Epigenetic factors differentially influence postnatal maturation of serotonin (5-HT) innervation in cerebral cortex of gerbils: interaction of rearing conditions and early methamphetamine challenge

Neddens, Joerg; Bagorda, Francesco; Busche, Andrea; Horstmann, S; Moll, Georg; Dawirs, Ralph R.; Teuchert-Noodt, Gertraud

doi:10.1016/j.devbrainres.2003.09.016

Cited by 32 publications

(7 citation statements)

References 69 publications

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“…Also serotonin, acetylcholine, and GABA were found to be modified by extrinsic activities during brain maturation [22–24], pointing to the crucial role of neurotransmitters in brain plasticity (rev. [22, 25]).…”

Section: Introductionmentioning

confidence: 99%

Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)

et al. 2009

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Still little is known about naturally occurring synaptogenesis in the adult neocortex and related impacts of epigenetic influences. We therefore investigated (pre)synaptic plasticity in various cortices of adult rodents, visualized by secondary lysosome accumulations (LA) in remodeling axon terminals. Twenty-two male gerbils from either enriched (ER) or impoverished rearing (IR) were used for quantification of silver-stained LA. ER-animals showed rather low LA densities in most primary fields, whereas barrel and secondary/associative cortices exhibited higher densities and layer-specific differences. In IR-animals, these differences were evened out or even inverted. Basic plastic capacities might be linked with remodeling of local intrinsic circuits in the context of cortical map adaptation in both IR- and ER-animals. Frequently described disturbances due to IR in multiple corticocortical and extracortical afferent systems, including the mesocortical dopamine projection, might have led to maladaptations in the plastic capacities of prefronto-limbic areas, as indicated by different LA densities in IR- compared with ER-animals.

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Section: Introductionmentioning

confidence: 99%

Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)

et al. 2009

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“…Rat hippocampal granule cell proliferation continues until postnatal day (P)19 (Bayer et al ., 1993) and we have demonstrated that MA administration from P11 to P20 produces deficits in spatial learning and memory but does not affect working memory, cued learning or swimming capabilities (Vorhees et al ., 1994a, 1998, 1999; Vorhees et al ., 2000; Williams et al ., 2002). Unlike in adult animals, neonatal exposure to MA in rats does not produce neurotoxicity as characterised by astrogliosis nor does it produce immediate reductions in dopaminergic and serotonergic markers (Cappon et al ., 1997), although neonatal exposure to MA in gerbils appears to induce long‐lasting changes in dopaminergic and serotonergic systems (Busche et al ., 2002; Neddens et al ., 2002; 2003). Perturbations of the hypothalamic–pituitary–adrenal (HPA) axis do occur in neonatal rats exposed to MA, as demonstrated by increases in corticosterone (CORT) and adrenocorticotropin hormone (Williams et al ., 2000).…”

Section: Introductionmentioning

confidence: 99%

Neonatal methamphetamine administration induces region‐specific long‐term neuronal morphological changes in the rat hippocampus, nucleus accumbens and parietal cortex

Williams¹,

Brown²,

Vorhees³

2004

Eur J of Neuroscience

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Previous studies have demonstrated that rats exposed to methamphetamine (MA) during the neonatal period display deficits in spatial learning and memory. The underlying correlates are unknown; therefore, this study was devised to determine whether neuronal changes occur in the dentate gyrus (DG), nucleus accumbens (NAcc) and cortex of adult rats exposed to 10 mg/kg MA administered four times daily from P11-20 using Golgi-Cox staining [Gibb, R. & Kolb, B. (1998) J. Neurosci. Meth., 79, 1-4]. The DG and NAcc demonstrated a decrease in the number of spines per neuron and the NAcc showed an associated decrease in dendritic length. Selective changes in cortex were observed because increased dendritic length in the parietal cortex occurred with no change in the number of spines, and no differences were noted for either dendritic length or spines in the medial frontal cortex. The data suggest a potential cause for the learning and memory deficits induced by neonatal MA exposure; however, the underlying mechanism that produces these neuronal changes is unknown.

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“…In vivo microdialysis experiments have also demonstrated reduced serotonin release in the hippocampus and prefrontal cortex [341–343]. These results are consistent with reduced immunohistochemical staining for serotonergic terminals in the hippocampus [344], although other brain regions may have increased serotonin levels [345], at least in gerbils. Changes in presynaptic serotonin function, like other neurochemical changes in isolation-reared rats, may be highly regionally dependent however.…”

Section: Deprivation Of Social Play In Rodentsmentioning

confidence: 55%

Have studies of the developmental regulation of behavioral phenotypes revealed the mechanisms of gene–environment interactions?

Hall

Perona

2012

Physiology & Behavior

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This review addresses the recent convergence of our long-standing knowledge of the regulation of behavioral phenotypes by developmental experience with recent advances in our understanding of mechanisms regulating gene expression. This review supports a particular perspective on the developmental regulation of behavioral phenotypes: That the role of common developmental experiences (e.g. maternal interactions, peer interactions, exposure to a complex environment, etc.) is to fit individuals to the circumstances of their lives within bounds determined by long-standing (evolutionary) mechanisms that have shaped responses to critical and fundamental types of experience via those aspects of gene structure that regulate gene expression. The phenotype of a given species is not absolute for a given genotype but rather variable within bounds that are determined by mechanisms regulated by experience (e.g. epigenetic mechanisms). This phenotypic variation is not necessarily random, or evenly distributed along a continuum of description or measurement, but often highly disjointed, producing distinct, even opposing, phenotypes. The potentiality for these varying phenotypes is itself the product of evolution, the potential for alternative phenotypes itself conveying evolutionary advantage. Examples of such phenotypic variation, resulting from environmental or experiential influences, have a long history of study in neurobiology, and a number of these will be discussed in this review: neurodevelopmental experiences that produce phenotypic variation in visual perception, cognitive function, and emotional behavior. Although other examples will be discussed, particular emphasis will be made on the role of social behavior on neurodevelopment and phenotypic determination. It will be argued that an important purpose of some aspects of social behavior is regulation of neurobehavioral phenotypes by experience via genetic regulatory mechanisms.

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Epigenetic factors differentially influence postnatal maturation of serotonin (5-HT) innervation in cerebral cortex of gerbils: interaction of rearing conditions and early methamphetamine challenge

Cited by 32 publications

References 69 publications

Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)

Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)

Neonatal methamphetamine administration induces region‐specific long‐term neuronal morphological changes in the rat hippocampus, nucleus accumbens and parietal cortex

Have studies of the developmental regulation of behavioral phenotypes revealed the mechanisms of gene–environment interactions?

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