenaline during the sensitive period may modulate the increase in intracellular Ca2+ concentration by N-methyl-D-aspartate to maintain a higher level of cortical plasticity during this period.
Kobayashi
M
M
Department of Neuroscience, Osaka Bioscience Institute, CREST, Japan Science and Technology Corporation, Suita.
Imamura
K
K
Kaub
P A
PA
Nakadate
K
K
Watanabe
Y
Y
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000375:Aging / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D005456:Fluorescent Dyes; D016257:Fura-2; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism; D016202:N-Methylaspartate / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D020318:Rats, Long-Evans; D014793:Visual Cortex / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism*
D000316:Adrenergic alpha-Agonists; D018690:Excitatory Amino Acid Agonists; D005456:Fluorescent Dyes; D005904:Glial Fibrillary Acidic Protein; D016202:N-Methylaspartate; D002118:Calcium; D016257:Fura-2; D009638:Norepinephrine