Tadao Kakegawa

Changes in plasma thyroid hormones, luteinizing hormone (LH), estradiol, progesterone and corticosterone of laying hens during a forced molt

1. Circulating concentrations of iodothyronines, luteinizing hormone(LH), estradiol(E2), progesterone and corticosterone were measured in hens before, during, and after a forced molt induced by fasting. 2. Corticosterone increased at the onset of molt, peaked at the maximal molt and returned to pre- and post-molt levels. LH, E2 and progesterone declined during the molt, and the decline was coincident with the cessation of egg production. 3. Thyroxine(T4), triiodothyronine (T3) and reverse triiodothyronine(rT3) increased during the molt. The increases of T4 and T3 were not abolished even if the forced molt was conducted in mild weather.

Modification by hypothalamic lesions of the release of growth hormone (GH) following stimulation of the ventromedial hypothalamic nucleus in the rat.

This study was designed to clarify the localization(s) of hypothalamic area(s) concerned with the regulation of growth hormone (GH) release evoked by electrical stimulation of the hypothalamic ventromedial nucleus (VMH) of rats. Bipolar concentric stimulating electrodes were implanted in the bilateral VMH or dorsal premammillary nucleus and the jugular vein was cannulated for blood sampling one week prior to the experiments. At the same time lesions of the anterior periventricular nucleus or dorsal premammillary nucleus were performed with an anodal current. The rats were pretreated with alpha-methyl-p-tyrosine to prevent spontaneous GH bursts. As previously reported, stimulation of the VMH for 10 min appeared to suppress GH release during the period of stimulation but within 10 min after termination of stimulation plasma GH had risen from a resting level of 19.3 +/- 2.3 ng/ml plasma, to 275.3 +/- 62.3 ng/ml. The apparent suppression of GH release during the VMH stimulation was abolished in the anterior periventricular nucleus-lesioned rats. In these rats, GH release occurred during the VMH stimulation and plasma GH increased to 905.4 ng/ml by 10 min, at which time the stimulus was terminated. On the other hand, the VMH stimulation completely failed to raise plasma GH levels in rats with dorsal premammillary nucleus lesions either during or after VMH stimulation. Although lesions of the dorsal premammillary nucleus blocked the delayed VMH-induced rise, stimulation of the dorsal premammillary nucleus itself caused no change in the plasma GH level.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth hormone release induced by electrical stimulation of the basolateral amygdala, observed in pentobarbital anesthetized rats

The aim of this study was to clarify the neural pathway leading to the growth hormone (GH) release when the basolateral amygdala (ABL) was electrically stimulated. Concentric bipolar stimulating electrode was implanted in the unilateral ABL. Blood samples were taken from a cannula implanted into the right atrium via the right external jugular vein. Electrical stimulation of the ABL for 10 min caused a significant increase in plasma GH level from resting value 27.5 +/- 5.7 ng/ml (mean +/- S.E.M.) to 62.2 +/- 7.5 ng/ml at the termination of stimulation. This increase in GH level was markedly augmented to 152.0 +/- 23.0 ng/ml after lesion of the periventricular hypothalamic nucleus (Pe), where somatostatinergic neurons send their axons to the median eminence. Lesion of the stria terminalis (st) fully or partly abolished GH release induced by ABL stimulation. These results suggest that stimulation of the ABL accelerates GH secretion. The st is an essential pathway for this release, whereas the activity of Pe-neurons is rather inhibitory to this release.

Electrical Stimulation of the Basolateral Amygdala Elicits Only Growth Hormone Secretion Among Six Anterior Pituitary Hormones in the Pentobarbital‐Anesthetized Male Rat

In order to investigate the role of the basolateral amygdala on secretion of the adenohypophyseal hormones, the basolateral amygdala was electrically stimulated for 10 min through a chronically implanted electrode in the pentobarbital‐anesthetized adult male rat. Blood samples were withdrawn through a Silastic cannula implanted in the right atrium. Electrical stimulation of the basolateral amygdala increased plasma growth hormone, decreased plasma follicle‐stimulating hormone and suppressed the increase in plasma adrenocorticotropin. Plasma prolactin, thyroid‐stimulating hormone and luteinizing hormone were not significantly changed. These results indicate that electrical stimulation of the basolateral amygdala in the pentobarbital‐anesthetized adult male rat causes a simultaneous change in secretion of several adenohypophyseal hormones.

Electrical Stimulation of Specific Brainstem Nuclei Suppresses Growth Hormone‐Releasing Hormone‐Induced Growth Hormone Secretion in the Pentobarbital Anaesthetized Rat

To clarify the neural mechanism related to suppression of growth hormone (GH) secretion, biphasic electrical stimulation was delivered into several brainstem nuclei in the pentobarbital anaesthetized rat. A concentric bipolar stimulating electrode was implanted chronically one week prior to the electrical stimulation. Ninety min before the electrical stimulation, the rats were anaesthetized by ip injection of pentobarbital and a silastic cannula was inserted into the right atrium for blood sampling. Blood samples were withdrawn five times (0, 10, 20, 30 and 60 min) during the experiment. Electrical stimulation was delivered for 10 min just after the first blood sampling. One min after the onset of the stimulation, human GH‐releasing hormone was injected iv to induce GH secretion. Electrical stimulation of several brainstem nuclei, i.e. the locus coeruleus, the rostral portion of the nucleus tractus solitarius and the lateral reticular nucleus suppressed GH secretion and the central gray of the pons showed a tendency for the suppression of GH secretion. On the other hand, electrical stimulation of the parabrachial nucleus and the caudal portion of the nucleus tractus solitarius did not suppress GH secretion. These suppressions were nullified by prior electrolytic lesioning of the hypothalamic periventricular nucleus where the major cell bodies of somatostatin immunoreactive fibres in the median eminence originate. These results indicate that electrical stimulation of several brainstem nuclei excites somatostatin neurons in the periventricular nucleus which are responsible for the suppression of GH secretion.

Changes in thyroxine and triiodothyronine during spontaneous molt in the hen, gallus domesticus

Abstract 1. 1. Changes in plasma concentrations of thyroxine (T 4 ) and triiodothyronine (T 3 ) were studied during spontanepus molt in 28-month-old white leghorn hens. The molt was accomplished over a long time period (2–5 months) with intermittent body and wing feather shedding. 2. 2. Plasma T 4 levels in molted hens did not rise in molting periods and were rather lower than those in non-molting hens, while plasma T3 levels in molted hens rose significantly during heavy molts. 3. 3. The results suggest that in natural molt of hens, the increased thyroidal activity is not necessarily a prerequisite for molt except that more T 3 is needed for thermoregulation due to the loss of feather insulation.

Thyrotropin Response to Thyrotropin-Releasing Hormone in Rats with Hypothalamic Knife Cuts

Regulation of the pituitary-thyroid axis in rats with hypothalamic knife cuts has been studied. Complete hypothalamic deafferentation, either limited to the median eminence and the arcuate nucleus, or including parts of the dorsomedial nucleus and the whole ventromedial nucleus caused an increase in thyrotropin (TSH)-releasing hormone (TRH)-induced TSH secretion. Using an immunocytochemical procedure, a few TRH-positive fibers were observed within the median eminence of the larger island, while almost no fibers were identified in the smaller island. The exaggerated TSH response to TRH appeared within 3 days after the surgery and lasted for at least 1 week, when blood thyroxine (T4) level was significantly lowered. Exogenously injected T4 could inhibit such responses of TSH in the deafferented rats in a dose-related manner. These results support the hypothesis that the increase in the TSH response to TRH following hypothalamic deafferentation is due, at least in part, to the lowered thyroid hormone level in the blood.