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Biomedical subjects

A J Patel

Publications and source records attributed to A J Patel.

At least 127 records · Page 7Linked to original sources
PubMed1977

Do drugs acting on the nervous system affect cell proliferation in the developing brain.

Drugs which alter the balance of neurotransmitter activity may, while failing to cause gross structural malformations of the brain, produce long-lasting functional disturbances if given when the brain is developing. Subtle anatomical changes may underlie such disturbances; reserpine has been shown to interfere with cell proliferation in the brain of suckling rats, and long-term alterations in behaviour reported after treatment with reserpine may be related to this effect of the drug. Neurotransmitters, apart from their conventional role, may also function as neurohumours and be involved in the regulation of cell proliferation in the nervous system. Thus drugs influencing central neurotransmitter activity, such as phenothiazines and adrenergic agonists and antagonists, which in clinical practice are often given to pregnant mothers, may affect the developing brain through mechanisms similar to those reported for reserpine. More experimental information is needed about the influence of such drugs on cell proliferation in the brain, and about their "behavioural teratogenicity".

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PubMed1976

Effect of thyroid deficiency on postnatal cell formation in the rat brain: a biochemical investigation.

In thyroid deficiency, interference with postnatal cell formation seems to be confined to those regions of the brain where postnatal neurogenesis is significant. In comparison with controls the increase in cell number in the cerebellum is retarded in the second week of life, but a normal number is reached by 35 days. In contrast the DNA content of the olfactory bulbs is apparently irreversibly depressed. Mitotic activity, in terms of incorporation of [2-14C]thymidine into DNA, is mainly affected in the cerebellum: in thyroid deficient rats, it is depressed below control levels at day 12, but it is about 4 times higher than in controls at day 21 when, under normal conditions, cell proliferation has virtually ceased. The time course (15-240 min) of [14C]thymidine metabolism at day 14 shows regional differences in control rats. The rate of conversion of [14C]thymidine to [14C]thymidine nucleotides, and of these in turn to [14C]DNA is slower in the forebrain - where cell proliferation occurs on a smaller scale - than in the cerebellum. Consequently, in the forebrain nearly linear DNA synthesis rate is maintained for a longer time than in the cerebellum (1 h vs. 0.5 h), and since less 14C is conserved in DNA a significant efflux of unconverted [14C]thymidine is evident during the experimental period. The effect of thyroid deficiency on [14C]thymidine metabolism in the brain is only slight, and is due to an abnormally large supply of [14C]thymidine consequent to depressed systemic utilization of this precursor.

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PubMed1976

Effect of thyroid deficiency on cell acquistion in the postnatal rat brain: a quantitative histological study.

The mechanisms underlying transient reduction of cell number in the developing cerebellum of thyroid-deficient rats have been studied by quantitative histological methods. Thyroid deficiency has no significant effect on the generation cycle of dividing cells in either the subependymal layer of the lateral ventricular walls or the external granulay layer of the cerebellum: the length of the cell cycle and the duration of the different phases of the cycle, including the DNA synthesis time appears to be normal. However, the external granular layer of the cerebellum contains fewer cells than in control at 12 days. Pyknotic nuclei are prominent in the granule cell layer of the hypothyroid cerebellum at this age. These amount to an estimated loss of about 1% of the total cerebellar cell population in 24 h. It is suggested that death of granule cells is for the most part a consequence of reduced Purkinje cell dendritic arborization, with failure of parallel fibre/Purkinje cell synaptogenesis. In the second postnatal week, granule cell death and reduced numbers of cells in the germinal zone can account to a great extent for the observed shortfall in cerebellar DNA content. The eventual attainment of normal cell numbers in the cerebellum of hypothyroid rats is related to a persistent external granular layer in the forth and fifth postnatal weeks.

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PubMed1975

The effect of undernutrition in early life on cell generation in the rat brain.

In undernourished rats aged up to 21 days, the DNA synthesis period in dividing cells of the subependymal and external granular layers is consistently and markedly prolonged, while rates of cell production from these layers are only slightly altered. Cell cycle times are unchanged up to the end of the first week of life and prolonged from day 12. The G1 phase is markedly shortened at 1, 6 and 12 days of age. It would appear that, in comparison with controls, disappearance of the external granular layer is delayed, and cell numbers in both germinal layers may be reduced.

Animals↗
PubMed1975

Effect of undernutrition on metabolic compartmentation of glutamate and on the incorporation of [14C] leucine into protein in the developing rat brain.

The effect of undernutrition on the rate of protein synthesis and the development of metabolic compartmentation of glutamate in the brain was investigated by using [U -14 C] leucine as precursor. In the brain of normal rats the incorporation rate of [14C] leucine into protein was at a maximum during the 3rd week after birth, but in the undernourished animal this rate was markedly lower. The biochemical maturation of the brain, followed in terms of the age-dependent increase in the glutamine/glutamate specific radioactivity ratio, was severly retarded in the undernourished animals, mainly as a result of a marked depression in the conversion of leucine carbon into glutamine. However these biochemical effects of undernutrition were reversible: on rehabilitation from Day 21-35 the rate of conversion of leucine carbon, both into proteins and glutamate and glutamine, was restored to normal.

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