The effects of early hypo- and hyperthyroidism on the development of the rat cerebellar cortex. II. Synaptogenesis in the molecular layer

doi:10.1016/0006-8993(72)90363-0

Brain Research

Volume 44, Issue 1, 15 September 1972, Pages 25-36

https://doi.org/10.1016/0006-8993(72)90363-0 Get rights and content

Abstract

The development of the molecular layer was studied in rats made hypo- and hyperthyroid at birth. The width and area of the molecular layer, packing density of granule cells in the internal granular layer, and synaptogenesis in the outer and inner halves of the molecular layer were determined. Hypothyroidism caused:

(1) transient developmental retardation in width and area of the molecular layer, with normal levels being approached by 30 days,
(2) a slight, but not significant, increase in packing density of granule cells, probably reflecting a reduction in glomeruli or synaptogenesis in the internal granular layer, as well as crowding produced by increased numbers of granule cells ²⁰,
(3) retardation of synaptogenesis in the molecular layer, especially in the outer half, as late as 55 days. This retardation was manifested by a decrease in the synaptic content of the Purkinje cell dendritic domain, and decreased size of the parallel fiber synaptic domain, resulting (along with the increase in granule cells) in a greater packing density of parallel fibers in the molecular layer.

Hyperthyroidism caused:

(1) an accelerated increase in width of the molecular layer from day 10 on, such that by 30 days the molecular layer was wider than in controls. This was accompanied by only a small, transient increase in the area of the molecular layer and a sharp leveling off by 15 days such that the area was greatly decreased by 30 days compared to controls. This was interpreted to mean that the length of the molecular layer was decreased in the sagittal plane, resulting in taller and narrower Purkinje cell dendritic trees. Possible reasons for this are discussed,
(2) a significant decrease in packing density of granule cells, probably reflecting both the decrease in the number of granule cells ²⁰ and an accelerated development of glomeruli,
(3) an acceleration of synaptogenesis in the inner and outer halves of the molecular layer and an increase in the number of synaptic profiles/cell at 30 days. This probably is the result of accelerated growth of the Purkinje cell dendritic tree and the deficit in granule cells and basket cells described previously ²⁰. Total synaptic profiles were decreased, however, due to the decreased sagittal length and area of the molecular layer.

Thus it was shown that early hypo- and hyperthyroidism both cause a terminal deficit in total synaptic profiles in the rat cerebellar cortex, but for different reasons.

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The effects of early hypo- and hyperthyroidism on the development of the rat cerebellar cortex. II. Synaptogenesis in the molecular layer

Abstract

Brain Research

Brain Research

Gen. comp. Endocr.

Brain Research

Brain Research

Brain Research

Autoradiographic and histological studies of postnatal neurogenesis. III. Dating the time of production and onset of differentiation of cerebellar microneurons

J. comp. Neurol.

Biochemical effects of thyroid deficiency on the developing brain

J. Neurochem.

Cytochemistry of synapses: a selective staining method for electron microscopy

Science

Effect of thyroid hormone on the biochemical maturation of rat brain: conversion of glucose-carbon into amino acids

J. Neurochem.