Thematische Bibliographien / Medical Neurobiology

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Auswahl der wissenschaftlichen Literatur zum Thema „Medical Neurobiology“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 26. Januar 2023

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Zeitschriftenartikel zum Thema "Medical Neurobiology"

&NA;. „Medical Neurobiology“. Medicine & Science in Sports & Exercise 44, Nr. 4 (April 2012): 769. http://dx.doi.org/10.1249/01.mss.0000413417.60137.a0.

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Enoka, R. M., und D. G. Stuart. „Neurobiology of muscle fatigue“. Journal of Applied Physiology 72, Nr. 5 (01.05.1992): 1631–48. http://dx.doi.org/10.1152/jappl.1992.72.5.1631.

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Muscle fatigue encompasses a class of acute effects that impair motor performance. The mechanisms that can produce fatigue involve all elements of the motor system, from a failure of the formulation of the descending drive provided by suprasegmental centers to a reduction in the activity of the contractile proteins. We propose four themes that provide a basis for the systematic evaluation of the neural and neuromuscular fatigue mechanisms: 1) task dependency to identify the conditions that activate the various mechanisms; 2) force-fatigability relationship to explore the interaction between the mechanisms that results in a hyperbolic relationship between force and endurance time; 3) muscle wisdom to examine the association among a concurrent decline in force, relaxation rate, and motor neuron discharge that results in an optimization of force; and 4) sense of effort to determine the role of effort in the impairment of performance. On the basis of this perspective with an emphasis on neural mechanisms, we suggest a number of experiments to advance our understanding of the neurobiology of muscle fatigue.

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Kuhad, A., und K. Chopra. „Neurobiology of diabetic encephalopathy“. Drugs of the Future 33, Nr. 9 (2008): 763. http://dx.doi.org/10.1358/dof.2008.033.09.1232462.

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Joffe, Russell T. „Book Review: Cambridge Medical Reviews: Neurobiology and Psychiatry“. Canadian Journal of Psychiatry 40, Nr. 1 (Februar 1995): 55. http://dx.doi.org/10.1177/070674379504000122.

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Salm, Adrienne K., und James L. Culberson. „Peer Presentations of Case Studies in Medical Neurobiology“. Medical Science Educator 25, Nr. 4 (24.07.2015): 407–12. http://dx.doi.org/10.1007/s40670-015-0157-z.

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HERRERA, DANIEL G. „Neurobiology and Psychiatry, vol. 2: Cambridge Medical Reviews“. American Journal of Psychiatry 152, Nr. 3 (März 1995): 469—a—470. http://dx.doi.org/10.1176/ajp.152.3.469-a.

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Joyce, Eileen M. „Cambridge medical reviews: Neurobiology and psychiatry, volume 1“. Journal of Psychosomatic Research 37, Nr. 2 (Februar 1993): 204. http://dx.doi.org/10.1016/0022-3999(93)90088-w.

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Haines, Duane E., James B. Hutchins und James C. Lynch. „Medical neurobiology: Do we teach neurobiology in a format that is relevant to the clinical setting?“ Anatomical Record 269, Nr. 2 (15.04.2002): 99–106. http://dx.doi.org/10.1002/ar.10073.

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Newberg, Andrew R., Lisa A. Catapano, Carlos A. Zarate und Husseini K. Manji. „Neurobiology of bipolar disorder“. Expert Review of Neurotherapeutics 8, Nr. 1 (Januar 2008): 93–110. http://dx.doi.org/10.1586/14737175.8.1.93.

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AHMED, IQBAL, und DAVID GANSLEB. „The Neurobiology of Memory“. Journal of Clinical Psychopharmacology 10, Nr. 4 (August 1990): 307. http://dx.doi.org/10.1097/00004714-199008000-00028.

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Dissertationen zum Thema "Medical Neurobiology"

Taliaferro, Linda Kay. „Psychiatric Disorders as Potential Predictors in Medical Disease Development“. ScholarWorks, 2011. https://scholarworks.waldenu.edu/dissertations/939.

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Millions of individuals suffer disability or death from immune-based inflammatory diseases. If psychiatric disorders could be empirically linked to the prediction of immune-based inflammatory diseases, there would be a basis for promoting disease prevention measures for individuals diagnosed with one of four psychiatric disorders. Psychoneuroimmunology provided the theoretical base for understanding emotionally induced medical disease development. In this quantitative study, a parallel archival research design was used to investigate the degree to which generalized anxiety disorder, posttraumatic stress disorder, major depression recurrent, and dysthymic disorder predicted the presence of atherosclerosis, cardiovascular heart disease, rheumatoid arthritis, cancer, and type II diabetes. There were 1,209 electronic medical records of adult patients obtained through purposive stratified sampling. A secondary data analysis was employed using descriptive cross tabulation, chi-square test of independence, and multinomial logistic regression. The findings revealed major depression recurrent was a statistically significant predictor for atherosclerosis, rheumatoid arthritis, type II diabetes and cancer. Generalized anxiety disorder was a statistically significant predictor for cancer. The results can promote positive social change by providing information that could be used to develop assessment plans that identity individuals who are at risk of developing the comorbid diseases. The prevention programs could effectively be used to minimize the subsequent development of inflammatory diseases, which in turn could decrease the onset of the medical diseases among individuals with psychiatric disorders.

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Salagic, Belma. „Regulation of COX-2 signaling in the blood brain barrier“. Thesis, Linköping University, Linköping University, Department of Physics, Chemistry and Biology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-18113.

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Upon an inflammation the immune system signals the brain by secreted cytokines to elicit central nervous responses such as fever, loss of appetite and secretion of stress hormones. Since the blood brain barrier, (BBB) protects the brain from unwanted material, molecules like cytokines are not allowed to cross the barrier and enter the brain. However, it is clear that they in some way can signal the brain upon an inflammation. Many suggestions concerning this signaling has been made, one being that cytokines bind to receptors on the endothelial cells of the blood vessels of the brain and trigger the production of prostaglandins that can cross the BBB. This conversion is catalyzed by the enzyme cyclooxygenase-2, (COX-2), which is induced by transcription factors like NF-κB in response to cytokines. One of the central nervous responses to inflammatory stimuli is activation of the HPA-axis whose main purpose is glucocorticoid production. Glucocorticoids inhibit the inflammatory response by suppressing gene transcription of pro-inflammatory genes including those producing prostaglandins through direct interference with transcription factors such as NF-κB or initiation of transcription of anti-inflammatory genes like IκB or IL-10. It has however not been clear if glucocorticoids can target the endothelial cells of the brain in order to provide negative feed-back on the immune-to-brain signaling, and in that way inhibit central nervous inflammatory symptoms. An anatomical prerequisite for such a mechanism would be that the induced prostaglandin production occurs in cells expressing GR. This has however never been demonstrated. Here I show that a majority of the brain endothelial cells expressing the prostaglandin synthesizing enzyme COX-2 in response to immune challenge also express the glucocorticoid receptor, (GR). This indicates that immune-to-brain signaling is a target for negative regulation of inflammatory signaling executed by glucocorticoids and identifies brain endothelial GR as a possible future drug target for treatment of central nervous responses to inflammation such as fever and pain.

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Whicker, Wyatt, W. Drew Gill und Russell W. Brown. „DISCOVERY OF A NOVEL ANTI-NEUROINFLAMMATORY TREATMENT FOR AUDITORY SENSORIMOTOR GATING IN TWO RODENT MODELS OF SCHIZOPHRENIA“. Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/204.

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Schizophrenia is primarily treated with the use of antipsychotic medications. However, antipsychotics used have severe, dose-dependent side effects in schizophrenia patients. Therefore, there is a need for new adjunctive drugs that lower the effective dose of first line schizophrenia drugs and improve patient symptoms. Neuroinflammation is associated with microglial activation in schizophrenia, and increased tumor necrosis factor-alpha (TNF) has shown to be associated with Metabolic Syndrome in schizophrenia patients. A newly developed anti-neuroinflammatory, PD2024, reduces TNF-alpha action in vitro and in vivo, and has been shown to be well-tolerated in rat and dog studies with no adverse effects. The purpose of this research is to evaluate the effect of PD2024 in two well-defined schizophrenia models in rats. The neonatal quinpirole model has been established through administration of the dopamine D2-like agonist quinpirole (NQ) or saline control (NS) postnatally from days 1-21. NQ treatment results in increases of dopamine D2 receptor sensitivity throughout the animal’s lifetime without changing receptor number, mimicking a hallmark of schizophrenia. The polyinosinic:polycytidylic acid (Poly I:C) model is based on mimicking an increase immune response during early brain development, which has been shown to increase the prevalence of schizophrenia. Poly I:C (2 mg/kg) was administered during the neonatal period at postnatal days (P)5-7 to produce this effect. Both models were given PD2024 at 10mg/kg orally through the diet from P30-67. Prepulse inhibition (PPI) was used to test sensorimotor gating deficits in the rats. PPI has past research showing its use as a quantitative phenotype for evaluating schizophrenia-associated behavioral and neurobiological deficits. In our PPI test, rats are exposed to three different, randomly ordered noise trials. The trials included a pulse trial with a 120-decibel startle pulse, a prepulse trial with an auditory click at 73, 76, or 82-decibels, and a no stimulus trial without any additional noise. The rats were given 25 randomized trials, comprised of 5 pulse, 15 prepulse (5 each of 73, 76, and 82dB) and 5 no stimulus trials. Background noise was 70dB, and the rats were tested during adolescence (days 45-46) and adulthood (60-65). In NQ adolescent rats, PPI was significantly improved in the PD2024-treated compared to NQ controls. NQ-PD2024 and NS rats were statistically equivalent throughout the trials. These results were reflected in the NQ adult model as well. The Poly I:C adolescents treated with PD2024 also demonstrated improved PPI performance compared to Poly I:C controls. This improvement was also shown in the adult Poly I:C rats. Overall, the PPI deficits in both models improved between 15 to 30% in adolescence and adulthood. These results indicate that PD2024 is effective in treating schizophrenia-associated behaviors.

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Batten, Seth R. „GLUTAMATE DYSREGULATION AND HIPPOCAMPAL DYSFUNCTION IN EPILEPTOGENESIS“. UKnowledge, 2013. http://uknowledge.uky.edu/medsci_etds/1.

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Epileptogenesis is the complex process of the brain developing epileptic acitivity. Due to the role of glutamate and the hippocampus in synaptic plasticity a dysregulation in glutamate neurotransmission and hippocampal dysfunction are implicated in the process of epileptogenesis. However, the exact causal factors that promote epileptogenesis are unknown. We study presynaptic proteins that regulate glutamate neurotransmission and their role in epileptogenesis. The presynaptic protein, tomosyn, is believed to be a negative regulator of glutamate neurotransmission; however, no one has studied the effects of this protein on glutamate transmission in vivo. Furthermore, evidence suggests that mice lacking tomosyn have a kindling phenotype. Thus, in vivo glutamate recordings in mice lacking tomosyn have the potential to elucidate the exact role of tomosyn in glutamate neurotransmission and its potential relationship to epileptogenesis. Here we used biosensors to measure glutamate in the dentate gyrus (DG), CA3, and CA1 of the hippocampus in tomosyn wild-type (Tom+/+), heterozygous (Tom+/-), and knock out (Tom-/-) mice. We found that, in the DG, that glutamate release increases as tomosyn expression decreases across genotype. This suggests that tomosyn dysregulation in the DG leads to an increase in glutamate release, which may explain why these mice have an epileptogenic phenotype.

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Ighodaro, Eseosa T. „STUDYING VASCULAR MORPHOLOGIES IN THE AGED HUMAN BRAIN USING LARGE AUTOPSY DATASETS“. UKnowledge, 2018. https://uknowledge.uky.edu/neurobio_etds/19.

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Cerebrovascular disease is a major cause of dementia in elderly individuals, especially Black/African Americans. Within my dissertation, we focused on two vascular morphologies that affect small vessels: brain arteriolosclerosis (B-ASC) and multi-vascular profiles (MVPs). B-ASC is characterized by degenerative thickening of the wall of brain arterioles. The risk factors, cognitive sequelae, and co-pathologies of B-ASC are not fully understood. To address this, we used multimodal data from the National Alzheimer’s Coordinating Center, Alzheimer’s Disease Neuroimaging Initiative, and brain-banked tissue samples from the University of Kentucky Alzheimer’s Disease Center (UK-ADC) brain repository. We analyzed two age at death groups separately: < 80 years and ≥ 80 years. Hypertension was a risk factor in the < 80 years at death group. In addition, an ABCC9 gene variant (rs704180), previously associated with aging-related hippocampal sclerosis, was associated with B-ASC in the ≥ 80 years at death group. With respect to cognition as determined by test scores, severe B-ASC was associated with worse global cognition in both age groups. With brain-banked tissue samples, we described B-ASC’s relationship to hippocampal sclerosis of aging (HS-Aging), a pathology characterized by neuronal cell loss in the hippocampal region not due to Alzheimer’s disease. We also studied MVPs, which are characterized by multiple small vessel lumens within a single vascular (Virchow-Robin) space. Little information exists on the frequency, risk factors, and co-pathologies of MVPs. Therefore, we used samples and data from the UK-ADC, University of Kentucky pathology department, and University of Pittsburgh pathology department to address this information. We only found MVPs to be correlated with age. Lastly, given the high prevalence of cerebrovascular disease and dementia in Black/African Americans, we discussed the challenges and considerations for studying Blacks/African Americans in these contexts.

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Xing, Bin. „THE EFFECT OF PPARγ ACTIVATION BY PIOGLITAZONE ON THE LIPOPOLYSACCHARIDE-INDUCED PGE₂ AND NO PRODUCTION: POTENTIALUNDERLYING ALTERATION OF SIGNALING TRANSDUCTION“. UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/629.

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Microglia-mediated neuroinflammation plays an important role in the pathogenesis of Parkinson's disease (PD). Uncontrolled microglia activation produces major proinflammatory factors including cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) that may cause dopaminergic neurodegeneration. Peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone has potent antiinflammatory property. We hypothesize pioglitazone protects dopaminergic neuron from lipopolysaccharide (LPS)-induced neurotoxicity by interacting with relevant signal pathways, inhibiting microglial activation and decreasing inflammatory mediators. First, the neuroprotection of pioglitazone was explored. Second, the signaling transductions such as jun N-terminal kinase (JNK) and the interference with these pathways by pioglitazone were investigated. Third, the effect of pioglitazone on these pathways-mediated PGE2 / nitric oxide (NO) generation was investigated. Finally, the effect of PPARγ antagonist on the inhibition of PGE2 / NO by pioglitazone was explored. The results show that LPS neurotoxicity is microglia-dependent, and pioglitazone protects neurons against LPS insult possibly by suppressing LPS-induced microglia activation and proliferation. Second, pioglitazone protects neurons from COX-2 / PGE2 mediated neuronal loss by interfering with the NF-κB and JNK, in PPARγ-independent mechanisms. Third, pioglitazone significantly inhibits LPS-induced iNOS / NO production, and inhibition of LPS-induced iNOS protects neuron. Fourth, inhibition p38 MAPK reduces LPS-induced NO generation but no effect is found upon JNK inhibition, and pioglitazone inhibits p38 MAPK phosphorylation induced by LPS. In addition, pioglitazone increases PPARγ phosphorylation, followed by the increased PI3K/Akt phosphorylation. Nevertheless, inhibition of PI3K increases LPS-induced p38 MAPK phosphorylation. Inhibition of PI3K eliminates the inhibitive effect of pioglitazone on the LPS-induced NO production, suggesting that the inhibitive effect of pioglitazone on the LPS-induced iNOS and NO might be PI3K-dependent.

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Fu, Weisi. „PROTEIN KINASE A AND EPAC MEDIATE CHRONIC PAIN AFTER INJURY: PROLONGED INHIBITION BY ENDOGENOUS Y1 RECEPTORS IN DORSAL HORN“. UKnowledge, 2016. https://uknowledge.uky.edu/physiology_etds/31.

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Inflammation or nerve injury sensitizes several populations of nociceptive neurons in the dorsal horn of the spinal cord, including those that express the neuropeptide Y (NPY) Y1 receptor (Y1R). Our overall hypothesis is that after tissue or nerve injury, these Y1R-expressing neurons enter a state of latent sensitization (LS) that contributes to vulnerability to the development of chronic pain; furthermore, LS is under the tonic inhibitory control of endogenous Y1R signaling. First, we evaluated the intracellular signaling pathways that become activated in Y1R-expressing neurons and participate in LS. To do this, we established behavioral models of inflammatory or neuropathic pain, allowed pain hypersensitivity to resolve, and then during this period of pain remission we administered the Y1R receptor antagonist, BIBO3304, by intrathecal injection. As observed previously with mu-opioid receptor antagonists/inverse agonists, we found that BIBO3304 reinstated pain hypersensitivity via an N-methyl-D-aspartate receptor (NMDAR)- and adenylyl cyclase type 1 (AC1)-dependent mechanism. Our subsequent behavioral pharmacological experiments then established two signaling pathways downstream of AC1 that maintain LS. The first pathway involves protein kinase A (PKA) and transient receptor potential cation channel A1 (TRPA1) and channel V1 (TRPV1). The second pathway involves exchange proteins activated by cAMP (Epac 1 and Epac 2). We next found that nerve injury decreases the co-expression of Y1R with markers of excitatory interneurons, suggesting that Y1R-expressing neurons acquire a pain-enhancing phenotype after peripheral nerve injury. In a separate set of experiments that utilized Y1R-receptor internalization as an index of NPY release, we found that nerve injury increased stimulus-evoked NPY release. We conclude that injury induces pain-facilitatory mechanisms of LS in the dorsal horn involving PKA→TRPA1 and PKA→TRPV1 at the central terminals of primary afferent neurons. Whether Epac mechanisms are located on these same presynaptic terminals and/or at Y1R-expressing excitatory interneurons remain to be determined. We also conclude that injury-induced LS is masked by a compensatory up-regulation of spinal NPY release that tonically inhibits pain. These results present a novel mechanism of injury-induced LS and endogenous control of the transition from acute to chronic pain by the NPY-Y1R system. Our work sheds light on novel targets for the treatment of chronic pain.

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Salmeron, Kathleen Elizabeth. „INVESTIGATIONS OF INTERLEUKIN-1 ALPHA AS A NOVEL STROKE THERAPY IN EXPERIMENTAL ISCHEMIC STROKE“. UKnowledge, 2018. https://uknowledge.uky.edu/neurobio_etds/20.

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Stroke is a leading cause of death and disability worldwide. Although rapid recognition and prompt treatment have dropped mortality rates, most stroke survivors are left with permanent disability. Approximately 87% of all strokes result from the thromboembolic occlusion of the cerebrovasculature (ischemic strokes). Potential stroke therapeutics have included anti-inflammatory drugs, as well as many other targets with the goal of mitigating the acute and chronic inflammatory responses typically seen in an ischemic stroke. While these approaches have had great success in preclinical studies, their clinical translation has been less successful. Master inflammatory cytokines, such as IL-1, are of particular interest. IL-1’s isoforms, IL-1α and IL-1β, were long thought to have similar function. While IL-1β has been extensively studied in stroke, the role of IL-1α during post stroke inflammation has been overlooked. Because IL-1 inhibitors have been unsuccessful in clinical application, we reasoned that IL-1α may provide previously unknown benefits to the brain after injury. We hypothesized that IL-1α could be protective or even accelerate reparative processes in the brain such as producing new blood vessels (angiogenesis) or neurons (neurogenesis). To test that IL-1α is protective after stroke, we tested IL-1α’s protective effects on primary cortical neurons in in vitro models of stroke. We showed that IL-1α was directly protective on primary cortical neurons in a dose-dependent fashion. We then performed mouse middle cerebral artery occlusion stroke studies to determine the safety of giving IL-1α in vivo. These studies showed that administering IL-1α acutely was neuroprotective. However, intravenous (IV) administration of IL-1α resulted in transient, hemodynamic changes following drug delivery. To minimize these systemic effects, we administered IL-1α intra-arterially (IA) directly into the stroke affected brain tissue, allowing us to significantly lower the concentration of administered IL-1α. In comparison to IV, IA IL-1α showed greater histological protection from ischemic injury as well as improved functional recovery following stroke, all without systemic side effects. To test that IL-1α could aid in neurorepair following stroke, we tested IL-1α’s ability to help damaged blood vessels repair in vitro. We found that IL-1α significantly increased brain endothelial cell activation, proliferation, migration, and capillary formation. We tested IL-1α’s proangiogenic properties in vivo by administering IL-1α three days following stroke. Delayed administration allowed us to separate IL-1α’s acute neuroprotective effects from potential subacute angiogenic effects. We found that mice receiving IL-1α performed significantly better on behavioral tests and also showed greater vascularization within the penumbra two weeks following stroke. We also found that IL-1α treated animals showed more endothelial activation than vehicle treated animals. Finally, our studies showed that IL-1α treated animals showed increased early-phase neurogenesis with evidence of increased proliferation at the subventricular zone suggesting that IL-1α’s beneficial effects are even more far-reaching than previously thought. In conclusion, our experiments suggest that the inflammatory cytokine IL-1α is neuroprotective and neuroreparative in experimental ischemic stroke and worthy of further study as a novel stroke therapy.

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Ivy, Devon. „DEFINING THE RADIORESPONSE OF MOSSY CELLS“. CSUSB ScholarWorks, 2018. https://scholarworks.lib.csusb.edu/etd/633.

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Clinical radiotherapy is used to treat a variety of brain tumors within the central nervous system. While effective, it can result in progressive and debilitating cognitive impairment that can diminish quality of life. These impairments have been linked to hippocampal dysfunction and corresponding deficits in spatial learning and memory. Mossy cells are a major population of excitatory neurons located within the dentate hilus and highly involved in hippocampal circuitry. They play critical roles in spatial navigation, neurogenesis, memory, and are particularly vulnerable to a variety of neurotoxic insults. However, their sensitivity to ionizing radiation has yet to be investigated in detail. I hypothesize that mossy cells are critical targets for ionizing radiation, whereby damage to these targets contributes to the mechanisms associated with radiation-induced hippocampal dysfunction. To test this idea, wild-type mice were exposed to clinically relevant doses of cranial x-ray irradiation and their hippocampi were examined 1 month and 3 months post treatment. A significant decline in both the number of mossy cells and their activity were observed. In addition, dentate granular cells demonstrated reduced levels of activity, as well as reduced proliferation within the subgranular zone. A second cohort of mice was introduced to a novel environment in order to induce the expression of immediate early genes. Analysis of c-Fos mRNA yielded a significant increase in control but not irradiated animals, suggesting that radiotherapy impaired immediate early gene expression and resultant functional behavioral outcomes. These findings support the proposition that radiation-induced damage to mossy cells contributes to hippocampal deficiencies which result in cognitive dysfunction.

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Bardgett, Megan Elyse. „NEURAL MECHANISMS OF SYMPATHETIC ACTIVATION DURING HYPERINSULINEMIA AND OBESITY-INDUCED HYPERTENSION“. UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/46.

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Obesity afflicts more than 30% of the U.S. population and is a major risk factor for the development of hypertension, type II diabetes, and cardiovascular disease. Studies in humans and animals indicate that obesity is associated with increased sympathetic outflow to the vasculature and kidneys. One mechanism postulated to underlie the increase in sympathetic nerve activity (SNA) in obesity is hyperinsulinemia. Little is known regarding the central circuitry underlying elevated SNA and arterial blood pressure (ABP) during hyperinsulinemia and obesity or if sympathoexcitatory circuits are still responsive to insulin in obesity. Hyperinsulinemic-euglycemic clamps elevate SNA to the hind limb vasculature in lean rodents but obesity is associated with resistance to the peripheral and anorexic effects of insulin. Therefore, the first aim was to determine whether diet-induced obesity causes development of insulin resistance in the central circuits mediating SNA. The sympathoexcitatory response to insulin was still intact in diet-induced obese rats indicating a role for insulin in the elevation in SNA and ABP in obesity. The second aim of this project was to identify the specific receptors in the rostral ventrolateral medulla (RVLM) that mediate the elevated SNA during hyperinsulinemia. The RVLM provides basal sympathetic tone and maintains baseline ABP. Glutamate is the major excitatory neurotransmitter and glutamate receptors of the RVLM are known to mediate multiple forms of hypertension. Blockade of RVLM NMDA-specific glutamatergic receptors reverses the increased lumbar SNA associated with hyperinsulinemia. In contrast, blockade of angiotensin II type 1 or melanocortin receptors in the RVLM had no effect on the sympathoexcitatory response to insulin. The goal of the third aim was to identify the cellular mechanisms within RVLM that mediate the elevated SNA and ABP in diet-induced obesity. Blockade of RVLM glutamate receptors reversed the elevated ABP and lumbar SNA associated with diet-induced obesity while it had no effect on rats on a low fat diet or those resistant to weight gain on the high fat diet. Similar to the findings during hyperinsulinemia, blockade of RVLM angiotensin II type 1 or melanocortin receptors had no effect on lumbar SNA or ABP during diet-induced obesity.

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Bücher zum Thema "Medical Neurobiology"

Medical neurobiology. New York: Oxford University Press, 2011.

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Arthur, Butt, Hrsg. Glial neurobiology: A textbook. Chichester, West Sussex: John Wiley & Sons, 2007.

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Minagar, Alireza. Neurobiology of dementia. Amsterdam: Elsevier/Academic Press, 2009.

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Basic neurochemistry: Principles of molecular, cellular, and medical neurobiology. 8. Aufl. Amsterdam: Elsevier/Academic Press, 2012.

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R, Bauer William, und Wong Dean F. 1949-, Hrsg. Neurokinetics: The dynamics of neurobiology in vivo. New York: Springer, 2011.

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Carlos, Zarate Juan, und SpringerLink (Online service), Hrsg. Behavioral Neurobiology of Bipolar Disorder and its Treatment. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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1940-, Bennett Robert M., Hrsg. The clinical neurobiology of fibromyalgia and myofascial pain: Therapeutic implications. Binghamton, N.Y: Haworth Medical Press, 2002.

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1931-, Huber Ivan, Masler Edward P. 1948- und Rao B. R. 1936-, Hrsg. Cockroaches as models for neurobiology: Applications in biomedical research. Boca Raton, Fla: CRC Press, 1990.

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B, Porto Pazos Ana, Pazos Sierra Alejandro und Buceta Washington Buno, Hrsg. Advancing artificial intelligence through biological process applications. Hershey, PA: Medical Information Science Reference, 2008.

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Symposium on Molluscan Neurobiology (2nd 1986 Amsterdam). Neurobiology: Molluscan models : proceedings of the Second Symposium on Molluscan Neurobiology, held at the Department of Zoology of the Free University, Amsterdam, the Netherlands, August 18-22, 1986. Herausgegeben von Boer H. H, Geraerts W. P. M, Joosse J und Koninklijke Nederlandse Akademie van Wetenschappen. Amsterdam: North-Holland, 1987.

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Buchteile zum Thema "Medical Neurobiology"

Manoharan, S., M. Mohamed Essa, A. Vinoth, R. Kowsalya, A. Manimaran und R. Selvasundaram. „Alzheimer’s Disease and Medicinal Plants: An Overview“. In Advances in Neurobiology, 95–105. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28383-8_6.

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Drew, Trevor, und S. Rossignol. „Studies on the Medial Reticular Formation during Locomotion in Chronic Cats Using Microstimulation and Unit Recording“. In Neurobiology of Vertebrate Locomotion, 73–76. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-09148-5_6.

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Vogt, Brent A., Robert W. Sikes und Leslie J. Vogt. „Anterior Cingulate Cortex and the Medial Pain System“. In Neurobiology of Cingulate Cortex and Limbic Thalamus, 313–44. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4899-6704-6_11.

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Mason, Peggy. „Introduction to the Nervous System“. In Medical Neurobiology, 3–20. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0001.

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Mason, Peggy. „Cells of the Nervous System: Neurons and Glia“. In Medical Neurobiology, 21–32. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0002.

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Mason, Peggy. „Developmental Overview of Neuroanatomy: The Tube Within the Brain“. In Medical Neurobiology, 33–52. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0003.

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Mason, Peggy. „The Neuron at Rest“. In Medical Neurobiology, 55–72. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0004.

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Mason, Peggy. „Electrical Communication Within a Neuron“. In Medical Neurobiology, 73–88. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0005.

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Mason, Peggy. „Neurotransmitter Release“. In Medical Neurobiology, 89–102. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0006.

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Mason, Peggy. „Synthesis, Packaging, and Termination of Neurotransmitters“. In Medical Neurobiology, 103–26. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780195339970.003.0007.

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