Thyroidectomy and Central Catecholamine Neurons of the Male Rat

Abstract

Using the Falck-Hillarp methodology in combination with quantitative microñuorimetry, catecholamine (CA) levels and utilization in discrete hypothalamic CA nerve terminal systems in the male rat have been analyzed 24 h, 1, 2 and 4 weeks following thyroidectomy as well as after T₃ or T₄ restitution therapy 4 weeks after thyroidectomy. By means of high pressure liquid chromatography (HPLC), dopamine (DA) and noradrenaline (NA) levels and utilization 4 weeks after thyroidectomy have been analyzed in various brain regions. Triiodothyronine treatment (10 µg/kg, s.c, twice daily during 10 days) of 4-week athyroidic rats increased serum T₃ levels, but not T₄ serum levels. Thyroxine treatment (36 µg/kg, s.c, twice daily during 10 days) of 4-week athyroidic rats increased serum T₄ levels and the T₃ levels were found to be even slightly higher than those found in normal animals. Triiodothyronine or T₄ restitution therapy reversed the changes induced by thyroidectomy on the anterior pituitary hormones (TSH, prolactin and growth hormone) and corticosterone secretion. It is suggested that removal of thyroid hormones may be responsible for the changes in the anterior pituitary hormones and corticosterone secretions. In the quantitative microfluorimetrical analysis 24 h, 1,2 and 4 weeks after thyroidectomy, decreases in DA levels and utilization and increases in NA levels and utilization were found in the lateral palisade zone (LPZ) of the median eminence and in the parvocellular and magnocellular parts of the paraventricular hypothalamic nucleus (PA), respectively. In addition, 1-, 2- and 4-week decreases were found in DA levels and turnover in the medial palisade zone (MPZ) as well as in NA turnover in the dorsomedial hypothalamic nucleus (DM) and in the ‘border zone’ (BZ) between the medial and lateral hypothalamus ventral to the fornix. In the HPLC analysis it could be demonstrated that 4 weeks after thyroidectomy decreases in DA levels and utilization in the mediobasal hypothalamus and increases in DA levels as well as NA levels and utilization in the hypothalamus had developed. The T₃ or T₄ restitution therapies after 4 weeks of thyroidectomy counteracted the effects on CA levels and utilization in all hypothalamic CA nerve terminal systems except for the reduced NA utilization found in the DM following 4 weeks after thyroidectomy. The demonstrated reductions in DA levels and utilization in the MPZ and LPZ of the median eminence and the increases in NA levels and utilization in the PA are suggested to reflect the existence of an inhibitory dopaminergic mechanism in the median eminence and a facilitatory noradrenergic mechanism in the PA involved in the regulation of TSH secretion. These mechanisms seem to be directly or indirectly regulated by thyroid hormones. The reduced NA utilization in the DM and in the BZ after thyroidectomy is suggested to be related to the lowering of growth hormone secretion and reduction of its pul...

Enhanced Tuberoinfundibular Dopaminergic Neuron Activity in Thyroidectomized, Ovariectomized and Estrogen-Treated Rats with Hyperprolactinemia

“…Hypothyroid male [5][6][7] or Tx + Ovx female rats with [8]. We [4] and others [9] have already shown that there is an increased PRL secretion in response to thyrotropinreleasing hormone (TRH) in estrogen-treated Ovx + Tx rats, which partially explains the high PRL levels in those animals.…”

“…Most studies showed increased activity of the TIDA neurons using indices such as DA turnover rate [5,10] or tyrosine hydroxylase activity [7,11] in the median eminence (ME) and DA level in hypophysial portal plasma [7]. On the other hand, reductions in DA level and utilization in the ME were also reported [6], The increased activity of TIDA neurons in male hypothyroid rats seems to corre late well with the decreased plasma PRL level [7], A simi lar relationship in the female hypothyroid rat, however, has not been reported. In this study, we measured the activity of TIDA neurons using a more appropriate ani mal model, i.e.…”

Effects of Combined Pre‐ and Postnatal Treatment with Nicotine on Hypothalamic Catecholamine Nerve Terminal Systems and Neuroendocrine Function in the 4‐Week Old and Adult Male and Female Diestrous Rat

“…Furthermore, upon TH inhibition a clearly significant lowering of LH serum levels was also demonstrated in these nicotine-treated female rats. These results may be explained on the basis of an increased dependency on release of CA from adrenaline and NA nerve terminal systems of the hypothalamus and preoptic area known to have a stimulatory role in the control of serum TSH and LH levels (12,(18)(19)(20)(21)(22)(23)(24). This increase in the dependency of stimulatory NA and adrenaline networks may be related to the increase in DA utilization in the tubero-infundibular DA neurons, which exhibit inhibitory effects on serum TSH, prolactin and LH levels.…”

Morphofunctional Characteristics of Pituitary Adrenocorticotropes in An Animal Model of Heat Stress

“…Considering the data about decreased concentration of serum corticosterone found in this study, we assume that the decreased activity of ACTH cells may be due, in some part, to the negative feed-back mechanism of glucocorticoids upon the HPA axis, and therefore, upon ACTH cells. Generally, there is a synergistic relationship between the adrenal and thyroid gland through the HP axis (27,28). The data from Rousset et al (25) have shown suppression of thyroid activity in the first two days of exposure to 34°C, and therefore decreased activity of the CRH and ACTH (27).…”

“…Generally, there is a synergistic relationship between the adrenal and thyroid gland through the HP axis (27,28). The data from Rousset et al (25) have shown suppression of thyroid activity in the first two days of exposure to 34°C, and therefore decreased activity of the CRH and ACTH (27). Our findings of a decreased plasma concentration of ACTH, as well as the decreased cell volume and volume density of the ACTH cells, might be, in some degree, the result of decreased activity of CRH via the thyroid gland.…”