Hyperthermia after intrahypothalamic injections of thyrotropin releasing hormone (TRH) in the pigeon

Thermoregulatory responses to intrahypothalamic injections of thyrotropin releasing hormone (TRH) were recorded from unanesthetized pigeons exposed to 6 degrees C, 20 degrees C and 32 degrees C. Our results suggest that TRH is a non-specific excitatory neuromodulator or neurotransmitter for heat production in the pigeon.     

Distribution of thyrotropin releasing hormone (TRH), alpha-melanocyte-stimulating hormone (alpha-MSH) and somatostatin in the skin of the green frog (Rana esculenta)]

High concentrations of Thyrotrophin-Releasing Hormone (TRH) have been found in the dorsal skin of the Frog Rana esculenta, lower levels being measured in the ventral skin. alpha-MSH and somatostatin were undetectable in these tissues. Nor was TRH detected in the blood of these animals. The concentration of somatostatin in the pancreas was similar to that of the hypothalamus and twice or one hundred times higher than in the intestine or stomach respectively.     

Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat

Summary At ambient temperatures (T_a) of both 8 and 22°C, intraventricular administration of TRH (10–80 g) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30°C T_a, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.This work was supported by the grants from the National Science Council of Republic of China and the Pjing-Ling Neurological Foundation (VGH, Taipei, Taiwan).     

Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat

At ambient temperatures (Ta) of both 8 and 22 degrees C, intraventricular administration of TRH (10-80 microgram) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30 degrees C Ta, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.     

Control of pituitary secretion of melanotropin in an anuran amphibian by thyrotropin releasing factor (TRH). Study in vitro]

Intermediate lobes from Rana esculenta pituitary glands were continuously superfused for 7 hrs at 28 degrees C with amphibian culture medium. alpha-MSH release was measured by use of a sensitive double antibody radio-immunoassay system. alpha-MSH secretion was inhibited by low temperatures. A large increase in alpha-MSH release was observed when Thyrotropin Releasing Hormone (TRH) at doses ranging from 10(-9) to 10(-7) molar was added to the superfusion medium. Since large amounts of TRH are to be found in the hypothalamus of amphibians but have no effect over pituitary TSH secretion, the action of TRH over alpha-MSH release may have a physiological significance.     

Papaverine enhances the negative inotropic effect of acetylcholine in rat auricles

Summary The negative inotropic effect of acetylcholine in rat left auricles is enhanced in the presence of the phosphodiesterase inhibitor papaverine. This result favours the idea of a cyclic GMP-mediated action of acetylcholine in the heart.I thank Lydia Paragnik for help. This research was supported by a grant from the Deutsche Forschungsgemeinschaft.     

Differential effects of the serotonin receptors on cultured rat cerebral cortical neurons

Effects of serotonin (5-HT) on cerebral cortical neurons were examined by patch clamp techniques. 5-HT produced a variety of responses such as outward (19/73 patches/neurons), slow inward (15/73 patches/neurons), fast inward (8/73 patches/neurons), and mixed currents (initially fast inward deflection followed by an outward response: 2/73 patches/neurons), with a latency of 12 sec, 15 sec, 0 sec, and 0 sec respectively, at a holding potential of −60 mV in whole-cell patches. The fast inward currents were again evoked by a selective 5-HT3 receptor agonist, 1-(m-chlorophenyl)-biguanide hydrochloride (CPBG). In the cell-attached patch clamp configuration, 5-HT inside the patch pipette elicited single channel currents with slope conductances of 42 pS and 132 pS (4/42 patches/neurons). CPBG inside the patch pipette evoked inward single channel currents with a lower slope conductance of 41 pS (3/23 patches/neurons). In contrast, application of 5-HT or a 5-HT₂ receptor agonist, α-methyl-5-hydroxytryptamine-maleate, outside the patch pipette induced outward single channel currents with a major slope conductance of 140 pS (8/30 patches/neurons) or 135 pS (6/20 patches/neurons), respectively. These results indicate that the outward and fast inward currents may be mediated respectively by the 5-HT₂ receptor, which is coupled to a G-protein, and by the 5-HT₃ receptor, which contains the non-selective cation channel, and that the mixed type may be caused by both the 5-HT₂ and 5-HT₃ receptors. Received 27 September 1996; received after revision 4 November 1996; accepted 7 November 1996     

Antagonism by thyrotropin-releasing hormone (TRH) of pentobarbital-induced hypothermia in rats with brain lesions

Summary Anesthesia with a large dose of pentobarbital (55 mg/kg, i.p.) caused a sustained decrease in brain temperature (Tb), which was monitored with a probe placed in the midbrain reticular formation. The administration of TRH to the lateral ventricle antagonized this hypothermia. None of the acute surgeries examined in this paper (adrenal-demedullectomy, septal knife cuts, electrolytic lesions of the hypothalamus and midbrain knife cuts) had any essential effect on this antagonism by TRH. These results suggest that centrally-administered TRH exerts its effect on thermoregulation, at least in part, through brain structure(s) caudal to the midbrain.     

Antagonism by thyrotropin-releasing hormone (TRH) of pentobarbital-induced hypothermia in rats with brain lesions

Anesthesia with a large dose of pentobarbital (55 mg/kg, i.p.) caused a sustained decrease in brain temperature (Tb), which was monitored with a probe placed in the midbrain reticular formation. The administration of TRH to the lateral ventricle antagonized this hypothermia. None of the acute surgeries examined in this paper (adrenal-demedullectomy, septal knife cuts, electrolytic lesions of the hypothalamus and midbrain knife cuts) had any essential effect on this antagonism by TRH. These results suggest that centrally-administered TRH exerts its effect on thermoregulation, at least in part, through brain structure(s) caudal to the midbrain.     

Is beta-(4-chlorophenyl)-GABA a specific antagonist of substance P on cerebral cortical neurons?

Beta-(4-chlorophenyl)-GABA (Baclofen, Lioresal) antagonized the excitant actions of acetylcholine and substance P to comparable extents. L-glutamate-induced excitation was affected to a lesser extent. These findings do not support the suggestion that beta-(4-chlorophenyl)-GABA is a specific substance P antagonist.     

Immunocytochemical localization of GnRH (gonadotropin releasing hormone) systems in the brain of a marine teleost fish,the sole

Summary The GnRH system was studied in the brain of the sole by immunocytochemistry (peroxidase-antiperoxidase method) (PAP) using antibodies to synthetic salmon GnRH (s-GnRH). Two centers containing immunoreactive cell bodies were observed in the forebrain, one located at the junction between the olfactory bulbs and the telencephalon and the other in the preoptic area. Numerous immunoreactive fibers were found, especially in the telencephalon, hypothalamus, pituitary, optic tectum and retina.     

Pancreastatin (33–49) enhances the priming effect of glucose in the rat pancreas

Short-term exposure to glusoe increases insulin secretion during subsequent stimulation. We investigated the effect of the new regulatory peptide pancreastatin on this priming effect of glucose in the perfused rat pancreas. Pancreastatin (33–49) at a concentration of 10^–8 M inhibited insulin release when stimulated by glucose at a concentration of 16.7 mM. However, after a second pulse of 16.7 mM glucose, pancreastatin potentiated the priming effect of glucose on insulin secretion. The modulation of insulin secretion by pancreastatin results in a potentiation of the priming effect of glucose in the rat pancreas, suggesting a role for pancreastatin in the adaptation of the B cell to glucose-stimulated insulin secretion.     

Pituitary gonadotropin releasing hormone (GnRH) receptor levels in intact and ovariectomized-adrenalectomized female golden hamsters on a short photoperiod

Both intact and ovariectomized + adrenalectomized hamsters on a short photoperiod, had a daily surge in plasma LH at approximately 16.00-18.00 h. The number of pituitary GnRH receptors was generally lower in ovariectomized + adrenalectomized hamsters than in intact animals, but both intact and ovariectomized + adrenalectomized hamsters had a decrease in the number of receptors just prior to the LH surge. These results show that gonadal steroids are not involved in regulating the pre-LH surge fall in the number of GnRH receptors.     

Pituitary gonadotropin releasing hormone (GnRH) receptor levels in intact and ovariectomized-adrenalectomized female golden hamsters on a short photoperiod

Summary Both intact and ovariectomized+adrenalectomized hamsters on a short photoperiod, had a daily surge in plasma LH at approximately 16.00–18.00 h. The number of pituitary GnRH receptors was generally lower in ovariectomized+adrenalectomized hamsters than in intact animals, but both intact and ovariectomized+adrenalectomized hamsters had a decrease in the number of receptors just prior to the LH surge. These results show that gonadal steroids are not involved in regulating the pre-LH surge fall in the number of GnRH receptors.     

An assessment of the effect of hormone and neurotransmitters on adenine and gluanine derivatives simultaneously in rat brain cortical slices

Summary A 2-dimensional thin-layer method has been developed for the separation on cellulose of adenine and guanine derivatives. Using incubated rat cerebral cortex slices it was shown that noradrenaline and acetylcholine stirnulated cAMP and cGMP production respectively but glutamate and -aminobutyric acid stimulated production of both cyclic nucleotides.