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Journal articles on the topic 'Central nervous system in rats'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Lang, Frederick F., Fred J. Epstein, Joseph Ransohoff, Jeffrey C. Allen, Jeffrey Wisoff, I. Richmond Abbott, and Douglas C. Miller. "Central nervous system gangliogliomas." Journal of Neurosurgery 79, no. 6 (December 1993): 867–73. http://dx.doi.org/10.3171/jns.1993.79.6.0867.

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The records of 58 patients with gangliogliomas surgically treated between January 1, 1980, and June 30, 1990, were retrospectively reviewed in order to determine long-term survival, event-free survival, and functional outcome resulting after radical resection and to assess the impact of histological grading on outcome. Tumors were located in the cerebral hemisphere in 19 cases, the spinal cord in 30, and the brain stem in nine. Forty-four patients had gross total resection and 14 had radical subtotal resection. Only six patients underwent postoperative irradiation or chemotherapy and, therefore, the outcome was generally related to surgery alone. Of the 58 gangliogliomas, 40 were classified as histological grade I, 16 were grade II, and two were grade III. The median follow-up period was 56 months. There were no operative deaths, and the operative morbidity rate was 5%, 37%, and 33% for cerebral hemisphere, spinal cord, and brain-stem gangliogliomas, respectively. The 5-year actuarial survival rates for cerebral hemisphere, spinal cord, and brain-stem gangliogliomas were 93%, 84%, and 73%, respectively (p = 0.7). The event-free survival rate at 5 years was 95% for cerebral hemisphere gangliogliomas and 36% for spinal cord gangliogliomas (p < 0.05); for brain-stem gangliogliomas the event-free survival rate at 3 years was 53% (p < 0.05). Neurological function at recent follow-up evaluation was stable or improved in 81% of patients. Multivariate analysis (Cox linear regression) revealed tumor location to be the only variable predictive of outcome, with spinal cord and brain-stem gangliogliomas having a 3.5- and 5-fold increased relative risk of recurrence, respectively, compared to cerebral hemisphere gangliogliomas. Histological grade was not predictive of outcome, although in each location there was a trend for higher-grade tumors to have a shorter time to recurrence. It is concluded that radical surgery leads to long-term survival of patients with gangliogliomas, regardless of location, and adjuvant therapy can probably be reserved for special cases.

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2

Hamidi, Mehrdad. "Central nervous system distribution kinetics of indinavir in rats." Journal of Pharmacy and Pharmacology 59, no. 8 (August 2007): 1077–85. http://dx.doi.org/10.1211/jpp.59.8.0004.

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3

Parham, D., A. Tereba, P. J. Talbot, D. P. Jackson, and V. L. Morris. "Analysis of JHM Central Nervous System Infections in Rats." Archives of Neurology 43, no. 7 (July 1, 1986): 702–8. http://dx.doi.org/10.1001/archneur.1986.00520070058019.

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4

Arieli, R., and G. Hershko. "Prediction of central nervous system oxygen toxicity in rats." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1903–6. http://dx.doi.org/10.1152/jappl.1994.77.4.1903.

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Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

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5

Fisher, L. A., C. R. Cave, and M. R. Brown. "Central nervous system cardiovascular effects of bombesin in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H425—H431. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h425.

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The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.

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6

Rykaczewska-Czerwińska, Monika, Piotr Oleś, Michał Oleś, Mariola Kuczer, Danuta Konopińska, and Andrzej Plech. "Effect of alloferon 1 on central nervous system in rats." Pharmacological Reports 62 (September 2010): 62–63. http://dx.doi.org/10.1016/s1734-1140(10)71168-3.

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7

Szenohradszky, János, Anthony J. Trevor, Philip Bickler, James E. Caldwell, Manohar L. Sharma, Ira J. Rampil, and Ronald D. Miller. "Central Nervous System Effects of Intrathecal Muscle Relaxants in Rats." Anesthesia & Analgesia 76, no. 6 (June 1993): 1304–9. http://dx.doi.org/10.1213/00000539-199306000-00020.

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8

Szenohradszky, János, Anthony J. Trevor, Philip Bickler, James E. Caldwell, Manohar L. Sharma, Ira J. Rampil, and Ronald D. Miller. "Central Nervous System Effects of Intrathecal Muscle Relaxants in Rats." Anesthesia & Analgesia 76, no. 6 (June 1993): 1304–9. http://dx.doi.org/10.1213/00000539-199376060-00020.

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9

Miyaguchi, Hideki, Ineko Kato, Tadashi Sano, Hisanori Sobajima, Shinji Fujimoto, and Hajime Togari. "Dopamine penetrates to the central nervous system in developing rats." Pediatrics International 41, no. 4 (August 1999): 363–68. http://dx.doi.org/10.1046/j.1442-200x.1999.01084.x.

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10

Crabb, David W., Sandra L. Morzorati, Jay R. Simon, and Ting-Kai Li. "Central nervous system control of alcohol dehydrogenase activity in rats." Life Sciences 37, no. 25 (December 1985): 2381–87. http://dx.doi.org/10.1016/0024-3205(85)90105-5.

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11

Bamshad, Maryam, Victor T. Aoki, M. Gregory Adkison, Wade S. Warren, and Timothy J. Bartness. "Central nervous system origins of the sympathetic nervous system outflow to white adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 1 (July 1, 1998): R291—R299. http://dx.doi.org/10.1152/ajpregu.1998.275.1.r291.

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White adipose tissue (WAT) is innervated by postganglionic sympathetic nervous system (SNS) neurons, suggesting that lipid mobilization could be regulated by the SNS [T. G. Youngstrom and T. J. Bartness. Am. J. Physiol. 268 ( Regulatory Integrative Comp. Physiol. 37): R744–R751, 1995]. A viral transsynaptic retrograde tract tracer, the pseudorabies virus (PRV), was used to identify the origins of the SNS outflow from the brain to WAT neuroanatomically. PRV was injected into epididymal or inguinal WAT (EWAT and IWAT, respectively) of Siberian hamsters and IWAT of rats. PRV-infected neurons were visualized by immunocytochemistry and found in the spinal cord, brain stem (medulla, nucleus of the solitary tract, caudal raphe nucleus, C1 and A5 regions), midbrain (central gray), and several areas within the forebrain. The general pattern of infection of WAT in both species was more similar than different and resembled that seen after PRV injections into the adrenal medulla in rats (A. M. Strack, W. B. Sawyer, J. H. Hughes, K. B. Platt, and A. D. Loewy. Brain Res. 491: 156–162, 1989). EWAT versus IWAT injected hamsters had relatively less labeling in the suprachiasmatic, dorsomedial, and arcuate nuclei. Overall, it appeared that the SNS innervation of WAT originates from the general SNS outflow of the central nervous system and therefore may play a significant role in lipid mobilization.

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12

Overton, J. M., G. Davis-Gorman, and L. A. Fisher. "Central nervous system cardiovascular actions of CRF in sinoaortic-denervated rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 3 (March 1, 1990): R596—R601. http://dx.doi.org/10.1152/ajpregu.1990.258.3.r596.

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Studies were performed in unrestrained conscious Sprague-Dawley rats to examine the central nervous system (CNS) mechanism by which corticotropin-releasing factor (CRF) produces simultaneous elevations of arterial pressure and heart rate. To test the hypothesis that CRF inhibits ongoing impulse transmission through and/or transmitter release from the CNS terminations of baroreceptor afferents, the cardiovascular effects of intracerebroventricular administration of CRF were compared in rats subjected to prior sham surgery (Sham) or sinoaortic denervation (SAD). Resting levels of arterial pressure and heart rate were elevated after SAD. In addition, SAD resulted in greater chronotropic sympathetic tone and reduced chronotropic parasympathetic tone as assessed by intravenous injections of atropine methyl nitrate and DL-propranolol. Intracerebroventricular administration of CRF in both surgical groups elicited significant increases in arterial pressure and heart rate, although a tendency for reduced tachycardic responses after SAD was apparent. Pretreatment with atropine or propranolol revealed that both the parasympathetic and sympathetic nervous systems contribute to CRF-induced heart rate responses in both surgical groups. These results suggest that ongoing baroreceptor afferent transmission is not requisite for the expression of CRF-induced cardiovascular changes. Thus it is unlikely that CRF elevates arterial pressure and heart rate through an exclusive action at the CNS terminations of baroreceptor sensory fibers.

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13

Modi, Manish, and Abhishek Garg. "Tuberculosis of Central Nervous System." Journal of Postgraduate Medicine, Education and Research 47, no. 4 (2013): 202–13. http://dx.doi.org/10.5005/jp-journals-10028-1086.

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ABSTRACT Meningitis is the most serious manifestation of extrapulmonary tuberculosis. Being a paucibacillary disease, no single diagnostic test is sensitive and specific. Despite recent advances in diagnostic methods and readily available effective chemotherapy, more than 50% of the patients either die or are left with major neurological deficits due to delay in the diagnosis. HIV coinfection is associated with higher complications and case fatality rates. The only way to reduce the mortality and morbidity is early diagnosis and initiation of chemotherapy and steroids. How to cite this article Modi M, Garg A. Tuberculosis of Central Nervous System. J Postgrad Med Edu Res 2013;47(4):202-213.

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14

Akins, V. F., and S. L. Bealer. "Central nervous system histamine regulates peripheral sympathetic activity." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H218—H224. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h218.

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Brain histamine (HA) was depleted in conscious Sprague-Dawley rats by central administration of alpha-fluoromethyl-histidine (alpha-FMH), an irreversible inhibitor of the HA synthesizing enzyme. Isotonic or hypertonic saline was infused intravenously at 10 microliters.100 g-1.min-1 for 30 min and mean arterial pressure (MAP) and heart rate (HR) were monitored. In addition, plasma vasopressin (AVP) and norepinephrine (NE) were measured pre- and postinfusion. Animals pretreated with alpha-FMH showed a delayed and attenuated pressor response and bradycardia during hypertonic saline (HTS) infusion and a significant reduction in plasma NE levels (-29 +/- 8% below control values). However, plasma concentrations of AVP were similar in both groups. Central pretreatment with the H1-antagonist pyrilamine (PYR) also delayed the onset and significantly attenuated the pressor response to HTS infusion, and caused dose-related decreases in plasma NE concentrations (-34 +/- 8, -47 +/- 5, and -52 +/- 7% after 60, 100, and 600 nmol PYR, respectively). These data indicate a role for central HA in peripheral sympathetic activation but not as a mediator of AVP release to a peripheral hyperosmotic stimulus.

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15

Batchelor, Tracy, and Sarah Löw. "Primary Central Nervous System Lymphoma." Seminars in Neurology 38, no. 01 (February 2018): 086–94. http://dx.doi.org/10.1055/s-0038-1627470.

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Primary central nervous system lymphoma (PCNSL) is an extranodal non-Hodgkin lymphoma limited to the brain, spinal cord, leptomeninges, and eyes. The majority of patients are immunocompetent, with a median age of 65 years at diagnosis. Historically, whole-brain radiation therapy (WBRT) was the first and sole treatment for PCNSL. Today, due to the recognized neurotoxicity of WBRT, this modality is usually avoided in the treatment. Most chemotherapy regimens are based on high-dose methotrexate plus the anti-CD20 monoclonal antibody rituximab, leading to high response rates, but 5-year survival is still poor at approximately 30% compared with other extranodal lymphomas. New treatment strategies including high-dose chemotherapy/autologous stem cell transplantation, targeted therapies focusing on, for example, genetic alterations in B cells or mammalian target of rapamycin signaling, and immunotherapy with inhibitors of the programmed cell death 1 receptor are only a few options to improve the armamentarium against PCNSL.

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16

VP, Vinodh, Rahmat Harun, Pulivendhan Sellamuthu, and Regunath Kandasamy. "Primary Central Nervous System Fibrosarcoma." Journal of Neurosciences in Rural Practice 08, S 01 (August 2017): S111—S113. http://dx.doi.org/10.4103/jnrp.jnrp_165_17.

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ABSTRACTWe report a rare case of a young female with primary brain fibrosarcoma, and to the best of our knowledge, we believe that only <50 cases have been reported or described worldwide so far. Fibrosarcoma is a malignant neoplasm, in which histologically the predominant cells are fibroblasts that divide excessively without cellular control and they can invade local tissues or metastasize. Primary central nervous system fibrosarcomas are very aggressive neoplasms and generally have a poor prognosis. This tumor is either from sarcomatous transformation of a meningioma or arises de novo within the brain parenchyma. Our patient, a 48-year-old woman, who presented with progressive speech disorder over the period of 4 months, showed a left temporoparietal lesion with surrounding edema and local mass effect. Total surgical resection was achieved. Histopathology revealed classical fibrosarcoma features and secondary screening revealed no other distant lesion as diagnosis of primary brain fibrosarcoma was established. This case is deemed to be extremely rare because most reports claim that recurrence is within 6 months with poor prognosis; however, this patient is currently recurrence-free at 3 years. This would suggest of the possibility for a relook into this disease's course and recurrence rate when complete excision is achieved. Due to extreme rarity of these tumors, more comparative studies will be needed to improve the disease outcome.

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17

Levin, E. R., M. A. Weber, and S. Mills. "Atrial natriuretic factor-induced vasodepression occurs through central nervous system." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (September 1, 1988): H616—H622. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h616.

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To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

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18

Ates, Ozkan, Suleyman R. Cayli, Neslihan Yucel, Eyup Altinoz, Ayhan Kocak, M. Akif Durak, Yusuf Turkoz, and Saim Yologlu. "Central nervous system protection by resveratrol in streptozotocin-induced diabetic rats." Journal of Clinical Neuroscience 14, no. 3 (March 2007): 256–60. http://dx.doi.org/10.1016/j.jocn.2005.12.010.

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19

Naseem, Syed M. "Toxicokinetics of [3H]saxitoxinol in peripheraland central nervous system of rats." Toxicology and Applied Pharmacology 141, no. 1 (November 1996): 49–58. http://dx.doi.org/10.1016/s0041-008x(96)80008-1.

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20

Inagaki, N., A. Yamatodani, T. Watanabe, M. Tohyama, K. Sinoda, and H. Wada. "Distribution of histaminergic terminals in the central nervous system of rats." Japanese Journal of Pharmacology 43 (1987): 262. http://dx.doi.org/10.1016/s0021-5198(19)58590-0.

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21

Zakaria, Mohamed Naguib, Hany M. El-Bassossy, and Waleed Barakat. "Targeting AGEs Signaling Ameliorates Central Nervous System Diabetic Complications in Rats." Advances in Pharmacological Sciences 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/346259.

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Diabetes is a chronic endocrine disorder associated with several complications as hypertension, advanced brain aging, and cognitive decline. Accumulation of advanced glycation end products (AGEs) is an important mechanism that mediates diabetic complications. Upon binding to their receptor (RAGE), AGEs mediate oxidative stress and/or cause cross-linking with proteins in blood vessels and brain tissues. The current investigation was designed to investigate the effect of agents that decrease AGEs signaling, perindopril which increases soluble RAGE (sRAGE) and alagebrium which cleaves AGEs cross-links, compared to the standard antidiabetic drug, gliclazide, on the vascular andcentral nervous system(CNS) complications in STZ-induced (50 mg/kg, IP) diabetes in rats. Perindopril ameliorated the elevation in blood pressure seen in diabetic animals. In addition, both perindopril and alagebrium significantly inhibited memory decline (performance in the Y-maze), neuronal degeneration (Fluoro-Jade staining), AGEs accumulation in serum and brain, and brain oxidative stress (level of reduced glutathione and activities of catalase and malondialdehyde). These results suggest that blockade of AGEs signaling after diabetes induction in rats is effective in reducing diabetic CNS complications.

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22

Karavelioglu, Ergun, Yucel Gonul, Hasan Aksit, Mehmet Gazi Boyaci, Mustafa Karademir, Nejdet Simsek, Mustafa Guven, Tugay Atalay, and Usame Rakip. "Cabazitaxel causes a dose-dependent central nervous system toxicity in rats." Journal of the Neurological Sciences 360 (January 2016): 66–71. http://dx.doi.org/10.1016/j.jns.2015.11.033.

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23

YATOMI, A., A. IGUCHI, S. YANAGISAWA, H. MATSUNAGA, I. NIKI, and N. SAKAMOTO. "Prostaglandins Affect the Central Nervous System to Produce Hyperglycemia in Rats*." Endocrinology 121, no. 1 (July 1987): 36–41. http://dx.doi.org/10.1210/endo-121-1-36.

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24

Mercer, L. Preston, Danita S. Kelley, Holly M. Bundrant, Akram-Ul Haq, and Laurie L. Humphries. "Gender Affects Rats' Central Nervous System Histaminergic Responses to Dietary Manipulation." Journal of Nutrition 126, no. 12 (December 1, 1996): 3128–35. http://dx.doi.org/10.1093/jn/126.12.3128.

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25

Held, Heather E., Raffaele Pilla, Geoffrey E. Ciarlone, Carol S. Landon, and Jay B. Dean. "Female rats are more susceptible to central nervous system oxygen toxicity than male rats." Physiological Reports 2, no. 4 (April 2014): e00282. http://dx.doi.org/10.14814/phy2.282.

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26

Chikley, Ben-Ami, and Kontoyiannis. "Mucormycosis of the Central Nervous System." Journal of Fungi 5, no. 3 (July 8, 2019): 59. http://dx.doi.org/10.3390/jof5030059.

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Mucormycosis involves the central nervous system by direct extension from infected paranasal sinuses or hematogenous dissemination from the lungs. Incidence rates of this rare disease seem to be rising, with a shift from the rhino-orbital-cerebral syndrome typical of patients with diabetes mellitus and ketoacidosis, to disseminated disease in patients with hematological malignancies. We present our current understanding of the pathobiology, clinical features, and diagnostic and treatment strategies of cerebral mucormycosis. Despite advances in imaging and the availability of novel drugs, cerebral mucormycosis continues to be associated with high rates of death and disability. Emerging molecular diagnostics, advances in experimental systems and the establishment of large patient registries are key components of ongoing efforts to provide a timely diagnosis and effective treatment to patients with cerebral mucormycosis.

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27

Arieli, R., and Y. Moskovitz. "Humidity does not affect central nervous system oxygen toxicity." Journal of Applied Physiology 91, no. 3 (September 1, 2001): 1327–33. http://dx.doi.org/10.1152/jappl.2001.91.3.1327.

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Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness when hyperbaric oxygen is breathed in diving and hyperbaric medical therapy. Lin and Jamieson ( J Appl Physiol 75: 1980–1983, 1993) reported that humidity in the inspired gas enhances CNS oxygen toxicity. Because alveolar gas is fully saturated with water vapor, we could not see a cause and effect and surmised that other factors, such as metabolic rate, might be involved. Rats were exposed to 507- and 608-kPa O2 in dry (31 or 14%) or humid (99%) atmosphere until the appearance of the first electrical discharge preceding the clinical convulsions. Each rat served as its own control. A thermoneutral temperature (28 ± 0.4°C) yielded resting CO2 production of 0.81 ± 0.06 ml · g−1 · h−1. Latency to the first electrical discharge was not affected by humidity. At 507-kPa O2, latency was 23 ± 0.4 and 22 ± 0.7 min in dry and humid conditions, respectively, and, at 608-kPa O2, latency was 15 ± 4 and 14 ± 3 min in dry and humid conditions, respectively. When no effects of CO2 and metabolic rate are present, humidity does not affect CNS oxygen toxicity. Relevance of the findings to diving and hyperbaric therapy is discussed.

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Alvarez, Azucena L., Alejandro Delorenzi, Daniel Santajuliana, Samuel Finkielman, Victor E. Nahmod, and Carlos J. Pirola. "Central bradykininergic system in normotensive and hypertensive rats." Clinical Science 82, no. 5 (May 1, 1992): 513–19. http://dx.doi.org/10.1042/cs0820513.

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1. The kinin antagonist des-Arg9−[Leu8]bradykinin, injected into the lateral ventricle, caused a long-lasting, dose-dependent reduction in arterial blood pressure and heart rate in spontaneously hypertensive rats but not in normotensive Wistar-Kyoto rats; the antagonist also blocked the pressor response to ventricularly infused bradykinin in both strains. 2. Bradykinin content was increased in the hypothalamus and septum and decreased in the dorsal medulla of spontaneously hypertensive rats when compared with those of normotensive Wistar-Kyoto rats, whereas similar bradykinin contents were observed in the pineal gland, hypophysis and rostroventrolateral medulla of both rat strains. 3. Increased concentrations of bradykinin and its precursor kininogen were found in the cerebrospinal fluid of spontaneously hypertensive rats. 4. Bradykinin receptor numbers, measured as the binding of [125I-Tyr1]bradykinin to nervous tissue, were found to be increased in the dorsal medulla and hypophysis, and to be decreased in the pineal gland, of spontaneously hypertensive rats. 5. Therefore, the central kinin system may participate, by both pre- and post-synaptic mechanisms, in the maintenance of hypertension in spontaneously hypertensive rats.

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29

Rauch, A. L., M. F. Callahan, V. M. Buckalew, and M. Morris. "Regulation of plasma atrial natriuretic peptide by the central nervous system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R531—R535. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r531.

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The anterior ventral region of the third ventricle (AV3V) is a major central site in the regulation of cardiovascular and renal function. To examine the role of the central nervous system in the regulation of atrial natriuretic peptide (ANP) secretion, the effect of lesions in this region on basal, volume-stimulated, and osmotic-stimulated plasma ANP was determined. Basal levels of plasma ANP were not different in sham- and AV3V-lesioned rats. Volume expansion with a continuous infusion of saline or with a bolus administration of saline increased plasma ANP in sham-lesioned rats. In AV3V-lesioned rats, continuous infusion of saline had no effect on plasma ANP, and a bolus administration of saline decreased plasma ANP. Osmotic stimulation with hypertonic saline increased plasma ANP in sham-lesioned rats but had no effect on plasma ANP in AV3V-lesioned rats. These results suggest that the central nervous system is involved in the regulation of ANP secretion and that altered ANP regulation may contribute to the cardiovascular and renal deficiencies in AV3V-lesioned rats.

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30

Song, Jian-gang, Hong-hai Li, Yun-fei Cao, Xin Lv, Ping Zhang, Ye-sheng Li, Yong-jun Zheng, et al. "Electroacupuncture Improves Survival in Rats with Lethal Endotoxemia via the Autonomic Nervous System." Anesthesiology 116, no. 2 (February 1, 2012): 406–14. http://dx.doi.org/10.1097/aln.0b013e3182426ebd.

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Background Recent advances have indicated a complex interplay between the autonomic nervous system and the innate immune system. Targeting neural networks for the treatment of sepsis is being developed as a therapeutic strategy. Because electroacupuncture at select acupoints can modulate activities of the autonomic nervous system, we tested the hypothesis that electroacupuncture at specific acupoints could modulate systemic inflammatory responses and improve survival via its impact on the autonomic nervous system in a rat model of sepsis. Methods Sprague-Dawley male rats received electroacupuncture for 45 min before and at 1, 2, or 4 h after a lethal dose of intraperitoneal lipopolysaccharide injection (6 mg/kg). Outcomes included survival and systemic cytokine responses. Also, the possible roles of neural circuitry, including the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, were evaluated. Results Electroacupuncture pretreatment at the Hegu acupoints significantly attenuate systemic inflammatory responses and improve survival rate from 20% to 80% in rats with lethal endotoxemia. Such a site-specific effect requires the activation of muscarinic receptors in the central nervous system, but not increasing central sympathetic tone. In the periphery synergistic, rather than independent, action of the sympathetic and parasympathetic systems is also necessary. Conclusions Electroacupuncture pretreatment has a dramatic survival-enhancing effect in rats with lethal endotoxemia, which involves the activation of efferent neural circuits of the autonomic nervous system (e.g., cholinergic antiinflammatory pathway). This approach could be developed as a prophylactic treatment for sepsis or perioperative conditions related to excessive inflammation.

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31

Kwak, Seung P., Jessica E. Malberg, David S. Howland, Ke-Yi Cheng, Jianying Su, Yin She, Myles Fennell, and Afshin Ghavami. "Ablation of central nervous system progenitor cells in transgenic rats using bacterial nitroreductase system." Journal of Neuroscience Research 85, no. 6 (2007): 1183–93. http://dx.doi.org/10.1002/jnr.21223.

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32

Ahmed, Amina. "Treatment of Central Nervous System Tuberculosis." Journal of Pediatric Infectious Diseases 13, no. 02 (January 15, 2018): 141–52. http://dx.doi.org/10.1055/s-0037-1607235.

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AbstractCentral nervous system tuberculosis (CNS-TB) manifests as tuberculous meningitis, intracranial tuberculoma, or spinal tuberculous arachnoiditis. Children are disproportionately affected, with high rates of mortality and morbidity reported even in the era of treatment. Most guidelines for the treatment of drug-susceptible CNS-TB recommend 9 to 12 months of a standard regimen of isoniazid, rifampin, pyrazinamide, and ethambutol, with the adjunctive use of corticosteroids early in therapy. Recent trials have demonstrated improved outcomes with intensified regimens using nonstandard regimens or higher dosages of standard drugs. Accumulating evidence also supports shorter duration of treatment. Further investigation is warranted to identify the optimal regimen and duration of treatment for CNS-TB. Complications such as hydrocephalus may be managed medically or surgically. Although outcomes have improved with effective chemotherapy and immunomodulation of disease, prompt diagnosis and treatment in the early stages of disease remain paramount to improve prognosis.

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33

Fazan, Rubens, Domitila A. Huber, Carlos Alberto A. Silva, Valdo J. Dias da Silva, Maria Cristina O. Salgado, and Helio C. Salgado. "Sildenafil acts on the central nervous system increasing sympathetic activity." Journal of Applied Physiology 104, no. 6 (June 2008): 1683–89. http://dx.doi.org/10.1152/japplphysiol.01142.2007.

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Sildenafil induces vasodilation and is used for treating erectile dysfunction. Although its influence on resting heart function appears to be minimal, recent studies suggest that sildenafil can increase sympathetic activity. We therefore tested whether sildenafil injected into the central nervous system alters the autonomic control of the cardiovascular system in conscious rats. The effect of sildenafil citrate injected into the lateral cerebral ventricle was evaluated in conscious rats by means of the recording of lumbar sympathetic nerve activity (LSNA), spectral analysis of systolic arterial pressure and heart rate variability, spontaneous baroreflex sensitivity, and baroreflex control of LSNA. Intracerebroventricular (ICV, 100 μg/5 μl) administration of sildenafil caused remarkable tachycardia without significant change in basal arterial pressure and was associated with a conspicuous increase (47 ± 14%) in LSNA. Spectral analysis demonstrated that systolic arterial pressure oscillations in the low frequency (LF) range were increased (from 6.3 ± 1.5 to 12.8 ± 3.8 mmHg2), whereas the high frequency (HF) range was not affected by ICV administration of sildenafil. Sildenafil increased pulse interval oscillations at LF and decreased them at HF. The LF-HF ratio increased from 0.04 ± 0.01 to 0.17 ± 0.06. Spontaneous baroreflex sensitivity measured by the sequence method and the baroreflex relationship between mean arterial pressure and LSNA were not affected by ICV administration of sildenafil. In conclusion, sildenafil elicited an increase in sympathetic nerve activity that is not baroreflex mediated, suggesting that this drug is able to elicit an autonomic imbalance of central origin. This finding may have implications for understanding the cardiovascular outcomes associated with the clinical use of this drug.

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34

Neumann, Hartmut P. H., Hans R. Eggert, Klaus Weigel, Hartmut Friedburg, Otmar D. Wiestler, and Peter Schollmeyer. "Hemangioblastomas of the central nervous system." Journal of Neurosurgery 70, no. 1 (January 1989): 24–30. http://dx.doi.org/10.3171/jns.1989.70.1.0024.

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✓ The findings of a 10-year study (1976 to 1986) conducted in southwest Germany on hemangioblastomas (HBL's) of the central nervous system (CNS) are presented. During that period, 47 HBL's were diagnosed and surgically removed in 44 patients, with a good postoperative survival rate and prognosis. The majority (83%) of these tumors were located in the cerebellum. By thorough clinical examination of the patients and careful evaluation of their family background, it was found that 23% of the HBL patients were afflicted with von Hippel-Lindau syndrome. In addition to the CNS tumors, 14 neoplastic or similar lesions were detected in other tissues. These included angiomatosis of the retinae, pheochromocytomas, pancreatic cysts, renal cysts, and renal carcinoma. The diagnosis of von Hippel-Lindau syndrome was thus established in seven families. The authors suggest the need for a screening program for patients with HBL of the CNS which is designed to confirm or exclude ocular or visceral lesions associated with von Hippel-Lindau syndrome.

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35

SUTO, G., J. CZIMMER, A. KIRALY, B. FALUSI, S. UNDI, and G. MOZSIK. "Interferon-α inhibits gastrie secretion through central nervous system CRF in rats." Gastroenterology 120, no. 5 (April 2001): A536. http://dx.doi.org/10.1016/s0016-5085(01)82661-5.

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36

Ates, Ozkan, Suleyman R. Cayli, Eyup Altinoz, Neslihan Yucel, Ayhan Kocak, Ozcan Tarim, Akif Durak, Yusuf Turkoz, and Saim Yologlu. "Neuroprotective effect of mexiletine in the central nervous system of diabetic rats." Molecular and Cellular Biochemistry 286, no. 1-2 (March 16, 2006): 125–31. http://dx.doi.org/10.1007/s11010-005-9102-6.

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37

Oshida, Kyoichi, Takashi Shimizu, Mitsunori Takase, Yoshitaka Tamura, Toshiaki Shimizu, and Yuichiro Yamashiro. "Effects of Dietary Sphingomyelin on Central Nervous System Myelination in Developing Rats." Pediatric Research 53, no. 4 (April 2003): 589–93. http://dx.doi.org/10.1203/01.pdr.0000054654.73826.ac.

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38

Suto, Gabor, Jozsef Czimmer, Agnes Kiraly, Boglarka Falusi, Sarolta Undi, and Gyula Mozsik. "Interferon-α inhibits gastrie secretion through central nervous system CRF in rats." Gastroenterology 120, no. 5 (April 2001): A536. http://dx.doi.org/10.1016/s0016-5085(08)82661-3.

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39

Sampaio, Waneli Cristine Morais, Mara Cláudia Ribeiro, Larice Feitosa Costa, Wânia Cristina de Souza, Goiara Mendonça de Castilho, Melissa Sousa de Assis, Fabiana Pirani Carneiro, et al. "Effect of music therapy on the developing central nervous system of rats." Psychology & Neuroscience 10, no. 2 (June 2017): 176–88. http://dx.doi.org/10.1037/pne0000087.

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40

Davisson, R. L., M. D. Travis, J. N. Bates, A. K. Johnson, and S. J. Lewis. "Stereoselective actions of S-nitrosocysteine in central nervous system of conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 5 (May 1, 1997): H2361—H2368. http://dx.doi.org/10.1152/ajpheart.1997.272.5.h2361.

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This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.

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YAMATE, Jyoji, Masanori TAJIMA, Tetsuo NUNOYA, and Satoru KUDOW. "Spontaneous tumors of the central nervous system of Fischer 344/DuCrj rats." Japanese Journal of Veterinary Science 49, no. 1 (1987): 67–75. http://dx.doi.org/10.1292/jvms1939.49.67.

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42

WU, GANGMING, BIN SUN, LI LIU, JUN ZHOU, LIQUN MO, CHANGHE REN, and CEHUA OU. "Lipid emulsion mitigates local anesthesia-induced central nervous system toxicity in rats." Experimental and Therapeutic Medicine 10, no. 3 (June 24, 2015): 1133–38. http://dx.doi.org/10.3892/etm.2015.2594.

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43

Cunningham, J. Thomas, Myrna Herrera-Rosales, Michelle A. Martinez, and Steve Mifflin. "Identification of Active Central Nervous System Sites in Renal Wrap Hypertensive Rats." Hypertension 49, no. 3 (March 2007): 653–58. http://dx.doi.org/10.1161/01.hyp.0000254481.94570.74.

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44

Hughes, Andy M., Barry J. Everitt, Stafford L. Lightman, and Kathryn Todd. "Oxytocin in the central nervous system and sexual behaviour in male rats." Brain Research 414, no. 1 (June 1987): 133–37. http://dx.doi.org/10.1016/0006-8993(87)91333-3.

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45

Nonogaki, Katsunori, Akihisa Iguchi, and Nobuo Sakamoto. "Bicuculline Methiodide Influences the Central Nervous System to Produce Hyperglycemia in Rats." Journal of Neuroendocrinology 6, no. 4 (August 1994): 443–46. http://dx.doi.org/10.1111/j.1365-2826.1994.tb00605.x.

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46

Van Huysse, J. W., and S. L. Bealer. "Central nervous system norepinephrine release during hypotension and hyperosmolality in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 6 (June 1, 1991): R1071—R1076. http://dx.doi.org/10.1152/ajpregu.1991.260.6.r1071.

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Extracellular norepinephrine (NE) levels in the paraventricular/anterior hypothalamic area (P/A) and in the dorsomedial medulla (DM) in conscious Sprague-Dawley rats were estimated by in vivo microdialysis before, during, and after sustained hypotension (75 mmHg mean arterial pressure) produced either by hemorrhage (Hem) or by 2-chloroadenosine infusion (2-Cl-ADO, 2.6-26.0 micrograms/min iv). P/A and DM NE were also measured before, during, and after hypertonic saline infusion (HTS; 1.5 M NaCl at 10 microliters.100 g-1.min-1 iv). P/A and DM NE increased during both Hem and 2-Cl-ADO and returned to baseline after reinfusion of hemorrhaged blood or after 2-Cl-ADO was stopped. However, Hem caused greater increases in P/A NE than 2-Cl-ADO despite equivalent decreases in blood pressure. Hem and 2-Cl-ADO produced equivalent changes in DM NE. HTS did not change P/A or DM NE despite increases in blood pressure of approximately 15 mmHg and plasma osmolality of approximately 30 mosmol/kgH2O. We conclude that 1) hypotension increases P/A and DM NE, which may mediate compensatory responses, 2) Hem is a more potent stimulus for NE release in the P/A than isovolemic hypotension induced by 2-Cl-ADO, and 3) the hypertensive response to HTS does not involve changes in P/A or DM NE.

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47

Li, Hui-Yun, Ling-Lin Wang, and Ru-Sung Yeh. "Leptin immunoreactivity in the central nervous system in normal and diabetic rats." NeuroReport 10, no. 2 (February 1999): 437–42. http://dx.doi.org/10.1097/00001756-199902050-00042.

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48

Del Bel, Elaine A., and Francisco S. Guimarães. "Social isolation increases cholecystokinin mRNA in the central nervous system of rats." NeuroReport 8, no. 16 (November 1997): 3597–600. http://dx.doi.org/10.1097/00001756-199711100-00035.

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49

UEMURA, K., A. IGUCHI, A. YATOMI, H. MIURA, A. HONMURA, M. YANASE, and N. SAKAMOTO. "Involvement of the Hippocampus in Central Nervous System-Mediated Glucoregulation in Rats." Endocrinology 124, no. 5 (May 1989): 2449–55. http://dx.doi.org/10.1210/endo-124-5-2449.

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50

Maeda-Hagiwara, M., and Y. Taché. "Central nervous system action of TRH to stimulate gastric emptying in rats." Regulatory Peptides 17, no. 4 (April 1987): 199–207. http://dx.doi.org/10.1016/0167-0115(87)90063-2.

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