The morphogenetic influences of serotonin on the differentiation of neurons synthesizing vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus were studied in rats. This was addressed by comparative morphofunctional analysis of VIP neurons in adult rats whose brains developed prenatally in conditions of normal and deficient serotonin metabolism. Serotonin deficiency was created in fetuses by treatment of their mothers with p-chlorophenylalanine (PCPA). Pregnant females in controls were treated with 0.9% NaCl. VIP neurons in experimental and control animals were found to show no differences in VIP mRNA concentrations and, probably, in the level of VIP synthesis. However, inhibition of serotonin synthesis led to an increase in the number of VIP-immunoreactive neurons and an increase in the VIP concentration within these cells. This was not associated with any change in neuron size, which was an indicator of the absence of functional hypertrophy accompanying activation of specific synthesis. Comparison of the data obtained here showed that during prenatal ontogenesis, serotonin has an imprinting influence on the differentiation of VIP neurons and is probably involved in the formation of the mechanism of VIP secretion.
"ained as collateral symptomatology to possible VN autoimmune dysfunction . Blockade of 5 - HT could elicit symptomatology consistent with a VN autoimmune disorders . This effect may be explained by the role of serotonin in controlling VIP release mechanisms . Altered VIP expression may occur prenatally through serotonin imprinting in ontogenesis ( Mirochnik et al . 2003 ) suggesting implications for monitoring the use of selective serotonin uptake inhibitor ( SSRI ) and tri - cyclic anti - depressants in pregnancy . However , decreased 5 - HT1A receptor numbers and affinity are noted in CFS particularly in the hippocampus ( Cleare et al . 2005 ) possibly indicating heterogenous modulating relationships"
[Show abstract][Hide abstract] ABSTRACT: Disorders such as chronic fatigue syndrome (CFS) and gulf war syndrome (GWS) are characterised by prolonged fatigue and a range of debilitating symptoms of pain, intellectual and emotional impairment, chemical sensitivities and immunological dysfunction. Sudden infant death syndrome (SIDS) surprisingly may have certain features in common with these conditions. Post-infection sequelae may be possible contributing factors although ongoing infection is unproven. Immunological aberration may prove to be associated with certain vasoactive neuropeptides (VN) in the context of molecular mimicry, inappropriate immunological memory and autoimmunity.
Adenylate cyclase-activating VNs including pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) act as hormones, neurotransmitters, neuroregulators, immune modulators and neurotrophic substances. They and their receptors are potentially immunogenic. VNs are widely distributed in the body particularly in the central and peripheral nervous systems and have been identified in the gut, adrenal gland, blood cells, reproductive system, lung, heart and other tissues. They have a vital role in maintaining cardio-respiratory function, thermoregulation, memory, concentration and executive functions such as emotional responses including social cues and appropriate behaviour. They are co-transmitters for a number of neurotransmitters including acetylcholine and gaseous transmitters, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system against toxic assault as well as being important in the maintenance of homeostasis.
This paper describes a biologically plausible mechanism for the development of certain fatigue-related syndromes based on loss of immunological tolerance to these VNs or their receptors following infection, other events or de novo resulting in significant pathophysiology possibly mediated via CpG fragments and heat shock (stress) proteins. These conditions extend the public health context of autoimmunity and VN dysregulation and have implications for military medicine where radiological, biological and chemical agents may have a role in pathogenesis. Possible treatment and prevention options are considered.
[Show abstract][Hide abstract] ABSTRACT: The transcriptome of a lager brewing yeast (Saccharomyces carlsbergensis, syn. of S. pastorianus), was analysed at 12 different time points spanning a production-scale lager beer fermentation. Generally, the average expression rapidly increased and had a maximum value on day 2, then decreased as the sugar got consumed. Especially genes involved in protein and lipid biosynthesis or glycolysis were highly expressed during the beginning of the fermentation. Similarities as well as significant differences in expression profiles could be observed when comparing to a previous transcriptome analysis of a laboratory yeast grown in YPD. The regional distribution of various expression levels on the chromosomes appeared to be random or near-random and no reduction in expression near telomeres was observed.
FEMS Yeast Research 01/2003; 2(4):563-73. DOI:10.1016/S1567-1356(02)00155-1 · 2.82 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Major advances have been made in understanding the relatively novel group of vasoactive (vasodilatory) neuropeptides (VNs) in humans. VNs comprise a novel but expanding group of substances having immunoregulation, inflammation modulation, neurotransmitter, neurotrophic, hormonal and metabolic functions. These substances may control gene expression for mRNA for themselves and their receptors. They have complex relationships with gaseous and other neurotransmitters and xenobiotic substances. Theoretical arguments have implicated these substances in autoimmune phenomena resulting in fatigue-related conditions such as chronic fatigue syndrome (CFS), sudden infant death syndrome (SIDS), fibromyalgia (FM) and Gulf War syndrome (GWS) but remain unproven. As well as possibly spontaneous onset, the precipitating causes of VN autoimmune dysfunction are likely to be a combination of genetic predisposition, infection and xenobiotic substances. Therapeutic and preventive possibilities for postulated VN autoimmune conditions will be influenced by the complex patholophysiology underpinning them. Some speculative possibilities are VN substitution/replacement, preservation of biological effect, epigenetic DNA modifications, plasma exchange, anti-cholinesterases, e.g., pyridostigmine, corticosteroids and other drug treatments, thymectomy, intravenous immunoglobulin and anti-idiotype antibodies, and CpG/DNA vaccines. Prevention and treatment of possible VN autoimmune fatigue-related disorders may prove to be important areas for future research and development.
Medical Hypotheses 02/2005; 65(4):797-803. DOI:10.1016/j.mehy.2005.03.007 · 1.07 Impact Factor
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