HORIZONS IN NEUROSCIENCE RESEARCH, VOLUME 1 -- CONTENTS -- PREFACE -- NERVOUS, IMMUNE, ENDOCRINE REGULATORY SYSTEMS AND DISEASES ASSOCIATED WITH NERVE GROWTH FACTOR CO-SECRETION -- SUMMARY -- ABBREVIATIONS -- INTRODUCTION -- 1. NERVE GROWTH FACTOR, ITS RECEPTORS AND THE SIGNALING MECHANISMS -- 1.1. The Characteristics of Nerve Growth Factor -- 1.2. Nerve Growth Factor Receptors -- 1.2.1. Tyrosin Kinase (TrkA) Receptor -- 1.2.2. P75ntr Receptor -- 1.3. Nerve Growth Factor Receptor Signaling Mechanisms -- 1.3.1. Tyrosine Kinase Receptor A Signaling -- 1.3.2. Cell Signaling Via P75ntr Receptor -- 1.3.3. Transactivation Between the Nerve Growth Factor-Bound Tyrosine Kinase A and the G Protein-Coupled Adenosine or Adrenergic Receptor Signalings -- 1.3.3.1. Transactivation Between the Tyrosine Kinase A and Adrenergic Receptors -- 1.3.3.2. Transactivation Between the TrkA and Adenosine A2 Receptors -- REFERENCES -- 2. CELLS SECRETING NERVE GROWTH FACTOR AND THEIR TISSUE LOCALIZATION -- 2.1. Neuronal Tissues -- 2.2. Nonneuronal Tissues -- 2.2.1. Bone Marrow -- 2.2.2. Lung Tissues -- 2.2.3. Adipose Tissues -- 2.2.4. Orbital Tissues -- 2.2.5 Endocrine Tissues -- 2.2.5.1. Adrenal Glands -- 2.2.5.2Pituitary Gland -- 2.2.5.3.Thyroid Glands -- REFERENCES -- 3. NERVE GROWTH FACTOR IN INFLAMMATORY, ALLERGIC AND AUTOIMMUNE PROCESSES -- 3.1. Nerve Growth Factor Modulates the Inflammatory Responses Via Prostaglandins -- 3.1.1. Nerve Growth Factor Associates with the Inflammatory Pain -- 3.2. Nerve Growth Factor in Allergic Diseases -- 3.2.1. Characterization of the Allergic Responses -- 3.2.2. The Sensory Neuronal Innervation and Nerve Growth Factor in Allergy -- 3.2.3. Nerve Growth Factor is Involved in the Allergic Inflammation Associated with Fibrosis -- 3.3. Relationship Between Nerve Growth Factor and Apoptosis.

3.4. Nerve Growth Factor in the Autoimmune Diseases -- 3.4.1. Suppressor Regulatory T Cells in the Autoimmune Diseases -- 3.4.2. Neurogenic Inflammation -- 3.4.2.1. Nerve Growth Factor Regulatory Role in the Autoimmune Diseases -- 3.5. Nerve Growth Factor Involvement in the Stress -- 3.5.1. Stress Induced Endocrine Alterations -- 3.5.2. The Relationship Between the Stress Induced Endocrine and Cytokine Processes -- 3.5.3. Nerve Growth Factor During Stress Links to the Endocrine and Immune Networks -- 3.5.4. The Network Between the Stress Induced Inflammation and the Actions of the Nerve Growth Factor. The Neurogenic Pain -- 3.6 Nerve Growth Factor Exerts an Effect Towards the Direction of T Helper 2 Dominance -- 3.6.1 The Effects of Stress, Glucocorticoids, Norepinephrines and CRH on the Direction Towards Th2 Dominance -- 3.6.2 The Immunocompetent Cells Express Glucocorticoid and Catecholamine Receptors -- 3.6.3 The Th1 Apoptosis-Susceptibility and the Th2 Apoptosis-Resistance Mediated by NGF -- 3.6.4 Cytokines Promote the Th2 Dominance -- REFERENCES -- 4. ENHANCED SYMPATHOADRENAL AND NERVE GROWTH FACTOR ACTIVITIES IN THE TISSUE HYPERTROPHY -- 4.1. The Enhanced Sympathoadrenal Activity and the Modulatory Effects of Catecholamines on the Nerve Growth Factor -- 4.2. Relationhip Between the Enhanced Sympathoadrenal Activity and the Tissue Hypertrophy -- 4.2.1. Catecholamines-Induced Cardiac Hypertrophy -- 4.2.2. Catecholamines in the Skeletal Muscle Hypertrophy -- 4.2.2.1. Phosphatidylinositol 3-Kinase (PI-3K) in the Myogenesis -- 4.2.2.2. Skeletal Muscle Hypertrophy -- REFERENCES -- 5. NERVE GROWTH FACTOR IN TISSUE RESTITUTION -- 5.1. Nerve Growth Factor in Wound Healing -- 5.2. Nerve Growth Factor Therapy -- REFERENCES -- 6. AUTOIMMUNE AND ENDOCRINE DISEASES WITH ENHANCED SYMPATHOADRENAL ACTIVITY -- 6.1. Graves'ophthalmopathy.

6.1.1. Autoimmune Processes in Graves' Ophthalmopathy -- 6.1.2. Enhanced Sympathoadrenal Activity in the Thyroid, Adipose and Eye Muscle Tissue Hypertrophy -- 6.2. Diabetes Mellitus -- 6.2.1. Regulation of the Sympathoadrenal System and the Hypothalamic-Pituitary-Adrenal Axis in Diabetes Mellitus -- 6.2.2. Diabetic Neuropathy and Nerve Growth Factor -- 6.2.3. The Role of Cellular Integrity and Function in Diabetic Vascular Complications -- REFERENCES -- NERVE GROWTH FACTOR AND PAIN: EVIDENCE FROM EXPERIMENTAL MODELS AND HUMANS, AND NEW PROSPECTIVES FOR TREATMENT -- ABSTRACT -- INTRODUCTION -- NGF AND NOCICEPTION -- INTRACELLULAR MECHANISMS OF NGF ACTION -- PATHOPHYSIOLOGICAL MECHANISMS OF INFLAMMATORY AND NEUROPATHIC PAIN -- EXPERIMENTAL EVIDENCE FOR THE INVOLVEMENT OF NGF IN INFLAMMATORY AND NEUROPATHIC PAIN -- PATHOPHYSIOLOGICAL MECHANISMS OF MIGRAINE -- PATHOPHYSIOLOGY OF FIBROMYALGIA -- INVOLVEMENT OF NGF IN THE PATHOPHYSIOLOGICAL MECHANISMS OF MIGRAINE AND FIBROMYALGIA -- POTENTIAL OF NGF TARGETING STRATEGIES IN NEUROPATHIC PAIN, CHRONIC MIGRAINE AND FIBROMYALGIA -- CONCLUSIONS -- REFERENCES -- HOMEOSTATIC ROLE OF THE PARASYMPATHETIC NERVOUS SYSTEM IN HUMAN BEHAVIOR -- ABSTRACT -- 1. INTRODUCTION -- 2. PARASYMPATHETIC ACTIVITY AND FATIGUE -- 2.1. Parasympathetic activity and chronic fatigue syndrome -- 2.1.1. Chronic fatigue syndrome and autonomic imbalance -- 2.1.2. Psychometric assessment of fatigue in CFS and relation with autonomic imbalance -- 2.2. Parasympathetic activity and overtraining -- 2.2.1. Overtraining syndrome and autonomic imbalance -- 2.2.2. Mood alterations and relation with autonomic imbalance -- 2.3. The multistage psychoautonomic model of adaptation to training -- Stage 1: Normal training adaptation -- Stage 2: Overreaching / Fatigue -- Stage 3: Overtraining / Chronic fatigue.

3. PARASYMPATHETIC NERVOUS SYSTEM AND EATING BEHAVIOR -- 3.1. HRV as a method of assessing postprandial sympathovagal balance -- 3.2. Prandial pattern and the problem of meal definition -- 3.3. Cephalic phase reflexes -- 3.3.1. Cephalic phases reflexes: roles and mechanisms -- 3.3.2. Cephalic phase of insulin release -- 3.4. Lipoprivic feeding -- 3.5. Putative role of the parasympathetic nervous system in eating behavior: The lessons of subdiaphragmatic vagal deafferentation -- 3.6. Portal glucose receptors, vagal afferents and eating behavior -- 4. CONCLUSION -- REFERENCES -- LIMK1: THE KEY ENZYME OF ACTIN REMODELING BRIDGES SPATIAL ORGANIZATION OF NUCLEUS AND NEURAL TRANSMISSION: FROM HETEROCHROMATIN VIA NON-CODING RN AS TO COMPLEX BEHAVIOR -- ABSTRACT -- INTRODUCTION -- THE MAIN PLAYERS IN THE SIGNAL CASCADE OF ACTIN REMODELING -- FROM CHROMATIN REMODELING TO NEUROGENESIS -- REGULATION OF GENE ACTIVITY AT POSTTRANSLATION LEVEL -- CHROMATIN STRUCTURE: STUDIES IN DROSOPHILA -- SECOND LEVEL OF GENOME ORGANIZATION: STRUCTURAL ORGANIZATION OF A CHROMOSOME, EUCHROMATIC AND HETEROCHROMATIC REGIONS OF THE DROSOPHILA POLYTENE CHROMOSOMES -- GENE SILENCING -- THIRD LEVEL O GENOME ORGANIZATION: SPATIAL ORGANIZATION OF CHROMOSOMES IN THE NUCLEUS -- EPIGENETIC MECHANISMS IN MEMORY FORMATION -- CONCLUSION -- REFERENCES -- "GLIOPATHY" MAINTAINS PERSISTENT HYPEREXCITABILITY OF SPINAL DORSAL HORN NEURONS AFTER SPINAL CORD INJURY: SUBSTRATE OF CENTRAL NEUROPATHIC PAIN -- INTRODUCTION -- ASCENDING PAIN PATHWAY -- HYPEREXCITABILITY OF SPINAL DORSAL HORN NEURONS -- P38 MAPK -- pERK -- pJNK -- pCREB -- PHENOTYPES OF SPINAL DORSAL HORN NEURONS -- SPINAL GLIA -- Physiological and Structural Neuronal Partners -- Glial Activation Following Spinal Cord Injury -- Neuronal-Glial Interactions -- CELLULAR MECHANISMS OF HYPEREXCITABILITY : LOSS OF DESCENDING INHIBITORY PATHWAYS.

Loss of Endogenous GABAergic Inhibitory Tone -- Modulation of Endogenous Inhibitory Circuits: Glial Modulation of GABAergic Tone -- Loss of Endogenous Opioidergic Inhibitory Tone -- Modulation of Endogenous Inhibitory Circuits : Glial Modulation of Opioid Effects -- CONCLUSION -- ACKNOWLEGEMENT -- REFERENCES -- MULTIPLE NEURONAL AND GLIAL MECHANISMS CAN BE INVOLVED IN THE RESPONSE TO THE ACTIVATION OF NICOTINIC RECEPTORS -- ABSTRACT -- INTRODUCTION -- 1. DIVERSITY AND COMPLEXITY OF THE NICOTINIC COMMUNICATION SYSTEM -- 1. 1. Diversity of Nicotinic Receptors in the Cns -- 1. 2. Complex Regulation of the Nachrs -- 1. 3. Complexity of the Nicotinergic System as a Neurotransmitter System -- 2. EFFECTS OF ACTIVATING NACHRS -- 2.1. Nicotine-Induced Dehydrogenase Activation -- 2.2. Nicotine -Induced Increases in Nerve Growth Factor -- 2.3. Nicotine -Induced Increase in Cyclooxygenase-2 -- 3. CONCLUSION -- REFERENCES -- CALCIUM SIGNALING IN GLIAL CELLS OF THE ENTERIC NERVOUS SYSTEM -- ABSTRACT -- 1. BASIC OF CALCIUM SIGNALING -- 1.1 Calcium Release from Intracellular Calcium Stores -- 1.2 Calcium Influx from Extracellular Source -- 1.3 Capacitative Calcium Entry -- 1.4 Recovery Following Calcium Signaling -- 2. INTRACELLULAR CALCIUM SIGNALING -- 2.1 Neurotransmitter-Mediated [Ca2+]I Response -- 2.2 Inflammatory Molecule-Evoked [Ca2+]I Response -- 2.3 Bioactive Lipid-Evoked [Ca2+]I Response -- 3. INTERCELLULAR CALCIUM SIGNALING -- 4. ROLE OF CALCIUM SIGNALING -- 4.1 Calcium Signaling and Information Processing in the Enteric Nervous System -- 4.2 Calcium Signaling and Cellular Functions in Enteric Glial Cells -- REFERENCES -- COCAINE AND CRAVING: FROM NORMAL TRANSMISSION TO PATHOLOGICAL FUNCTIONING -- ABSTRACT -- INTRODUCTION -- CLASSICAL CONDITIONING -- COCAINE, SENSORY PROCESSING AND LEARNING -- Cocaine and Sensory Processing in Humans.

Cocaine and Attention in Humans.