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Université Lyon 1, Villeurbanne, France
Université de Lyon, Lyon, France
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Université Lyon 1, Villeurbanne, France
Université de Lyon, Lyon, France
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the hormonal signals that the gut releases in blood in response to nutrient assimilation and which modulate hunger sensations and glucose homeostasis, such as cholecystokinin and glucagon-like peptide 1, a set of processes referred to as the gut–brain
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Introduction Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family expressed in many areas of the adult mammalian brain. Its biological action is mediated by the specific tyrosine kinase receptor trkB (Tapia Aranciba et al
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Introduction The brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family having the nerve growth factor as prototype. The main biological effects of BDNF are mediated by specific tyrosine kinase (TrkB
Department of Child Health, University of Arizona College of Medicine, Phoenix, Arizona, USA
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Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom
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Introduction Annually, approximately 70 million people worldwide suffer from a traumatic brain injury (TBI) ( Dewan et al. 2018 ), with 1.5 million of these individuals residing in the USA. Among the 1.5 million, around 50,000–60,000 are
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Laboratory of Experimental Endocrinology, Department for Public Health and Community Medicine, AstraZeneca R&D, Institute for Neuroscience and Physiology, Department of Primary Health Care, Department of Internal Medicine, The Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 5, SE-413 45 Gothenburg, Sweden
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Laboratory of Experimental Endocrinology, Department for Public Health and Community Medicine, AstraZeneca R&D, Institute for Neuroscience and Physiology, Department of Primary Health Care, Department of Internal Medicine, The Sahlgrenska Academy, Sahlgrenska University Hospital, University of Gothenburg, Blå Stråket 5, SE-413 45 Gothenburg, Sweden
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-proliferative effects ( Åberg et al . 2009 , 2010 ). The fact that GH-receptors are expressed in both glial cells and neurons ( Lobie et al . 1993 ) and that GH crosses the blood–brain barrier (BBB) ( Lopez-Fernandez et al . 1996 , Ye et al . 1997 ) indicates that
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). We aimed to answer this question in the present study by using the transgenic rats with low brain angiotensinogen (TGR(ASrAOGEN)) ( Schinke et al . 1999 ). In TGR(ASrAOGEN), angiotensinogen protein concentration was reduced to 10% in medulla, pons
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From Galen in the 2nd century AD, medical orthodoxy held that the brain–pituitary axis terminated in the nostrils and palate. Blood was allegedly endowed with vital spirit in the left ventricle of the heart and with animal spirit, the substance
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conventional reverse transcription-polymerase chain reaction (RT-PCR) method, which allows detection of only the final amplified product, has been employed to study expression patterns of GnRH mRNAs in discrete brain areas of rainbow trout ( Ferriere et al
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regulation of energy homeostasis. However, the underlying mechanisms are poorly understood. In the brain, and in agreement with its role in the control of energy balance, NUCB2/nesfatin-1 is highly expressed in several hypothalamic nuclei such as
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SUMMARY
1. Following the demonstration [Chance & Yaxley, 1950] that the brain glycogen of the mouse rises during a convulsion, an attempt has been made to study the effect of various substances on the level of brain glycogen in the mouse both when resting and after a convulsion induced by metrazol. The substances used were glucose, adrenaline, insulin, deoxycorticosterone glucoside, cortisone acetate and the anti-insulin principle of the anterior pituitary. The effect of fasting on the brain glycogen of the resting mouse was also examined.
2. The level of glycogen in the brain rose in the presence of a raised blood sugar or following injection of the anti-insulin principle. Insulin antagonized the effect of the latter without altering the level of the blood sugar.
3. During convulsions induced by metrazol after the administration of insulin, the level of the blood-sugar was reduced, and the usual increment in brain glycogen was suppressed. It reappeared when sufficient glucose was injected to restore the blood-sugar level to normal. None of the other substances tested affected the rise in glycogen level of the brain induced by a convulsion.
4. During certain types of normal behaviour [Chance, 1953 a] the levels of the blood sugar and brain glycogen generally change independently of each other, but on occasion both rise simultaneously. It is concluded that they represent independent responses resulting from central nervous activity.
