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Comparative Effects of Ethanol and Malnutrition on the Development of Catecholamine Neurons: Changes in Specific Activities of Enzymes
Author(s) -
Detering Nancy,
Edwards Elvira,
Ozand Pinar,
Karahasan Alp
Publication year - 1980
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1980.tb06596.x
Subject(s) - endocrinology , medicine , offspring , tyrosine hydroxylase , lactation , dopamine , neurochemical , catecholamine , gestation , weanling , ethanol , liquid diet , biology , pregnancy , biochemistry , genetics
A rat model was developed in which the comparative effects of malnutrition and ethanol on the neurochemical maturation of catecholamine neurons in brain were studied. The animals were offspring of rats optimally nourished (control pups), fed a diet with 35% of the calories supplied by ethanol (EtOH pups), or a diet calorically equivalent to the latter but lacking ethanol (isocaloric = IC pups). These latter two groups were calorically deprived since rats fed the diet containing ethanol ate 40–60% less than the optimally nourished group. The diets were administered to dams either during the last week of gestation (prenatal) or during lactation (postnatal). The protein content per gram wet weight was not significantly different between brains of control and experimental pups. Developmental changes in EtOH pups were noted in the activities of tyrosine hydroxylase (TOH) and dopamine β‐hydroxylase (DBH). The specific activity of TOH was increased in EtOH and IC pups preand postnatally. In the postnatal experimental group TOH activity in the brains of EtOH pups was higher not only when compared with control pups but also with IC pups. Prenatal caloric deprivation or ethanol exposure also caused increased specific activity of DBH in the neonatal rat brain. In contrast, exposure to ethanol postnatally caused a significant and persistent reduction in the specific activity of DBH, not only compared with control pups but also to matched IC pups exposed postnatally to the IC diet. The specific activity of 3,4‐dihydroxyphenylalaninedecarboxylase (DOPADC) was significantly elevated in the brains of prenatal and postnatal EtOH and IC pups, with little difference between the groups. Activities of monoamine oxidase (MAO) or catecholamine‐0‐methyltransferase (COMT) were generally lower in EtOH or IC pups than in control pups, again with little difference between EtOH and IC pups. These results suggest that an impaired metabolism of dopamine and norepinephrine is detectable in the brains of pups as a consequence of malnutrition, ethanol exposure, or both.