scholarly journals Recurrent Hypoglycemia Is Associated with Loss of Activation in Rat Brain Cingulate Cortex

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1908-1914 ◽  
Author(s):  
Paul Hurst ◽  
Alastair S. Garfield ◽  
Claire Marrow ◽  
Lora K. Heisler ◽  
Mark L. Evans
Keyword(s):  
Stress Responses ◽  
Cingulate Cortex ◽  
Brain Regions ◽  
Control Area ◽  
Sprague Dawley ◽  
Brain Areas ◽  
Sprague Dawley Rats ◽  
Brain Circuitry ◽  
Acute Hypoglycemia ◽  
Recurrent Hypoglycemia

A subset of people with diabetes fail to mount defensive counterregulatory responses (CRR) to hypoglycemia. Although the mechanisms by which this occurs remain unclear, recurrent exposure to hypoglycemia may be an important etiological factor. We hypothesized that loss of CRR to recurrent exposure to hypoglycemia represents a type of stress desensitization, in which limbic brain circuitry involved in modulating stress responses might be implicated. Here, we compared activation of limbic brain regions associated with stress desensitization during acute hypoglycemia (AH) and recurrent hypoglycemia (RH). Healthy Sprague Dawley rats were exposed to either acute or recurrent 3-d hypoglycemia. We also examined whether changes in neuronal activation were caused directly by the CRR itself by infusing epinephrine, glucagon, and corticosterone without hypoglycemia. AH increased neuronal activity as quantified by c-fos immunoreactivity (FOS-IR) in the cingulate cortex and associated ectorhinal and perirhinal cortices but not in an adjacent control area (primary somatosensory cortex). FOS-IR was not observed after hormone infusion, suggesting that AH-associated activation was caused by hypoglycemia rather than by CRR. Importantly, AH FOS-IR activation was significantly blunted in rats exposed to RH. In conclusion, analogous with other models of stress habituation, activation in the cingulate cortex and associated brain areas is lost with exposure to RH. Our data support the hypothesis that limbic brain areas may be associated with the loss of CRR to RH in diabetes.

Enzymatic condensation of dopamine and acetaldehyde: a salsolinol synthase from rat brain

Biologia ◽  
2011 ◽  
Vol 66 (6) ◽  
Author(s):  
Xuechai Chen ◽  
Abida Arshad ◽  
Hong Qing ◽  
Rui Wang ◽  
Jianqing Lu ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Substantia Nigra ◽  
Human Subjects ◽  
Enzymatic Reaction ◽  
Brain Regions ◽  
Activity Detection ◽  
Reaction Products ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salsolinol Synthase

AbstractSalsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; Sal) is structurally similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is supposed to have a role in the development of Parkinson-like syndrome in both human and non-human subjects. In the human brain, the amount of (R)-enantiomer of Sal is much higher than (S)-enantiomer, suggesting that a putative enzyme may participate in the synthesis of (R)-salsolinol, called (R)-salsolinol synthase. In this study, the (R)-salsolinol synthase activity in the condensation of dopamine and acetaldehyde was investigated in the crude extracts from the brains of Sprague Dawley rats. Identification of the enzymatic reaction products and enzyme activity detection were achieved by HPLC-electrochemical detection. The discovery of this enzyme activity in rat’s brain indicates the natural existence of (R)-salsolinol synthase in the brains of humans and rats, and it is distributed in most brain regions of rat with higher activity in soluble proteins extracted from striatum and substantia nigra.

Cardiovascular and renal sympathetic activation by blood-borne TNF-α in rat: the role of central prostaglandins

2003 ◽  
Vol 284 (4) ◽  
pp. R916-R927 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Shun-Guang Wei ◽  
Joseph Francis ◽  
Robert B. Felder
Keyword(s):  
Lateral Ventricle ◽  
Biological Effects ◽  
Brain Regions ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Hypothalamic Level ◽  
Renal Sympathetic

In pathophysiological conditions, increased blood-borne TNF-α induces a broad range of biological effects, including activation of the hypothalamic-pituitary-adrenal axis and sympathetic drive. In urethane-anesthetized adult Sprague-Dawley rats, we examined the mechanisms by which blood-borne TNF-α activates neurons in paraventricular nucleus (PVN) of hypothalamus and rostral ventrolateral medulla (RVLM), two critical brain regions regulating sympathetic drive in normal and pathophysiological conditions. TNF-α (0.5 μg/kg), administered intravenously or into ipsilateral carotid artery (ICA), activated PVN and RLVM neurons and increased sympathetic nerve activity, arterial pressure, and heart rate. Responses to intravenous TNF-α were not affected by vagotomy but were reduced by mid-collicular decerebration. Responses to ICA TNF-α were substantially reduced by injection of the cyclooxygenase inhibitor ketorolac (150 μg) into lateral ventricle. Injection of PGE2 (50 ng) into lateral ventricle or directly into PVN increased PVN or RVLM activity, respectively, and sympathetic drive, with shorter onset latency than blood-borne TNF-α. These findings suggest that blood-borne cytokines stimulate cardiovascular and renal sympathetic responses via a prostaglandin-dependent mechanism operating at the hypothalamic level.

Neurotransmitter Levels in Brains of Chronically Jiawey Siwu-Treated Rats

2002 ◽  
Vol 30 (04) ◽  
pp. 507-519
Author(s):  
Sue Yu ◽  
Yee-Yung Ng ◽  
Zhi-Hong Jian ◽  
Chien-Chih Chen ◽  
Mei-Shiun Lu ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Medulla Oblongata ◽  
Excitatory Amino Acids ◽  
Aminobutyric Acid ◽  
Vanillylmandelic Acid ◽  
Dose Dependency ◽  
Sprague Dawley ◽  
Brain Areas ◽  
Sprague Dawley Rats ◽  
Body Weights

Levels of monoamines and metabolites, excitatory amino acids, and γ-aminobutyric acid (GABA) were investigated in discrete brain areas of chronic Jiawey Siwu (JS)-treated rats. Male Sprague-Dawley rats were dosed orally for 3 months with normal saline or JS at 0.21, 1.05 or 4.2 g/kg/day. Body weights of these four groups were similar over 3 months. Most effects of JS revealed a dose dependency with levels of neurotransmitters. Levels of norepinephrine (NE) and epinephrine (EPI) in cerebral cortex; EPI, vanillylmandelic acid (VMA), dopamine (DA) and 5-hydroxytryptamine (5-HT) in medulla oblongata; DA in midbrain; NE and 5-HT in amygdala; and 5-HT in hypothalamus had decreased in JS-treated rats. 3-Methoxytyramine (3-MT) in cerebral cortex; 5-hydroxyindole-3-acetic acid (5-HIAA) in medulla oblongata; NE, 3-MT and homovanillic acid (HVA) in pons; EPI and 3-MT in midbrain; 3-MT and HVA in amygdala; 3-MT, 3,4-dihydroxyphenylacetic acid (DOPAC), HVA and 5-HIAA in cerebellum; HVA in hypothalamus; and DOPAC and HVA in hippocampus had all increased in JS-treated rats. In pons, 5-HT increased with low and decreased with high JS doses. Ratios of DA/3-MT in pons and midbrain; DA/HVA in pons and cerebellum; and 5-HT/5-HIAA in medulla oblongata, cerebellum and hypothalamus had decreased. Furthermore, aspartate (ASP) and glutamate (GLU) levels had decreased in cerebral cortex, midbrain, hypothalamus and hippocampus or amygdala, and increased in pons. GABA levels were reduced in cerebral cortex, and higher in medulla oblongata, pons, amygdala, cerebellum, hippocampus and striatum of JS-treated rats. These results indicate that the synthesis and (or) metabolism of NE, DA, EPI and 5-HT, and the levels of ASP, GLU and GABA in rat brains were differentially regionally altered by JS, which may contribute to the central manifestations of JS treatment.

Level of satiety: GABA and pentose shunt activities in three brain sites associated with feeding

1985 ◽  
Vol 248 (4) ◽  
pp. R453-R458 ◽  
Author(s):  
T. R. Kasser ◽  
R. B. Harris ◽  
R. J. Martin
Keyword(s):  
Area Postrema ◽  
Ventromedial Hypothalamus ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Energy Status ◽  
Sprague Dawley ◽  
Brain Areas ◽  
Gastric Intubation ◽  
Glucose Flux ◽  
Sprague Dawley Rats

The hypothesis addressed was that metabolic activity within specific brain areas may be altered to depict peripheral metabolic status. Sixty-three female Sprague-Dawley rats (225 g) received 150, 100, or 50% of normal intake by gastric intubation for 7 days. The incentive for spontaneous feeding would be inhibited in 150% fed rats (anoretic), stimulated in 50% fed rats (hungry), and maintained in 100% fed rats (control). Glucose flux through the gamma-aminobutyric acid shunt of the ventrolateral hypothalamus was 32% lower in hungry rats and 35% higher in anoretic rats relative to control values. Glucose flux through the pentose shunt of the ventromedial hypothalamus was 111% lower in hungry rats and 152% higher in anoretic rats relative to control values. Pentose shunt activity in the area postrema nucleus of the solitary tract (AP NTS) was 116% lower in hungry rats and 60% higher in anoretic rats relative to control values; however, hungry and anoretic rats had AP NTS pentose shunt activities that were not different from control values but were different from each other. The data demonstrate that within selective brain sites, specific pathways for glucose oxidation are affected by energy intake and may be used by the rat to assess and respond to changes in peripheral energy status.

Subfornical organ and supraoptic nucleus connections with septal neurons in rats

1985 ◽  
Vol 249 (2) ◽  
pp. R214-R218 ◽  
Author(s):  
A. V. Ferguson ◽  
C. W. Bourque ◽  
L. P. Renaud
Keyword(s):  
Supraoptic Nucleus ◽  
Medial Septum ◽  
Brain Regions ◽  
Subfornical Organ ◽  
Sprague Dawley ◽  
Indirect Pathway ◽  
Antidromic Activation ◽  
Diagonal Band ◽  
Sprague Dawley Rats ◽  
Septal Neurons

Extracellular single unit recordings obtained in pentobarbital-anesthetized male Sprague Dawley rats were utilized to examine the electrophysiology of connections of medial septum-diagonal band of Broca (MS-DBB) neurons with the subfornical organ (SFO), hippocampal commissure (HC), and supraoptic nucleus (SON). Of the 119/216 cells tested that demonstrated antidromic activation from SON, many (60%) were orthodromically excited by SFO stimulation, whereas most (68%) were unresponsive to stimulation in the adjacent HC. Separate populations of MS-DBB neurons that displayed antidromic activation from the SFO (11/140 cells tested) or HC (24/78 tested) were orthodromically excited by SON stimulation. Three cells were activated antidromically from both the SFO and SON. These observations reveal some possible interconnections between these three brain regions and point to the existence of an indirect pathway whereby the SFO can influence SON neurons through an influence on MS-DBB neurons.

Lactation alters the effects of conditioned stress on immune function

1997 ◽  
Vol 272 (1) ◽  
pp. R16-R25 ◽  
Author(s):  
N. Shanks ◽  
A. Kusnecov ◽  
M. Pezzone ◽  
J. Berkun ◽  
B. S. Rabin
Keyword(s):  
Immune Function ◽  
Stress Responses ◽  
Lymphocyte Proliferation ◽  
Physiological State ◽  
Cell Receptor ◽  
Plasma Corticosterone ◽  
Endocrine Function ◽  
Nitrite Accumulation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

During lactation, endocrine function is altered and stress responses are dampened. Stress effects on immune function are partially determined by endocrine factors; therefore, we assessed whether stress similarly alters immune function during lactation. Sprague-Dawley rats were conditioned by exposure to a tone paired with foot shock (2 sessions, 16 shocks each) prior to breeding or were left undisturbed. Lactating (day 10) (Lac) and nonlactating diestrous virgin controls (C) were killed immediately after reexposure to the tone or removal from their home cage. Plasma corticosterone stress responses were dampened in Lac relative to C animals. Peripheral blood lymphocyte proliferation to T cell receptor antibody stimulation was reduced to a similar extent in both experimental groups. Conditioned stress reduced splenocyte proliferation and increased nitrite accumulation in C animals, but not in Lac animals. Mesenteric lymph node lymphocyte proliferation was significantly increased after stress in Lac compared with C animals. Both plasma interleukin-6 (IL-6) and phytohemagglutinin-stimulated splenic IL-6 production were increased in Lac animals compared with C animals after stress exposure. These data indicate that stress-induced alterations may be determined by different regulatory mechanisms within immune compartments and that these effects depend on the physiological state of the organism.

Opioidergic system and N-methyl D-aspartate receptor (NMDA-R) hypofunction: Translational implications for the pathophysiology of psychosis and drug addiction

2011 ◽  
Vol 26 (S2) ◽  
pp. 1231-1231
Author(s):  
E.F. Buonaguro ◽  
F. Marmo ◽  
L. Avvisati ◽  
G. Latte ◽  
R. Rossi ◽  
...  
Keyword(s):  
Drug Addiction ◽  
Drugs Of Abuse ◽  
Premotor Cortex ◽  
Region Of Interest ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Preclinical Model ◽  
Sprague Dawley ◽  
Somatosensory Cortices ◽  
Sprague Dawley Rats

Enkephalin is an opioidergic neuromodulator that has been implicated in long-term behavioural sensitization after administration of drugs of abuse. Enkephalin is also a molecular marker of GABAergic neurons in the striato-pallidal pathway that is involved in sensory-motor gating and has been considered dysfunctional in the pathophysiology of psychosis.In this study we investigated in male Sprague Dawley rats putative changes in Enkephalin transcripts by in situ hybridization after acute or subchronic administration of ketamine in either high or low subanaesthetic doses (50 mg/kg and 12 mg/kg respectively). Ketamine is a non-competitive NMDA-R antagonist that perturbs glutamate neurotransmission and provides a preclinical model of psychosis-like behaviour in rats.In the acute paradigm the expression of Enkephalin was reduced in the motor, premotor, somatosensory cortices as well as in anterior cingulate. In the subchronic paradigm Enkephalin expression was reduced in the premotor cortex, in the ventromedial caudate-putamen and in the shell of nucleus accumbens. Comparative analysis showed that the relative decrement in gene expression was not significantly different between the acute and subchronic paradigm for each region of interest.Changes in distribution of Enkephalin expression and correlation analysis of functionally related brain regions suggest that Enkephalin transcripts reduction may be implicated in the motivational aspects of drug addiction and may help explaining some aspects of the pathophysiology in ketamine-induced psychosis.

Effects of prolonged exendin-4 administration on hypothalamic-pituitary-adrenal axis activity and water balance

2013 ◽  
Vol 304 (10) ◽  
pp. E1105-E1117 ◽  
Author(s):  
Manuel Gil-Lozano ◽  
Marina Romaní-Pérez ◽  
Verónica Outeiriño-Iglesias ◽  
Eva Vigo ◽  
Patricia L. Brubaker ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Hpa Axis ◽  
Stress Responses ◽  
Fold Increase ◽  
Acute Administration ◽  
Sprague Dawley ◽  
Hypothalamic Pituitary Adrenal ◽  
Sprague Dawley Rats ◽  
Glucagon Like Peptide 1 ◽  
Hpa Axis Activity

Exendin-4 (Ex-4) is a natural agonist of the glucagon-like peptide-1 (GLP-1) receptor, currently being used as a treatment for type 2 diabetes mellitus due to its insulinotropic properties. Previous studies have revealed that acute administration of both GLP-1 and, in particular, Ex-4 potently stimulates hypothalamic-pituitary-adrenal (HPA) axis activity. In this work, the effects of prolonged Ex-4 exposure on HPA function were explored. To this end, Sprague-Dawley rats were subjected to a daily regimen of two Ex-4 injections (5 μg/kg sc) for a minimum of 7 days. We found that subchronic Ex-4 administration produced a number of effects that resemble chronic stress situations, including hyperactivation of the HPA axis during the trough hours, disruption of glucocorticoid circadian secretion, hypertrophy of the adrenal gland, decreased adrenal gland sensitivity, impaired pituitary-adrenal stress responses, and reductions in both food intake and body weight. In addition, a threefold increase in diuresis was observed followed by a 1.5-fold increase in water intake; these latter effects were abolished by adrenalectomy. Together, these findings indicate that Ex-4 induces a profound dysregulation of HPA axis activity that may also affect renal function.

Sign in / Sign up

Export Citation Format

Share Document