https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793%2876%2980289-X

The development of monoamine oxidase in rat liver and brain.

The distribution of monoamine-containing neurons in the CNS of the developing and adult axolotl, Ambystoma mexicanum, has been investigated using the histochemical fluorescence technique of Falck and Hillarp combined with microspectrofluorimetry. The earliest catecholamine-containing neurons to be detected are located in the ventral ependymal zone of the spinal cord at the time of hatching (Stage 41). Between stages 43 and 46, catecholamine fluorescence can be detected in neurons in the following regions: nucleus preopticus, the hypothalamic-infundibular region, and the brain stem reticular fomation. 5-HT-containing neurons are only observed in the midbrain raphe region and are first detected at stage 44. In contrast to these early monoamine fluorescing groups, catecholamine-containing neurons are not routinely detectable in the nucleus interpeduncularis until six months of age. All monoamine-containing neuronal groups detected in developing axolotls are also present in both sexes of the adult. However, the fluorescence intensity is less in monoamine-containing neurons observed in adults than in early developing subjects.



All catecholamine-containing neuronal groups, with the exception of those located in the midbrain region (nucleus interpeduncularis, reticular zone) have fluorescent processes that contact the cerebrospinal fluid (CSF). The presence of CSF-containing processes in the hypothalamic and spinal cord regions suggest that the CSF may act as a medium through which bioactive substances are transported from one brain region to another. Intense catecholamine fluorescence is observed in cells of the notochord prior to the detection of monoamine-containing neurons in the CNS. A possible involvement of catecholamines in the inductive effects of the notochord during development is discussed.

The development of monoamine‐containing neurons in the brain and spinal cord of the salamander, Ambystoma mexicanum

This article explores the possibility that malfunction of the enzyme monoamine oxidase (E.C. 1.4.3.4., MAO) could lead to aberrations in the catabolism of biogenic amines in the central nervous system and give rise to certain mental abnormalities. No conclusive evidence could be presented to substantiate this. Data on the normal function of the enyzme (for example its existence in multiple forms, the control of MAO activity by hormones or the independent development of MAO activities towards different substrates during maturation) are reviewed.

Physiological and pathological changes in tissue monoamine oxidase activity.

Male Wistar rats (TNO W. 70) were kept under controlled conditions of light and darkness (12¬12 h). The cardiac turnover of noradrenaline was determined with two methods, either by the decay of the specific activity after i.v. injection of3H-(−)-noradrenaline or by inhibition of the tyrosine-hydroxylase withd,l-α-methyl-p-tyrosine. During the 12 h of darkness at night the turnover was significantly faster than during daytime (12h illumination). Reversal of the light schedule shifted the noradrenaline turnover by approximately 12 h. The experiments show that the cardiac turnover of noradrenaline can be influenced by environmental lighting. This may be of importance when effects of drugs are studied.

Influence of light and darkness on the turnover of noradrenaline in the rat heart.

The maturation of monoamine oxidase and 5-hydroxyindole acetic acid in regions of the mouse brain

A NUMBER of studies have been concerned with changes in tissue monoamine oxidase (MAO) activity with age. Such knowledge is useful in understanding sympathetic function and age-related disease states involving alterations in catecholamine metabolism. There is now a discrete amount of data on the age-related variations of M A 0 activity in brain, liver and heart tissue but only few data on other organs. KARKI, KUNTZMAN and BRODIE (1962) showed a marked increase of M A 0 activity in brain from the newborn period to adult life. PRANGE, WHITE, LIPTON and KINKEAD (1967) on the contrary reported constant MA0 activity throughout the life-span of both male and female rats, which was confirmed by HORITA (1967). The assays were however limited to rats older than 14 days of age. According to ROBINSON (1967) there is little or no MA0 activity histochemically detectable before 10 days of age in rat brain; at 15 days, some differentiation of enzyme activity was apparent. According to PRANGE et al. (1967), MA0 activity of rat livers appears to rise at about the 9th week and to decline about the 35th. HORITA (1967) showed that MA0 activity of the rat liver, as in brain, reached a relative maximum at the 6th week. MA0 activity of heart tissue gradually increased during development (NOVICK, 1961). GEY, BURKARD and PLETSCHER (1963,1964,1965) observed that MA0 activity measured in the total homogenate and in the mitochondria1 fraction of rat heart, was increased several fold during the course of the whole life span (1-24 months of age), which was supported by PRANCE et al. (1967) and HORITA (1967). Most activity measurements during development were made on animals closer to weaning than to the first days of life. Relatively little attention appears to have been paid to the days immediately after birth, when abrupt changes in enzyme activity may occur. The present study was carried out to measure MA0 activity of brain, heart, liver and spleen through the first 18 days of life, and to compare the newborn activity with that of young adultand old rats. Previously shown hyposensitivity to 5-hydroxytryptamine in fundal strips of the newborn rat (VACCARI and CUGURRA, 1968), led us also to determine if such hyposensitivity could be due to higher M A 0 activity of the fundus of newborn rats.

M. Marchi

Papers

Development of monoamine oxidase in several tissues in the rat1,2