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T Katafuchi

Publications and source records attributed to T Katafuchi.

85 records · Page 5Linked to original sources
PubMed1986

Hypothalamic regulation of sodium-potassium pump activity in skeletal muscle.

The suppression of active Na+-K+ transport in rat skeletal muscle during hypokalemia was counteracted by bilateral electrolytic lesion of the ventromedial hypothalamic nucleus. This reversal effect was unaffected even after pancreatectomy or adrenalectomy. The anomalous electrolyte content in hypokalemic rat muscles was aggravated by lesion of the dorsomedial hypothalamic nucleus and of the anterior hypothalamus. The results indicate that the hypothalamus is involved in the regulation of the Na+-K+ transport system in skeletal muscle during hypokalemia.

Animals↗
PubMed1986

Responses of adrenal catecholamine secretion to lateral hypothalamic stimulation and lesion in rats.

The effects of electrical stimulation and lesion of the lateral hypothalamic area (LHA) on catecholamine (CA) secretion from the adrenal medulla were investigated in anesthetized rats. A differential secretion of epinephrine (E) and norepinephrine (NE) was observed, in which a single stimulating site could produce different effects on E and NE secretion. On the basis of change in the E secretion rate during stimulation, stimulation sites could be classified into 3 groups: group A which showed increase in E secretion (no change in NE), group B which showed decrease in E (and also decrease in NE), and group C which showed no change in E (but a decrease in NE). No relationship was observed between the sites of stimulation in the LHA and the direction of the responses. Lesions of the stimulation sites decreased CA secretion to different extent among the three groups and these differences could be predicted by the effects of stimulation at the same sites. These results suggest that the LHA has both facilitatory and inhibitory effects on the sympatho-adrenal function and that the former is predominant.

Adrenal Medulla↗
PubMed1986

Effects of hypothalamic lesions on active sodium-potassium transport in the extensor digitorum longus muscles of hypokalemic rat.

The CNS-induced suppression on muscle Na+-K+ pump was studied in "twitch" muscle, extensor digitorum longus (EDL), of hypokalemic rats which were fed a K+ deficient diet for several weeks. Peripheral nerve section or bilateral lesion of the ventromedial hypothalamic nucleus had no effect on the Na+ and K+ contents in EDL of hypokalemic rats. However, lesions of the paraventricular nucleus caused the net Na+ loss and the net K+ uptake in the muscles. Lesions in either the dorsomedial nucleus or anterior hypothalamus also caused significant net K+ uptake but the net Na+ loss was not significant. The results were compared with those of "tonic" muscle, soleus, reported previously.

Animals↗
PubMed1985

Single neuron activity in the rat lateral hypothalamus during 2-deoxy-D-glucose induced and natural feeding behavior.

Single neuron activity in the lateral hypothalamic area (LHA) was recorded extracellularly in freely moving rats. Intra-third-cerebroventricular injection of 2-deoxy-D-glucose (2-DG) increased the activity in 38% of 69 neurons and decreased it in 19%. The remaining 43% of the neurons were not affected. Of the neurons excited, 50% showed definite inhibition of activity after long-lasting excitation. In 58% of the 69 neurons, the following changes in neuronal activity were observed during spontaneous feeding. Most of the tonic type neurons, which increased activity throughout the period of a meal, were excited by 2-DG, while the phasic type, which showed an abrupt increase in activity just before eating followed by a decrease, tended to be inhibited by 2-DG. Although injection of 2-DG induced feeding for a brief period in 61 cases (88%), the total food intake during 24 h was reduced significantly below normal. These findings indicate that 2-DG both excites and inhibits LHA neurons and induces facilitation followed by inhibition of feeding behavior.

Animals↗
PubMed1985

Lesions of the ventromedial hypothalamic nucleus enhance sympatho-adrenal function.

The effects of lesions of the ventromedial hypothalamic nucleus (VMH) on the sympatho-adrenal function were investigated in anesthetized rats using electrophysiological and biochemical techniques. Lesions of this nucleus produced a gradual but strong increase in the efferent activity of the adrenal sympathetic nerves. Catecholamine secretion from the adrenal medulla was also facilitated by VMH lesions. The results indicate that the catecholamines from the adrenal medulla might be involved in the development of metabolic disorders seen during VMH syndrome.

Adrenal Glands↗
PubMed1984

Effects of hypothalamic lesion on pancreatic autonomic nerve activity in the rat.

The effects of hypothalamic lesions and intravenous glucose infusion on the efferent activity of vagal and splanchnic nerves to the pancreas were studied in anesthetized rats. Lesions of the ventromedial hypothalamic (VMH), the dorsomedial hypothalamic (DMH) and the paraventricular (PVN) nuclei increased vagal and reduced splanchnic nerve activity. Lesion of the lateral hypothalamic area (LHA) decreased pancreatic vagal nerve activity, and produced either increased or decreased activity of pancreatic splanchnic nerve. Intravenous glucose infusion increased activity of the vagal nerve and reduced that of the splanchnic nerve. These glucose responses were influenced by hypothalamic lesions only slightly or not at all. The findings suggest that hypothalamic modulation of pancreatic hormone secretion involves both the parasympathetic and sympathetic nervous systems, and provide evidence that not only the VMH and the LHA but also the DMH and the PVN are involved in this mechanism.

Animals↗
PubMed1984

Responses of lateral hypothalamic neurons to simulative hypogravic condition induced by body suspension.

In unanesthetized rats, neuronal activity in the lateral hypothalamic area was recorded during horizontal and head-down tilt suspension. When the rat was raised in the horizontally suspended position, 21 of 44 neurons changed activity as follows: immediate increase (7/21, Type I), immediate decrease (3/21, Type II), and gradual decrease (11/21, Type III). When the rat was raised with a head-down tilt position, the responses were suppressed in about half of the neurons tested. These results showed that the LHA neurons altered their activity in response to low G simulation induced by body suspension. Possible signals which induce the changes in the LHA neuronal activity, and an involvement of the LHA in the autonomic reflexes under hypogravic condition are discussed.

Animals↗
PubMedDate not supplied

Immune cytokines and regulation of body temperature, food intake and cellular immunity.

Interleukin-1 (IL-1) and interferon alpha (IFN alpha), cytokines originally detected in immunological cells, now have been shown to produce nonimmunological host defense responses of central and peripheral origins. These cytokines are released from glial cells in the brain in pathological states. Local application of IL-1 beta and IFN alpha to thermosensitive neurons in the preoptic and anterior hypothalamus and glucose responsive neurons in the ventromedial hypothalamus in vivo and in vitro, altered the activity in appropriate ways to explain the cytokines-induced fever and anorexia, respectively. The responses to IL-1 beta, but not to IFN alpha, were blocked by sodium salicylate, suggesting the involvement of synthesis of prostaglandins. alpha MSH, an endogenous antipyretic and a possible antagonist of IL-1 beta at lymphocytes, specifically depressed the responses to IL-1 beta, but not those to IFN alpha. In contrast, the action of IFN alpha was reversibly blocked by naloxone, suggesting the opioid receptor mediation. Intracerebral injection of IFN alpha and beta-endorphin in the rat and mouse resulted in the suppression of cytotoxic activity of natural killer cells in the spleen by activation of brain opioid receptor, which was shown to be mediated predominantly by splenic sympathetic nerves. The results suggest a view that immune cytokines may provide afferent links for the regulatory circuits between the brain and the immune system.

Animals↗
PubMedDate not supplied

Impairment of spatial learning and hippocampal synaptic potentiation in c-kit mutant rats.

The c-kit receptor tyrosine kinase encoded by the white-spotting (W) gene is highly expressed in rat hippocampal CA1-CA4 regions. We found an impaired spatial learning and memory in homozygous c-kit (Ws/Ws) mutant rats that have a 12-base deletion in the tyrosine kinase domain of the c-kit gene and a very low kinase activity. Electrophysiological studies in hippocampal slices revealed that the long-term potentiation (LTP) induced by the tetanic stimulation (100 Hz, 1 sec) in the mossy fiber (MF)-CA3 pathway, but not in the Schaffer collaterals/commissural-CA1 pathway, was significantly reduced in c-kit mutants compared with wild-type (+/+) rats. The paired-pulse facilitation (PPF) was measured before the tetanus and after the establishment of the LTP in each slice. The initial PPF in the MF-CA3 pathway positively correlated with the amplitude of the LTP in the wild-type rats but not in the c-kit mutant rats. Furthermore, they failed to show the normal characteristics observed in the MF-CA3 pathway of +/+ rats; that is, the negative correlation between the initial PPF and the changes in PPF measured after the LTP. These findings suggest an involvement of SCF/c-kit signaling in hippocampal synaptic potentiation and spatial learning and memory.

Animals↗
PubMedDate not supplied

Neuroimmunomodulatory actions of hypothalamic interferon-alpha.

Recent studies have revealed that the brain produces interferon-alpha (IFN-alpha) in response to noninflammatory as well as inflammatory stress and that it might have a role in normal physiology. When administered intracerebrally, IFN-alpha causes diverse effects including fever, anorexia, analgesia and changes in the central neuronal activities. These responses are inhibited by the opioid receptor antagonist naloxone. This is consistent with the reports suggesting that recombinant human (rh) IFN-alpha binds to opioid receptors in rodent brain membrane. We revealed that rhIFN-alpha altered the activity of thermosensitive neurons in the medial preoptic area (MPO) and glucose-responsive neurons in the ventromedial hypothalamus in an opioid-receptor-dependent way. As a stress which produces opioid-dependent analgesia is known to suppress the cytotoxicity of splenic natural killer cells, we investigated whether the administration of beta-endorphin and rhIFN-alpha may induce a similar immunosuppression. We found that central, but not peripheral, injection of both compounds inhibited natural killer (NK) cytotoxicity. Further studies revealed that rhIFN-alpha decreased the activity of MPO neurons via opioid receptors and the altered activity of MPO neurons in turn resulted in the activation of corticotropin-releasing factor neurons, thereby suppressing NK cytotoxicity predominantly through activation of the splenic sympathetic nerve and beta-receptor mechanisms in splenocytes. Thus, IFN-alpha may alter the brain activity to exert a feedback effect on the immune system. Further detailed whole-cell clamping analyses on neuronal mechanisms in rat brain tissue slices showed that the inhibitory effect of rhIFN-alpha on N-methyl-D-aspartate-induced membrane current responses of MPO neurons was mediated not only by opioid receptors but also by the local production of reactive oxygen intermediates, nitric oxide and prostanoids, possibly due to neuron-glial cell interaction.

Animals↗
PubMedDate not supplied

The autonomic nervous system as a communication channel between the brain and the immune system.

Much evidence from various fields has revealed multiple channels of communication between the brain and the immune system. Among the routes of signal transmission, this review focuses on the roles and mechanisms of neural communication between the two systems. As for the centrifugal neural pathway by which the brain modulates immunity, there are various requirements for the noradrenergic sympathetic innervation of the primary and secondary lymphoid organs. In addition to the presence of beta- and alpha-adrenergic receptors on different types of immunocompetent cells, histological studies have demonstrated direct contact between tyrosine-hydroxylase-positive nerve terminals and lymphocytes in the spleen and thymus. The exposure of lymphocytes and macrophages to adrenergic agonists in vitro modulates their functions. A surgical or chemical sympathectomy is known to alter the immune responses in rodents. Recent data from the rat show that stress-induced immunosuppression is only slightly affected, if at all, by hypophysectomy or adrenalectomy, whereas it is largely dependent on sympathetic innervation. The splenic sympathetic nerve alters the firing rate by an ablation or stimulation of the hypothalamus, the administration of cytokines or neuropeptides, and an exposure to stress. Furthermore, such procedures provoke the increase in the release of noradrenaline in the rat spleen as assessed by in vivo microdialysis. The altered activities of the splenic sympathetic nerves mentioned above have been found to be causally related to the alteration in immunological responses including natural killer cytotoxicity. The splenic sympathetic nerve may thus constitute a communication channel that mediates central modulation of peripheral cellular immunity. Although the roles and mechanisms of parasympathetic control of lymphoid organs still remain obscure, recent data suggest that the thymic vagal efferent nerve may be involved in central modulation of immunity. Finally, electrophysiological studies have shown that hepatic vagal afferents may be one of the pathways through which blood-borne cytokines signal the brain.

Animals↗