scholarly journals Artificial Cerebrospinal Fluid V (ACSF.V) v1 (protocols.io.bd8xi9xn)

protocols.io ◽  
2020 ◽  
Author(s):  
Allen Institute
Keyword(s):  
Cerebrospinal Fluid ◽  
Artificial Cerebrospinal Fluid

PVN lesions prevent the endothelin 1-induced increase in arterial pressure and vasopressin

2001 ◽  
Vol 280 (2) ◽  
pp. E349-E356 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Arterial Pressure ◽  
Paraventricular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
Baseline Values ◽  
Long Evans

Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study assessed the role of the paraventricular nuclei (PVN) in these actions. Intracerebroventricular ET-1 (10 pmol) or the ETA antagonist BQ-123 (40 nmol) was administered in conscious intact or sinoaortic-denervated (SAD) Long-Evans rats with sham or bilateral electrolytic lesions of the magnocellular region of the PVN. Baseline values did not differ among groups, and artificial cerebrospinal fluid (CSF) induced no significant changes. In sham-lesioned rats, ET-1 increased mean arterial pressure (MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD ( P < 0.001 ET-1 vs. CSF) rats. PVN lesions abolished the rise in MAP: −0.1 ± 2.8 mmHg in intact and 0.0 ± 2.9 mmHg in SAD. AVP increased in only in the sham-lesioned SAD group 8.6 ± 3.5 pg/ml ( P < 0.001 ET-1 vs. CSF). BQ-123 blocked the responses. Thus the integrity of the PVN is required for intracerebroventricularly administered ET-1 to exert pressor and AVP secretory effects.

Regional effect of naltrexone in the nucleus of the solitary tract in blockade of NPY-induced feeding

2000 ◽  
Vol 278 (2) ◽  
pp. R499-R503 ◽  
Author(s):  
C. M. Kotz ◽  
M. J. Glass ◽  
A. S. Levine ◽  
C. J. Billington
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Opioid Receptors ◽  
The Other ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Regional Effect ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid

Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey

1989 ◽  
Vol 67 (1) ◽  
pp. 128-133 ◽  
Author(s):  
M. D. Owen ◽  
R. D. Matthes ◽  
C. V. Gisolfi
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Sweat Rate ◽  
Recovery Period ◽  
Erythrocebus Patas ◽  
Artificial Cerebrospinal Fluid ◽  
Skin Temperatures ◽  
Central Stimulation ◽  
Osmotic Stimuli

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255–413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.

Creatinine, potassium, and calcium flux from chicken cerebrospinal fluid

1975 ◽  
Vol 228 (2) ◽  
pp. 415-419 ◽  
Author(s):  
DK Anderson ◽  
SR Heisey
Keyword(s):  
Cerebrospinal Fluid ◽  
Transport Process ◽  
Calcium Flux ◽  
Brain Blood Flow ◽  
Artificial Cerebrospinal Fluid ◽  
Bulk Absorption ◽  
Perfusion Time ◽  
Active Transport Process ◽  
Tracer Molecules ◽  
Lateral Cerebral Ventricle

Brains of methoxyflurane-anesthetized chickens were perfused from a lateral cerebral ventricle to cisterna magna with an artificial cerebrospinal fluid (CSF) containing trace quantities of radioiodinated human serum albumin (RIHSA) or inulin (1.0 mg/ml) to measure CSF bulk absorption. In addition, it contained either trace quantities of 22Na, 42K, 45Ca or [14C]creatinine; the concentrations of the latter three were varied to determine permeability coefficients (K-D's) as a function of concentration. A mass balance for the tracer molecules was calculated to determine their movement into brain or blood. K-D's for 45Ca, 42K, 22Na, and creatinine (Cr) were unaffected by perfusion time and the latter two were larger than previously reported (3). The lack of effect of time on K-D and the large values for K-D22Na and K-D-Cr are attributed to anesthetic effects on brain blood flow. K-D-Cr and K-D42K were larger than K-D22Na or K-D45Ca and K-D's for 45Ca, Cr, and 42K were independent of their inflow concentrations. An active transport process is suggested for potassium and creatinine, but one that is located at sites other than the ependymal wall. Bulk flow clearance accounted for RIHSA movement from CSF, whereas nonbulk clearance accounted for 50% of 22Na and 45Ca movement and 90% of 42K clearance. Fifty percent of 42K and 25% of 22Na and 45Ca were found in brain. The large recovery of 42K in brain supports the hypothesis that intracellular potassium serves as an exchangeable pool for the tracer.

Effects of a new magnesium-rich artificial cerebrospinal fluid on contractile 5-hydroxytryptamine and endothelin receptors in rat cerebral arteries

2019 ◽  
Vol 41 (11) ◽  
pp. 1015-1023
Author(s):  
Ya-Wen Cheng ◽  
Yi-Chen Guo ◽  
Guo-Liang Li ◽  
Yong-Ning Deng ◽  
Wen-Juan Li ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Arteries ◽  
Endothelin Receptors ◽  
Artificial Cerebrospinal Fluid

Central role for angiotensin in control of adrenal catecholamine secretion

1985 ◽  
Vol 248 (3) ◽  
pp. R363-R370 ◽  
Author(s):  
E. J. Corwin ◽  
J. F. Seaton ◽  
M. Hamaji ◽  
T. S. Harrison
Keyword(s):  
Cerebrospinal Fluid ◽  
Catecholamine Secretion ◽  
Ang Ii ◽  
Artificial Cerebrospinal Fluid ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Adrenal Response ◽  
Adrenal Secretion ◽  
Lateral Cerebral Ventricle

Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion of catecholamines after hemorrhage in the dog. To test if ANG II acts centrally, experiments were performed under general anesthesia on bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg. Ventriculocisternal perfusion of ANG II or its antagonist saralasin was accomplished via needles inserted in the left lateral cerebral ventricle and cisterna magna. Mean arterial pressure and adrenal secretion of catecholamines were measured before and after hemorrhage. Nephrectomized dogs receiving only artificial cerebrospinal fluid (CSF) by ventriculocisternal perfusion had a very small adrenal response to hemorrhage compared with animals receiving ANG II intraventricularly (IVT) (at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 . min-1) had no effect on adrenal catecholamine secretion. Animals with intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not blunt the response to hemorrhage. Thus ANG II appears to support catecholamine secretion via a central mechanism. This mechanism is physiologically significant because either nephrectomy or functional elimination of ANG II by saralasin greatly attenuates the adrenal medullary response to hemorrhage in vivo.

Finite Element Analysis of Laser Fabricated Microjoint Performance in Cerebrospinal Fluid

2007 ◽  
Author(s):  
Ahsan Mian ◽  
Jesse Law
Keyword(s):  
Finite Element ◽  
Cerebrospinal Fluid ◽  
Mechanical Performance ◽  
Degradation Mechanism ◽  
Polyimide Film ◽  
Element Analysis ◽  
Critical Feature ◽  
Artificial Cerebrospinal Fluid ◽  
Bond Degradation ◽  
Before And After

Assessment of neural biocompatibility requires that materials be tested with exposure in neural fluids. Laser bonded microjoint samples made from titanium foil and polyimide film (TiPI) were evaluated for mechanical performance before and after exposure in artificial cerebrospinal fluid (CSF) for two, four and twelve weeks at 37°C. These samples represent a critical feature i.e., the microjoint — a major weakness in the bioencapsulation system. The laser microbonds showed initial degradation up to four weeks which then stabilized afterwards and retained similar strength until twelve weeks. To understand this bond degradation mechanism better, a finite element modeling approach was adopted. From the finite element results, it was revealed that the bond degradation was not owing to the hygroscopic expansion of polyimide. Rather, relaxation of the process induced residual stresses may have resulted in weakening of the bond strength as observed from experimental measurements.

scholarly journals TRH microdialysis into the RTN of the conscious rat increases breathing, metabolism, and temperature

1999 ◽  
Vol 87 (2) ◽  
pp. 673-682 ◽  
Author(s):  
Carlos Cream ◽  
Eugene Nattie ◽  
Aihua Li
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Random Order ◽  
Conscious Rat ◽  
Tissue Volume ◽  
Retrotrapezoid Nucleus ◽  
Sustained Effects ◽  
Artificial Cerebrospinal Fluid ◽  
E 32 ◽  
Stimulation Of

Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792–799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 ± 1.7 mM), ventilation (V˙e) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group ( n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group ( n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increasedV˙e (32%, P < 0.02, by 10 min, with recovery by 60 min), O2 consumption (V˙o 2; 19%, P < 0.03), and body (rectal) temperature (Tre; 0.5°C, P < 0.09). TRH (10 mM) increasedV˙e (78%, P < 0.01, by 10 min, with no recovery at 60 min), V˙o 2(48%, P < 0.01), and Tre (1.0°C, P < 0.01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 ± 256 nl for 10 mM ( n = 5) and 590 ± 128 nl for 1 mM ( n = 5). We conclude that 1) the RTN is involved in the integration ofV˙e,V˙o 2, Tre, and arousal and 2) TRH may establish the responsiveness of RTN neurons.

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