PSYCHOLOGICAL STRESS REDUCES CYCLIC 3',5'-ADENOSINE MONOPHOSPHATE LEVELS IN THE CEREBRAL CORTEX OF CONSCIOUS RATS, AS DETERMINED BY A NEW CRYOGENIC METHOD OF RAPID TISSUE FIXATION

This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.

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A different mode of action of potassium ions and veratridine on the formation of cyclic adenosine monophosphate in the cerebral cortex

Neuroscience ◽

10.1016/0306-4522(78)90081-7 ◽

1978 ◽

Vol 3 (3) ◽

pp. 333-338 ◽

Cited By ~ 7

Author(s):

J. Krˇivánek

Keyword(s):

Cerebral Cortex ◽

Mode Of Action ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Potassium Ions

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Pentobarbital Enhances Cyclic Adenosine Monophosphate Production in the Brain by Effects on Neurons but Not Glia

Anesthesiology ◽

10.1097/00000542-199605000-00017 ◽

1996 ◽

Vol 84 (5) ◽

pp. 1148-1155 ◽

Cited By ~ 4

Author(s):

Jerry M. Gonzales ◽

Iris Mendez-Bobe

Keyword(s):

Cerebral Cortex ◽

Cyclic Amp ◽

Cortical Neurons ◽

Neuronal Excitability ◽

Primary Cultures ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Camp Accumulation ◽

Camp Production ◽

The Brain

Background Cyclic adenosine monophosphate (cAMP) is an important regulator of neuronal excitability. The effects of barbiturates on cAMP production in intact neurons are not known. This study used cultures of cortical neurons, cultures of glia, and slices of cerebral cortex from the rat to study the effects of barbiturates on cAMP regulation in the brain. Methods Primary cultures of cortical neurons or glia were prepared from 17-day gestational Sprague-Dawley rat fetuses and were used after 12-16 days in culture. Cross-cut slices (300 microns) were prepared from cerebral cortex of adult rats. Cyclic AMP accumulation was determined by measuring the conversion of [3H]adenosine triphosphate (ATP) to [3H]cAMP in cells preloaded with [3H]adenine. Results Pentobarbital enhanced isoproterenol- and forskolin-stimulated, but not basal, cAMP accumulation in cultures of cerebral neurons. Cyclic AMP production was enhanced by pentobarbital in a dose-dependent fashion up to a concentration of 250 microM; This concentration of pentobarbital increased cAMP production by 40-50% relative to that in controls without pentobarbital. At 500 microM pentobarbital, the magnitude of the enhancement was less. Pentobarbital had no effect on isoproterenol-stimulated cAMP production in cultures containing only glia. Pentobarbital also enhanced isoproterenol-stimulated, but not basal, cAMP production in slices of cerebral cortex by approximately 30% at concentrations of 62.5-250 microM and by almost 100% at 500 microM. Conclusions Pentobarbital enhances stimulated cAMP accumulation in cultured preparations from brain and fresh cortical slices. Neurons are required for this effect. Because cAMP modulates neuronal excitability, this effect of pentobarbital may be an important mechanism by which this anesthetic influences brain function.

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Adenosine Metabolism in the Cerebral Cortex from Several Mice Models during Aging

International Journal of Molecular Sciences ◽

10.3390/ijms21197300 ◽

2020 ◽

Vol 21 (19) ◽

pp. 7300

Author(s):

Alejandro Sánchez-Melgar ◽

José Luis Albasanz ◽

Mercè Pallàs ◽

Mairena Martín

Keyword(s):

Cerebral Cortex ◽

Excitatory Amino Acid ◽

Adenosine Monophosphate ◽

Murine Models ◽

Excitatory Amino Acid Transporter ◽

Phosphorylated Form ◽

Purine Metabolites ◽

Amp Activated Protein Kinase ◽

Samp8 Mice ◽

Senescence Accelerated Mouse

Adenosine is a neuromodulator that has been involved in aging and neurodegenerative diseases as Alzheimer’s disease (AD). In the present work, we analyzed the possible modulation of purine metabolites, 5’nucleotidase (5′NT) and adenosine deaminase (ADA) activities, and adenosine monophosphate (AMP)-activated protein kinase (AMPK) and its phosphorylated form during aging in the cerebral cortex. Three murine models were used: senescence-accelerated mouse-resistant 1 (SAMR1, normal senescence), senescence-accelerated mouse-prone 8 (SAMP8, a model of AD), and the wild-type C57BL/6J (model of aging) mice strains. Glutamate and excitatory amino acid transporter 2 (EAAT2) levels were also measured in these animals. HPLC, Western blotting, and enzymatic activity evaluation were performed to this aim. 5′-Nucleotidase (5′NT) activity was decreased at six months and recovered at 12 months in SAMP8 while opposite effects were observed in SAMR1 at the same age, and no changes in C57BL/6J mice. ADA activity significantly decreased from 3 to 12 months in the SAMR1 mice strain, while a significant decrease from 6 to 12 months was observed in the SAMP8 mice strain. Regarding purine metabolites, xanthine and guanosine levels were increased at six months in SAMR1 without significant differences in SAMP8 mice. In C57BL/6J mice, inosine and xanthine were increased, while adenosine decreased, from 4 to 24 months. The AMPK level was decreased at six months in SAMP8 without significant changes nor in SAMR1 or C57BL/6J strains. Glutamate and EAAT2 levels were also modulated during aging. Our data show a different modulation of adenosine metabolism participants in the cerebral cortex of these animal models. Interestingly, the main differences between SAMR1 and SAMP8 mice were found at six months of age, SAMP8 being the most affected strain. As SAMP8 is an AD model, results suggest that adenosinergic metabolism is involved in the neurodegeneration of AD.

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Labeling of Metabolic Pools by [6-14C]Glucose during K+-Induced Stimulation of Glucose Utilization in Rat Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1995.11 ◽

1995 ◽

Vol 15 (1) ◽

pp. 97-110 ◽

Cited By ~ 50

Author(s):

Keiji Adachi ◽

Nancy F. Cruz ◽

Louis Sokoloff ◽

Gerald A. Dienel

Keyword(s):

Cerebral Cortex ◽

Rat Brain ◽

Brain Tissue ◽

Glucose Utilization ◽

Visual Stimulation ◽

Cerebral Metabolism ◽

Significant Loss ◽

Metabolic Fate ◽

Conscious Rats ◽

Stimulation Of

[6-14C]Glucose is the tracer sometimes recommended to assay cerebral glucose utilization (CMRglc) during transient or brief functional activations, but when used to study visual stimulation and seizures in other laboratories, it underestimated CMRglc. The metabolic fate of [6-14C]glucose during functional activation of cerebral metabolism is not known, and increased labeling of diffusible metabolites might explain underestimation of CMRglc and also reveal trafficking of metabolites. In the current studies cerebral cortex in conscious rats was unilaterally activated metabolically by KCl application, and CMRglc was determined in activated and contralateral control cortex with [6-14C]glucose or 2-[14C]deoxyglucose ([14C]DG) over a 5- to 7-min interval. Local 14C concentrations were determined by quantitative autoradiography. Labeled precursor and products were measured bilaterally in paired cortical samples from funnel-frozen brains. Left-right differences in 14C contents were small with [6-14C]glucose but strikingly obvious in [14C]DG autoradiographs. CMRglc determined with [6-14C]glucose was slightly increased in activated cortex but 40–80% below values obtained with [14C]DG. [14C]Lactate was a major metabolite of [6-14C]glucose in activated but not control cortex and increased proportionately with unlabeled lactate. These results demonstrate significant loss of labeled products of [6-14C]glucose from metabolically activated brain tissue and indicate that [14C]DG is the preferred tracer even during brief functional activations of brain.

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