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Early Gene Expression (early + gene_expression)
Kinds of Early Gene Expression Selected AbstractsEthanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene ExpressionALCOHOLISM, Issue 6 2009Catherine Vilpoux Background:, Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol-dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stages. Methods:, This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure. Results:, The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin-containing cells population (pIIIu), also known as Edinger-Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse-inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue-induced relapse to ethanol self-administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions. Discussion:, Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive-related processes (area postrema, nucleus of solitary tract). Conclusion:, A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies. [source] Hippocampal lesions impair spatial memory performance, but not song,A developmental study of independent memory systems in the zebra finchDEVELOPMENTAL NEUROBIOLOGY, Issue 8 2009David J. Bailey Abstract Songbirds demonstrate song- and spatial-learning, forms of memory that appear distinct in formal characteristics and fitting the descriptions and criteria of procedural and episodic-like memory function, respectively. As in other vertebrates, the neural pathways underlying these forms of memory may also be dissociable, and include the corresponding song circuit and hippocampus (HP). Whether (or not) these two memory systems interact is unknown. Interestingly, the HP distinguishes itself as a site of immediate early gene expression in response to song and as a site of estrogen synthesis, a steroid involved in song learning. Thus, an interaction between these memory systems and their anatomical substrates appears reasonable to hypothesize, particularly during development. To test this idea, juvenile male or female zebra finches received chemical lesions of the HP at various points during song learning, as did adults. Song structure, singing behavior, song preference, and spatial memory were tested in adulthood. Although lesions of the HP severely compromised HP-dependent spatial memory function across all ages and in both sexes, we were unable to detect any effects of HP lesions on song learning, singing, or song structure in males. Interestingly, females lesioned as adults, but not as juveniles, did lose the characteristic preference for their father's song. Since compromise of the neural circuits that subserve episodic-like memory does very little (if anything) to affect procedural-like (song learning) memory, we conclude that these memory systems and their anatomical substrates are well dissociated in the developing male zebra finch. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009 [source] C-type natriuretic peptide (CNP) regulates cocaine-induced dopamine increase and immediate early gene expression in rat brainEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2001Nathalie Thiriet Abstract The neuropeptide C-type natriuretic peptide (CNP) is the primary biologically active natriuretic peptide in brain. Using in situ hybridization, the present report demonstrates that CNP regulates egr-1, c-fos and junB immediate early gene expression in rat brain. In the frontal cortex, CNP induced immediate early gene expression whereas it inhibited dose-dependently the cocaine-induced early gene expression in the dopaminergic projection fields nucleus accumbens and caudate,putamen. CNP may produce its effect directly on dopaminergic neurons because we found that its receptor, guanylyl cyclase GC-B, was expressed in the mesencephalon where dopaminergic neurons originate, as well as in their projection fields. The inhibition by CNP of the early gene expression elicited by cocaine in the caudate,putamen is correlated with a CNP-evoked decrease in cocaine-induced rise in extracellular dopamine, measured by in vivo microdialysis experiments. The significance of the inhibition of cocaine-induced dopamine release and early gene induction by the endogenous peptide CNP is demonstrated by data indicating that CNP reduced the cocaine-induced spontaneous locomotor activation. By inhibiting dopaminergic neuronal activity, CNP represents a potential negative regulator of related behavioural effects of cocaine. [source] c-DNA Microarray to determine molecular events in neurodegeneration and neuroprotectionJOURNAL OF NEUROCHEMISTRY, Issue 2002M. B. H. Youdim Cell death in CNS involves complex processes, many of which have not been identified biochemically. At the present biochemical techniques cannot adequately establish these. However, the advent of cDNA microarray or microchips, in which the expression of thousands of genes can be measured at once to give a global assessment in disease pathology, its progress or animal models, has simplified this. We have employed this technique to study the mechanism of neurotoxicity of MPTP and 6-hydroxydoapmine induced in neuronally derived cells in culture, in the animal models of Parkinson's disease and neuroprotection initiated by monoamine oxidase B inhibitor, rasagiline; iron chelators, R-apomorphine and EGCG and other neuroprotective drugs. Our studies have clearly indicated that MPTP induced early gene expression, prior to cell death (first 24 h), are prerequirement for 51 late gene expression changes implicated at the time of neuronal death. The latter genes include those involved in iron metabolism, oxidative stress, inflammatory processes, glutaminergic excitotoxicity, nitric oxide, growth factors, transcription factors, cell cycle, intermediatory metabolism and other gene previously not identified. The expressions of many of the latter genes, also identified by in situ hybridization, are prevented when the animals are pretreated with the above neuroprotective drugs. These studies have clearly shown that neurodegeneratrion is a complex cascades of ,domino' effect. Thus a single neuroprotective drug treatment may not be adequate to prevent it, but, that a cocktail of drugs might. [source] Plasma Vasopressin Concentrations and Fos Protein Expression in the Supraoptic Nucleus Following Osmotic Stimulation or Hypovolaemia in the Ovariectomized Rat: Effect of Oestradiol ReplacementJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2004D. E. Hartley Abstract The set points for vasopressin release in response to increasing plasma osmolality and hypovolaemia alter with reproductive status. Here, we studied stimulated vasopressin release following ovariectomy and oestrogen replacement, neuronal activity being measured in terms of immediate early gene expression. Observations were carried out on three groups of female Sprague-Dawley rats. The first group were ovariectomized. The second group were given a subcutaneous oestrogen implant (20 µg/ml oestradiol-17,) at the time of ovariectomy. The final group were left intact and observations performed at oestrus. Two weeks after ovariectomy, vascular cannulae were implanted under anaesthesia and at least 48 h allowed for recovery before hormone release was stimulated by infusion of 1.5 m NaCl for 90 min, or hypovolaemia induced by the removal of 10 mg/kg body weight taken in 1-ml aliquots. Blood pressure was monitored, and blood samples were taken for determination of packed cell volume and plasma vasopressin and osmolality. After a minimum of 48 h, the challenge was repeated, the rats anaesthetized, and perfused with 4% paraformaldehyde. Brain sections were processed for immunocytochemical detection of Fos protein. Vasopressin release in response to both stimuli was reduced in ovariectomized compared to intact rats and the response could be substantially restored by oestradiol replacement. The number of Fos positive cells in the supraoptic nucleus of oestrogen-replaced rats was significantly higher than in the ovariectomized group and not statistically different from the intact group. [source] Technical Aspects of RadiofrequencyPAIN PRACTICE, Issue 3 2002M. Sluijter MD If the resulting current flows through a percutaneously introduced electrode, heat will be produced around the electrode because the body tissue acts as a resistor. RF can, therefore, be used to ablate nervous tissue in the treatment of chronic pain. This method has gained acceptance for percutaneous cordotomy and for the treatment of trigeminal neuralgia. For spinal pain, the method had little success initially, but since the introduction of small diameter instrumentation, the results have markedly improved. he mechanism of action of RF has not been challenged until recently even though there was awareness that some observations were not consistent with the heat concept. The formation of heat is not the only occurrence during RF treatment, however. The tissue surrounding the electrode is also exposed to the RF electric field. This exposure has a biological effect as has been demonstrated both in cells in a cell culture and in the exposure to RF of dorsal root ganglia, resulting in transsynaptal induction of early gene expression in the dorsal horn. The mode of action of RF is, therefore, uncertain at the moment. The method of pulsed RF is based on the concept that the production of heat has been a by-product of RF treatment and that the clinical effect is due to exposure to the electric field. In pulsed RF, the generator output is interrupted to allow for the elimination of heat in the silent period. The early results have been encouraging, but the results of controlled, prospective studies are not yet available. Since there are now 2 almost diametrically opposed views on the mode of action of RF, it is difficult to give recommendations for treatment. The decision is easy for indications for which heat RF has traditionally been contraindicated such as the treatment of peripheral nerves and trigger points. When the application of heat carries a potential risk, for instance if the dorsal root ganglion is the target structure, the use of pulsed RF is also recommended. As for the medial branch the situation is controversial. Since there are controlled studies available showing the effect of heat lesions, it is recommended that the technique should not be changed until further studies have been completed. Finally, the equipment for RF treatment is described and safety issues are discussed. [source] Unique Early Gene Expression Patterns in Human Adult-to-Adult Living Donor Liver Grafts Compared to Deceased Donor GraftsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2009J. De Jonge Because of inherent differences between deceased donor (DD) and living donor (LD) liver grafts, we hypothesize that the molecular signatures will be unique, correlating with specific biologic pathways and clinical patterns. Microarray profiles of 63 biopsies in 13 DD and 8 LD liver grafts done at serial time points (procurement, backbench and postreperfusion) were compared between groups using class comparisons, network and biological function analyses. Specific genes were validated by quantitative PCR and immunopathology. Clinical findings were also compared. Following reperfusion, 579 genes in DD grafts and 1324 genes in LDs were differentially expressed (p < 0.005). Many upregulated LD genes were related to regeneration, biosynthesis and cell cycle, and a large number of downregulated genes were linked to hepatic metabolism and energy pathways correlating with posttransplant clinical laboratory findings. There was significant upregulation of inflammatory/immune genes in both DD and LD, each with a distinct pattern. Gene expression patterns of select genes associated with inflammation and regeneration in LD and DD grafts correlated with protein expression. Unique patterns of early gene expression are seen in LD and DD liver grafts, correlating with protein expression and clinical results, demonstrating distinct inflammatory profiles and significant downregulation of metabolic pathways in LD grafts. [source] Resident Macrophages are Involved in Intestinal Transplantation-Associated Inflammation and Motoric Dysfunction of the Graft MuscularisAMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2007N. Schaefer Gut manipulation and ischemia/reperfusion evoke an inflammatory response within the intestinal muscularis that contributes to dysmotility. We hypothesize that resident macrophages play a key role in initiating the inflammatory cascade. Isogenic small bowel transplantation was performed in Lewis rats. The impact of recovery of organs on muscularis inflammation was investigated by comparing cold whole-body perfusion after versus prior to recovery. The role of macrophages was investigated by transplantation of macrophage-depleted gut. Leukocytes were counted using muscularis whole mounts. Mediator expression was determined by real-time RT-PCR. Contractility was assessed in a standard organ bath. Both organ recovery and ischemia/reperfusion induced leukocyte recruitment and a significant upregulation in IL-6, MCP-1, ICAM-1 and iNOS mRNAs. Although organ recovery in cold ischemia prevented early gene expression, peak expression was not changed by modification of the recovery technique. Compared to controls, transplanted animals showed a 65% decrease in smooth muscle contractility. In contrast, transplanted macrophage-depleted isografts exhibited significant less leukocyte infiltration and only a 19% decrease in contractile activity. In summary, intestinal manipulation during recovery of organs initiates a functionally relevant inflammatory response within the intestinal muscularis that is massively intensified by the ischemia reperfusion injury. Resident muscularis macrophages participate in initiating this inflammatory response. [source] | |||||||||||||