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Regulation of metallothionein‐I+II levels in specific brain areas and liver in the rat: Role of catecholamines
Author(s) -
Gasull Teresa,
Giralt Mercedes,
Garcia Agustina,
Hidalgo Juan
Publication year - 1994
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440120207
Subject(s) - dopamine , medicine , endocrinology , striatum , astrocyte , biology , tyrosine hydroxylase , phentolamine , cerebellum , catecholamine , hypothalamus , central nervous system , propranolol
The role of the catecholamines noradrenaline, adrenaline and dopamine on metallothionein (MT) levels of specific areas of the rat brain has been studied. MT‐I or MT‐I+II levels were measured by radioimmunoassay using specific antibodies that cross‐react only slightly with human MT‐III (growth inhibitory factor, GIF). The inhibition of tyrosine hydroxylase with α‐methyl‐p‐tyrosine (MPT), which depletes brain dopamine, noradrenaline, and adrenaline, increased MT levels in all brain areas studied (frontal cortex, cortex, medulla oblongata plus pons, midbrain, striatum, hippocampus, hypothalamus, and cerebellum) when considering the results of two separate experiments. The α‐ and β‐receptor blockers, phentolamine, and propranolol, alone or together, did not increase brain MT levels in any area of the brain, suggesting that the effect of MPT in vivo is related to inhibition of the synthesis of dopamine rather than of noradrenaline and adrenaline. Dopamine, noradrenaline, and serotonin increased MT‐I levels in primary cultures of neurons, whereas decreased them in astrocyte‐enriched primary cultures. Since MT‐I levels are about ten times higher in astrocytes than in neurons, the increased brain MT levels induced by MPT may reflect the supperssion of the normal inhibitory effect of dopamine on astrocyte MT levels. The increase in MT concentrations induced in most parts of the brain by immobilization stress was not prevented by MPT, phentolamine, or propranolol, suggesting that it was not mediated by the central monoamines.