Neural Responses to Injury: Prevention, Protection and Repair; Volume 3: The Neuro-Immunology of Stress, Injury and Infection
Neural Responses to Injury: Prevention, Protection and Repair; Volume 3: The Neuro-Immunology of Stress, Injury and Infection

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Published: 1996

Total Pages: 0

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The hypothesis on which this investigation is based is that stressors such as transient temperature changes and restraint signal the central nervous system eliciting the release of catecholamines and adrenal steroids which, in turn, affect the immune system resulting in the reactivation of latent viruses. Employing a mouse model of stress-induced reactivation of herpes simplex virus type 1 (HSV-1), we are determining the time course of viral reactivation relative to the alteration of immune parameters including lymphocyte functions and numbers. Specifically, we are correlating the expression of various immunomodulatory cytokine genes with the levels of neuroendocrine monoamines, as well as the activation of the hypothalamic-pituitary-adrenal (HPA) axis and relating these to the reactivation of infectious virus in the nervous system. Alterations in serum corticosterone and shifts in monoamines in the brains, trigeminal ganglia, and brain stems of latently infected and reactivated mice following the application of stress are being studied. Differences between control (not stressed) and stressed animals are being determined relative to the incidence of viral reactivation and the affect of stress on immunological regulation of the reactivation process.

Naural Responses to Injury: Prevention, Protection, and Repair. Revised. Volume 3, Part I. The Neuroimmunology of Stress, Injury and Infection
Naural Responses to Injury: Prevention, Protection, and Repair. Revised. Volume 3, Part I. The Neuroimmunology of Stress, Injury and Infection

Author: Nicolas Bazan

Publisher:

Published: 1997

Total Pages: 252

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The hypothesis on which this investigation is based is that stressors such' as transient temperature changes and restraint signal the central nervous system eliciting the release of catecholamines and adrenal steroids which, in turn, affect the immune system resulting in the reactivation of latent viruses. Employing a mouse model of stress-induced reactivation of herpes simplex virus type 1 (HSV-1), we are determining the time course of viral reactivation relative to the alteration of immune parameters including lymphocyte functions and numbers. Specifically, we are correlating the expression of various immunomodulatory cytokine genes with the levels of neuroendocrine monoamines, as well as the activation of the hypothalamic- pituitary-adrenal (HPA) axis and relating these to the reactivation of infectious virus in the nervous system. Alterations in serum corticosterone and shifts in monoamines in the brains, trigeminal ganglia, and brain stems of latently infected and reactivated mice following the application of stress are being studied. Differences between control (not stressed) and stressed animals are being determined relative to the incidence of viral reactivation and the affect of stress on immunological regulation of the reactivation process. The knowledge gained from this investigation will provide an understanding of the interaction between the nervous system, the neuroendocrine system, and the immune system during times of stress at the molecular and cellular levels.

Naural Responses to Injury: Prevention, Protection, and Repair. Volume 3: Part II. The Neuro-immunology of Stress, Injury and Infection
Naural Responses to Injury: Prevention, Protection, and Repair. Volume 3: Part II. The Neuro-immunology of Stress, Injury and Infection

Author: Nicolas Bazan

Publisher:

Published: 1997

Total Pages: 283

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Since the previous review on the role of oplolds in the immune system, numerous Investigative teams have contributed to the growing pool of Information Illustrating the tangible relationship between opiolds and Immune function, particularly as this association pertains to bacterial and viral pathogens. In addition, the recent cloning of both neural and immunederived opiold receptors will ultimately facilitate the Identification of molecular events that are responsible for the Immunomodulatory effects that are mediated by receptor ligation. Specifically, the administration of oplolds In vivo can potentially affect the Immune system either through direct interactIon with receptors on the effector cells or Indirectly, through the ligation of receptors found within the central nervous system. This indirect routing Is hypothesized to Involve secondary pathways Including the hypothalamic pituitary adrenal (lIPA) axis and the sympathetic nervous system ultimately resulting in immunomodulatlon. Consequently, a portion of this review addresses the recent data on leukocvte-derlved oplold receptors and the potential Immunoregulatory role relative to opiold receptors found within the central nervous system. In addition, recent observations on the effects of oplolds and immunocompetence is reviewed from both a molecular and cellular perspective. Finally, the consequence of oplold exposure on the competence of the host Immune system to microbial pathogens is summarized.

Neural Responses to Injury: Prevention, Protection, and Repair. The Neuroimmunology of Stress, Injury, and Infection
Neural Responses to Injury: Prevention, Protection, and Repair. The Neuroimmunology of Stress, Injury, and Infection

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Published: 1994

Total Pages: 198

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The SU Neuroscience Center is a comprehensive, multidisciplinary, and transdepartmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of the present program is to find solutions to neuroscience-related problems of interest to the U.S. Army Medical Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed. JMD.

Neural Responses to Injury: Prevention, Protection and Repair; Volume 4: Neurochemical Protection of the Brain, Neural Plasticity and Repair
Neural Responses to Injury: Prevention, Protection and Repair; Volume 4: Neurochemical Protection of the Brain, Neural Plasticity and Repair

Author: Nicolas Bazan

Publisher:

Published: 1996

Total Pages: 171

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The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Neurochemical Protection of the Brain, Neural Plasticity and Repair, are as follows: Species Number Allowed Number Used LSU IACUC# Rat (sprague-Dawle) 125 125 1046 Rat (Sprague-Dawle) 91 91 1045 The development of chronic epilepsy is a very serious complication of head injury, neurodegenerative diseases, brain tumors, and exposure to neurotoxic agents. Head injury is often associated with loss of short-term memory, indicating trauma to the hippocampal formation, the brain region most commonly associated with epileptic brain damage. Underlying the formation of epilepsy (epileptogenesis) is proposed to be a vicious cycle initiated by the loss of neurons. In an attempt to repair and/or replace lost synaptic connections, the brain can develop aberrant synaptic circuits that permit the propagation and amplification of waves of excitatory neurotransmission, eventually resulting in prolonged or repeated seizures (status epilepticus). The massive amounts of excitatory amino acids released during these episodes can stimulate further neuronal loss (excitotoxic damage), the formation of more aberrant synaptic circuits, and further seizures (Choi and Rothinan, 1990). Excitotoxic damage has been demonstrated in several experimental models of status epilepticus (Meldmm et al, 1973; Ben-Ari, 1995; Sloviter, 1987).

Neural Responses to Injury: Prevention, Protection, and Repair. Core Research Facility
Neural Responses to Injury: Prevention, Protection, and Repair. Core Research Facility

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Publisher:

Published: 1994

Total Pages: 34

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The LSU Neuroscience Center is a comprehensive, multidisciplinary, and transdepartmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of the present program is to find solutions to neuroscience-related problems of interest to the U.S. Army Medical Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed.

Neural Responses to Injury: Prevention, Protection, and Repair. Neurochemical Protection of the Brain, Neural Plasticity and Repair
Neural Responses to Injury: Prevention, Protection, and Repair. Neurochemical Protection of the Brain, Neural Plasticity and Repair

Author:

Publisher:

Published: 1994

Total Pages: 78

ISBN-13:

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The LSU Neuroscience Center is a comprehensive, multidisciplinary, and transdepartmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of the present program is to find solutions to neuroscience-related problems of interest to the U.S. Army Medical Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuropharmacology, molecular biology and virology are proposed. JMD.

Neural Responses to Injury: Prevention, Protection, and Repair
Neural Responses to Injury: Prevention, Protection, and Repair

Author:

Publisher:

Published: 1995

Total Pages: 23

ISBN-13:

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The LSU Neuroscience Center is a comprehensive, multidisciplinary, and trans-departmental entity that unites fundamental neurobiology and the clinical neurosciences in the common goal of elucidating the workings of the brain and contributing to the treatment of currently incurable diseases of the nervous system. The objective of this program is to find solutions to neuroscience-related problems of interest to the US Army Medical Research and Development Command. The program is focused on exploiting novel neuroprotective strategies that lead to prevention of and repair after neural injury. Converging approaches using state-of-the-art tools of cell biology, neurochemistry, neuroimmunology, neurophysiology, neuroppharmacology, molecular biology and virology are ongoing. Over the four years covered in this proposal, this program aims to: (1) carry out seven research projects in the basic and clinical neurosciences; (2) expand central, shared facilities with the addition of highly specialized instrumentation not currently available to our scientists; (3) develop laboratory space to permit the physical consolidation and coordination of this research effort; and (4) institute a coordination unit to monitor, facilitate, and administrate the cooperative research programs, as well as to meet the associated budgetary, human resources, facilities, and communications needs for the attainment of the program goals.

Naural Responses to Injury: Prevention, Protection, and Repair. Revised. Volume 4. Neurochemical Protection of the Brain, Neural Plasticity and Repair
Naural Responses to Injury: Prevention, Protection, and Repair. Revised. Volume 4. Neurochemical Protection of the Brain, Neural Plasticity and Repair

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Publisher:

Published: 1997

Total Pages: 0

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Traumatic brain injury is characterized by multiple phases of damage; including primary tissue damage and bleeding at the site of impact; secondary damage, including brain edema, ischemia, the diffusion of toxic substances beyond the initial site of injury and delayed neuronal death; and long-term epileptogenic changes in synaptic plasticity. A common motif at the cellular level of these various forms of neurotrauma is the over-release of neurotransmitters, the stimulation of post-synaptic receptors, and the subsequent accumulation of abnormally high concentrations of second messengers. The major neurotransmitter involved in neuronal damage is thought to be the excitatory amino acid L-glutamate. Glutamate triggers calcium entry into post-synaptic neurons via the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors (Rotlunan and Olney, 1986, 1987; Choi 1988), and so the activation of many calcium-dependent signaling pathways. The major focus of research in our laboratory has been the activation of calcium- dependent phospholipases A2, the release from membrane phospholipids of bioactive lipids, including free arachidonic acid (AA) and platelet-activating factor (PAF), and the signaling pathways then activated. We and other groups have shown the neuroprotective properties of pharmacological agents targeting bioactive lipid signaling cascades. Detailed characterization of these processes, and the downstream events that link the over-accumulation of bioactive lipids to long-term changes in brain physiology, is important in identifying the best therapeutic targets for the treatment of traumatic brain injury.