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Journal Article 2014; 35(8): 655-665 PubMed PMID: 25702292 Citation  Keywords:  Humans, Irritable Bowel Syndrome:etiology, Neuronal Plasticity:physiology,.   

: Neuroplasticity is the nervous system's ability to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. And the nervous system monitors and coordinates internal organ function. Thus neuroplasticity may also be associated with the pathogenesis of other diseases besides neuropsychiatric diseases, such as cardiovascular disease. The digestive system is controlled by the nervous system, mainly by the autonomic nervous system. Stress may lead to depression/anxiety and irritable bowel syndrome (IBS). IBS is commonly comorbid with depression/anxiety, which are disorders of decreased neuroplasticity. And the mechanisms of depression/anxiety and IBS are related. The hypothalamo-pituitary-adrenal axis, hippocampus, amygdala and stress-related factors and hormones, such as corticotropin-releasing factor, glucocorticoids and brain-derived neurotrophic factor are involved in both neuroplasticity and the pathogenesis of depression/anxiety and IBS. So we conclude that decreased neuroplasticity causes the comorbidity of depression/anxiety and IBS, and increased neuroplasticity may be beneficial against the development of IBS. This theory provides another angle that can explain some of the reported phenomena related to IBS and neuropsychiatry, and provide a potential treatment to protect against IBS....

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Journal Article 2010; 31(5): 609-615 PubMed PMID: 21173750 Citation  Keywords:  Animals, Disease Models, Animal, Immunohistochemistry, Injections, Intraperitoneal, Injections, Intraventricular, Interleukin-1beta, Lipopolysaccharides, Male, Neuronal Plasticity, Neuropeptides:biosynthesis, Paraventricular Hypothalamic Nucleus:immunolog.   

OBJECTIVES AND METHODS: Neuropeptides, as the main neuroendocrine system effectors, regulate notably the response to different stressors via a secretory plasticity within their respective hypothalamic neuronal populations. The aim of the present study was to explore by immunocytochemistry the occurrence and the potential expression plasticity of the novel neuropeptide EM66 in the CRH neurones of stressed rats.

RESULTS: The secretogranin II (SgII)-derived peptide EM66 is strongly expressed within hypothalamic neuroendocrine areas such as the parvocellular aspect of the paraventricular nucleus (pPVN) as well as the median eminence, suggesting a probable hypophysiotropic effect of this peptide. As a first approach to investigate such a role, we evaluated by immunohistochemistry EM66 expression within the pPVN following acute immune stress induced by lipopolysaccharide (LPS) or interleukin-1β (IL-1β) injection in rat. This study showed that EM66 is present in the pPVN but the number of EM66 immunolabeled cells did not fluctuate in this structure following LPS peripheral injection. In line with this observation, an intracerebroventricular injection of IL-1β did not provoke any significant variation of the number of intraparaventricular EM66 neurones.

CONCLUSION: The present data revealed for the first time that EM66 expression would be insensitive to the central and peripheral cytokines within the neurosecretory hypothalamic pPVN. This result indicates that EM66 does not participate to the phenotypic plasticity of hypothalamic parvicellular neurones in response to acute inflammatory stress....

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Journal Article 2010; 31(5): 602-608 PubMed PMID: 21173739 Citation  Keywords:  Animals, Brain:metabolism, Depression:metabolism, Humans, Hypothalamo-Hypophyseal System:metabolism, Neural Pathways:pathology, Neurogenic Inflammation:complications, Neuronal Plasticity, Peripheral Nerves:metabolism, Pituitary-Adrenal System:metabolism, .   

: The etiopathogenesis of depression is a highly complex process characterized by several neurobiological alterations including decreased monoamine neurotransmission in the brain, dysregulated hypothalamic-pituitary-adrenal axis activity, decreased neuronal plasticity, and chronic inflammation in the brain and peripheral tissues. Experimental and clinical studies indicate that the vagus nerve may influence these processes. The importance of the vagus nerve in the etiopathogenesis of depression is further supported by its involvement in the induction of sickness behavior, as well as by clinical studies confirming a beneficial effect of vagus nerve stimulation in depressed patients. The aim of this article is to describe current knowledge of afferent and efferent vagal pathways role in the development and progression of depression....

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Journal Article 2009; 30(6): 694-699 PubMed PMID: 20038923 Citation  Keywords:  Animals, Cell Membrane:physiology, Humans, Lipid Bilayers, Membrane Proteins:physiology, Neuronal Plasticity:physiology, Neurons:physiology, Synapses:physiology,.   

: Lipoid character of plasma membrane namely the presence of polyenic fatty acids enables to interact with membrane proteins and in certain extent also to modulate their function. During the development, molecules of membrane fatty acids become more and more complex, and the ratio of polyenic fatty acids/saturated fatty acids in the brain rises, while the concentration of monoenic fatty acids remained relatively stable. This phenomenon is apparent also in the ratio of unsaturated fatty acids OMEGA-3 in plasma of newborns which correlates with the birth weight. Plasma membrane reflects local specializations of nerve cells. Its composition varies in functionally specialized regions called domains. Specialized domains of nerve cells determine the function of dendrites, soma, axon, axon hillock ect. Premature weaning of laboratory rats results in structural changes and in the increase of excitability of neuronal circuits in hypothalamus, septum and hippocampus which indicate the possibility of membrane composition changes. In synapses, transport proteins of synaptic vesicles, act together with the specific proteins of the presynaptic membrane. Membrane proteins determine the release of neurotransmitter at different conditions of synaptic activity, and they can contribute to the recovery of neurotransmitter content after the repeated hyperactivity. In the model of experimental kindling, repeated seizures bring about decreases and distribution changes of synaptic vesicles....

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Journal Article 2009; 30(4): 429-436 PubMed PMID: 20010491 Citation  Keywords:  Animals, Autistic Disorder:pathology, Cell Adhesion Molecules, Neuronal:physiology, Cell Movement:physiology, Disease Models, Animal, Extracellular Matrix Proteins:physiology, Humans, Nerve Tissue Proteins:physiology, Neuronal Plasticity:physiology, Neuro.   

: Autism is the most genetically influenced neuropsychiatric disorder with heritability of approximately 90%. Since genetic factors seem to play a crucial role in autism etiology, enormous attention is focused on genetic analyses of the disorder. Reelin, one of the autism candidates, is necessary in regulation of neuronal migration during brain development and also in maintaining synaptic plasticity during postnatal life period. Reduced reelin levels were observed in sera and brain cortices of autistic patients. In this review, abnormalities in reelin signaling and the relationship between reelin deficiency and principal neuroendocrine pathways are discussed....

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Journal Article 2008; 29(6): 831-836 PubMed PMID: 19112396 Citation  Keywords:  Adolescent, Adolescent Development, Age of Onset, Brain:growth & development, Child, Child Development, Critical Period (Psychology), Humans, Neuronal Plasticity:physiology, Neuropsychology, Schizophrenia:physiopathology, Schizophrenic Psychology,.   

: Schizophrenia is a disorder characterized by delay in neurodevelopment and by a central disorder of recognition (i.e. with generalized cognitive deficit). Connectivity impairments in the areas of the social brain and cerebellum are the "messenger" of abnormal CNS development in schizophrenia. Processes of neuronal reorganization in cortical and subcortical structures, aberrant forms of pruning, sprouting, and myelinization may play a major role in the pathogenesis of a schizophrenic breakdown. Models of neuroplasticity during adolescence can be connected with models of neurodevelopmental vulnerability and models of neurotoxicity to form an integrated approach in order to better understand premorbid adjustment, onset, and course of schizophrenia. The loss of plasticity and aberrant myelinization lead to a deterioration in cognitive functions, social dysfunction and, in individuals with specific genetic vulnerability, to expression of schizophrenia. This article discusses brain development in relation to the diagnosis of schizophrenia and the basic symptoms of childhood schizophrenia (with early and very early onset) and of adolescent schizophrenia....

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Journal Article 2008; 29(4): 547-551 PubMed PMID: 18766146 Citation  Keywords:  Animals, Female, Male, Neuronal Plasticity:physiology, Neurons:cytology, Oxytocin:metabolism, Paraventricular Hypothalamic Nucleus:cytology, Rats, Restraint, Physical, Rodentia, Stress, Psychological,.   

OBJECTIVES AND METHODS: The presence of oxytocin (OT) and its putative participation to the phenotypic plasticity of CRH neurones in the stressed jerboa was investigated. We analysed by immunocytochemistry the OT expression within the hypothalamic parvicellular paraventricular nucleus (pPVN) of male jerboas submitted to an acute immobilization (30 min).

RESULTS: OT presence was clearly demonstrated in the pPVN of the jerboa and no significant difference in the number of OT immunolabeled cells was observed whatever the experimental conditions. Interestingly, CRH-immunoreactive neurons coexpressed OT within cell bodies and terminals in a similar way both in control and stressed animals. The level of coexpression was regionally heterogeneous and was not sensitive to the stress immobilization.

CONCLUSION: The present data reveal for the first time the occurrence of OT in hypothalamic pPVN neurons of the jerboa. Moreover, this OT expression level does not change upon an acute immobilization stress. These new data, coupled together with our previous work in the jerboa, incontestably establish a clear dichotomy between a stress-responsive CRH/CCK system and a stress non-responsive OT/VP system in the pPVN....

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Journal Article 2002; 23(5-6): 447-451 PubMed PMID: 12500170 Citation  Keywords:  Animals, Cell Differentiation:physiology, Gene Expression Regulation:physiology, Humans, Immune System:physiology, Neuroendocrine Tumors:metabolism, Neuronal Plasticity:physiology, Neuropeptides:metabolism, Neurosecretory Systems:cytology,.   

: The term neuroendocrine has been used to define cells that secrete their products in a regulated manner, in response to a specific stimulus. The neuroendocrine system includes neurons and endocrine cells sharing a common phenotypic program characterized by the expression of markers such as neuropeptides, chromogranins, neuropeptide processing enzymes SPC2 and SPC3 (subtilase-like pro-protein convertases) or dense core secretory granules. Various theories such as the APUD (amine precursor uptake decarboxylation) concept, the diffuse neuroendocrine system (DNES) or the paraneuron concept have been put forth to classify neuroendocrine cells as a cohesive group. Neuroendocrine characteristics have been used as evidence of a common embryological origin for normal and neoplastic cells. However, it is now recognized that neuroendocrine characteristics can be observed in various cell types, such as immunocytes, that are not of a common embryological origin with either neurons or endocrine cells. We propose to redefine previous "neuroendocrine" concepts to include the notion that activation of specific genetic switches can lead to the expression of a partial or full neuroendocrine phenotype in a variety of cell types, including immune cells....

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