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Kent D Dunlap - One of the best experts on this subject based on the ideXlab platform.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g. olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury, and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in any non-mammal. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g., olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed the social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in a non-mammalian model. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
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simulated predator stimuli reduce Brain Cell proliferation in two electric fish species brachyhypopomus gauderio and apteronotus leptorhynchus
The Journal of Experimental Biology, 2017Co-Authors: Kent D Dunlap, Michael Ragazzi, Geoffrey Keane, Elise Lasky, Vielka L. SalazarAbstract:ABSTRACT The Brain structure of many animals is influenced by their predators, but the Cellular processes underlying this Brain plasticity are not well understood. Previous studies showed that electric fish (Brachyhypopomus occidentalis) naturally exposed to high predator (Rhamdia quelen) density and tail injury had reduced Brain Cell proliferation compared with individuals facing few predators and those with intact tails. However, these field studies described only correlations between predator exposure and Cell proliferation. Here, we used a congener Brachyhypopomus gauderio and another electric fish Apteronotus leptorhynchus to experimentally test the hypothesis that exposure to a predator stimulus and tail injury causes alterations in Brain Cell proliferation. To simulate predator exposure, we either amputated the tail followed by short-term (1 day) or long-term (17–18 days) recovery or repeatedly chased intact fish with a plastic rod over a 7 day period. We measured Cell proliferation (PCNA+ Cell density) in the telencephalon and diencephalon, and plasma cortisol, which commonly mediates stress-induced changes in Brain Cell proliferation. In both species, either tail amputation or simulated predator chase decreased Cell proliferation in the telencephalon in a manner resembling the effect of predators in the field. In A. leptorhynchus, Cell proliferation decreased drastically in the short term after tail amputation and partially rebounded after long-term recovery. In B. gauderio, tail amputation elevated cortisol levels, but repeated chasing had no effect. In A. leptorhynchus, tail amputation elevated cortisol levels in the short term but not in the long term. Thus, predator stimuli can cause reductions in Brain Cell proliferation, but the role of cortisol is not clear.
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predators inhibit Brain Cell proliferation in natural populations of electric fish brachyhypopomus occidentalis
Proceedings of The Royal Society B: Biological Sciences, 2016Co-Authors: Kent D Dunlap, Michael Ragazzi, Alex Tran, Rudiger Krahe, Vielka L. SalazarAbstract:Compared with laboratory environments, complex natural environments promote Brain Cell proliferation and neurogenesis. Predators are one important feature of many natural environments, but, in the ...
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glucocorticoid receptor blockade inhibits Brain Cell addition and aggressive signaling in electric fish apteronotus leptorhynchus
Hormones and Behavior, 2011Co-Authors: Kent D Dunlap, Denisa Jashari, Kristina M PappasAbstract:Glucocorticoids were among the first hormones discovered that influence neurogenesis in the adult Brain (Gould et al., 1992). In most cases, exogenous glucocorticoid treatment or stressful conditions that elevate endogenous glucocorticoids inhibit both the production and survival of newborn Cells (Mirescu and Gould, 2006; Wong and Herbert, 2005; Wong and Herbert, 2006). However, the relationship between glucocorticoids and neurogenesis is not always inhibitory (reviewed in Lucassen et al., 2008). For example, in rodents and primates, moderate increases in glucocorticoid levels that occur during environmental enrichment, mild stress or physical exercise are positively associated with neurogenesis (Kempermann et al., 1997; Lucassen et al., 2008; Lyons et al., 2010; Parihar et al., 2011). Although the mechanisms of glucocorticoid action in stress-induced inhibition of neurogenesis has been explored at length, relatively little is known about how glucocorticoids might mediate environmentally induced enhancement of neurogenesis. Here we examine the causal role of glucocorticoid receptors (GRs) in social enhancement of Brain Cell addition and communication behavior in adult weakly electric fish. Brown ghost knife fish, Apteronotus leptorhynchus, communicate with weak electric discharges produced by modified motorneurons in the tail (Zakon and Smith, 2009). The electric organ discharge (EOD) frequency is very stable within an individual and conveys the fish’s sex and individual identity. This continuous EOD is controlled by the spontaneous rhythmic firing of the pacemaker nucleus in the hindBrain. During social interaction, particularly during male-male aggression, fish transiently elevate EOD frequency to produce communication signals termed chirps (Dunlap, 2002; Hagedorn and Heiligenberg, 1985; Larimer and MacDonald, 1968). Chirps are emitted when the prepacemaker nucleus (PPn-C) located in the diencephalon briefly increases the pacemaker firing rate. Social interaction, chirping behavior, glucocorticoid levels and Brain Cell addition are all interrelated in Apteronotus leptorhynchus. Previously, we showed that both short-term and long-term social interaction influenced chirp production. In short term interactions, chirp rate increased in the first 2 min and decreased over the next 3 min, though still remaining elevated above background chirp rate (Dunlap, 2002). Long-term interaction potentiated chirp rate (Dunlap et al., 2002). That is, fish paired with another fish for 7d chirp more than isolated fish to a standardized, synthetic EOD playback. This latter study showed that long-term interaction modified the propensity to chirp, but nothing was known about chirp production toward another fish in long-term pairings. In addition to changing chirping behavior, long-term social interaction increases plasma cortisol levels (Dunlap et al., 2002) and promotes Cell addition to the periventricular zone (PVZ) of the Brain (Dunlap et al., 2006). (We define Cell addition as the two part process of Cell birth plus 4d survival.) The effect of social interaction on Cell addition is regionally and temporally specific. It enhances Cell addition in the PVZ region that contributes adult-born Cells to the PPn (the Brain region that controls chirping), but has no effect on neighboring PVZ regions. Moreover, enhanced Cell addition coincides with the period that social interaction potentiates chirping behavior. This regional and temporal specificity suggest that social enhancement of Cell addition may contribute to socially induced changes in chirping behavior. Cortisol treatment to isolated fish mimics many aspects of social interaction on chirping behavior and Cell addition. Fish implanted with cortisol show potentiated chirping (Dunlap et al., 2002) and enhanced Brain Cell addition (Dunlap et al., 2006). The primary difference between cortisol treatment and social interaction is that cortisol treatment, at least at certain time scales, seems to have a more generalized effect on Cell addition, increasing Cell addition in all the PVZ examined, not just the region adjacent to the PPn (Dunlap et al., 2006). Given the association between endogenous cortisol levels, chirping and Brain Cell addition in socially-interacting fish and the similar effects of exogenous cortisol in isolated fish, we hypothesized that cortisol plays a causal role in mediating the effect of social interaction on Cell addition and chirping behavior. However, it is possible that socially induced changes in cortisol are epiphenomenal and do not directly influence Cell addition and chirping. To address this possibility, we treated fish with RU486, a GR antagonist (Bury et al., 2003; Scott et al., 2005; Shaw et al., 2007), to see if socially induced changes in Brain and behavior still occur without GR activation. Given that glucocorticoids can influence locomotor behavior in fish (Gregory and Wood, 1999; Overli et al., 2002), and physical activity can enhance Brain Cell production in mammals (van Praag et al., 1999; van Praag, 2008), we also examined swimming behavior in RU486 –treated animals to evaluate whether GR blockade might affect Brain Cell production via its influence on physical activity. Our study is presented in two parts: first a behavioral comparison of paired and isolated fish to characterize electrocommunication and locomotor behavior in social conditions that promote Brain Cell addition and, secondly, an experimental analysis of the effect of GR blockade on electrocommunication, locomotion and Brain Cell addition.
Joshua H Corbo - One of the best experts on this subject based on the ideXlab platform.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g. olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury, and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in any non-mammal. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g., olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed the social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in a non-mammalian model. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
Margarita M Vergara - One of the best experts on this subject based on the ideXlab platform.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g. olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury, and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in any non-mammal. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
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reduced Brain Cell proliferation following somatic injury is buffered by social interaction in electric fish apteronotus leptorhynchus
Developmental Neurobiology, 2020Co-Authors: Kent D Dunlap, Margarita M Vergara, Joshua H CorboAbstract:In many species, the negative effects of aversive stimuli are mitigated by social interactions, a phenomenon termed social buffering. In one form of social buffering, social interactions reduce the inhibition of Brain Cell proliferation during stress. Indirect predator stimuli (e.g., olfactory or visual cues) are known to decrease Brain Cell proliferation, but little is known about how somatic injury, as might occur from direct predator encounter, affects Brain Cell proliferation and whether this response is influenced by conspecific interactions. Here, we assessed the social buffering of Brain Cell proliferation in an electric fish, Apteronotus leptorhynchus, by examining the separate and combined effects of tail injury and social interactions. We mimicked a predator-induced injury by amputating the caudal tail tip, exposed fish to paired interactions that varied in timing, duration and recovery period, and measured Brain Cell proliferation and the degree of social affiliation. Paired social interaction mitigated the negative effects of tail amputation on Cell proliferation in the foreBrain but not the midBrain. Social interaction either before or after tail amputation reduced the effect of tail injury and continuous interaction both before and after caused an even greater buffering effect. Social interaction buffered the proliferation response after short-term (1 d) or long-term recovery (7 d) from tail amputation. This is the first report of social buffering of Brain Cell proliferation in a non-mammalian model. Despite the positive association between social stimuli and Brain Cell proliferation, we found no evidence that fish affiliate more closely following tail injury.
Nathan G Skene - One of the best experts on this subject based on the ideXlab platform.
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genetic identification of Brain Cell types underlying schizophrenia
Nature Genetics, 2018Co-Authors: Nathan G Skene, Helena Gaspar, Trygve E Bakken, Julien Bryois, James J Crowley, Gerome Breen, Paola GiustirodriguezAbstract:With few exceptions, the marked advances in knowledge about the genetic basis of schizophrenia have not converged on findings that can be confidently used for precise experimental modeling. By applying knowledge of the Cellular taxonomy of the Brain from single-Cell RNA sequencing, we evaluated whether the genomic loci implicated in schizophrenia map onto specific Brain Cell types. We found that the common-variant genomic results consistently mapped to pyramidal Cells, medium spiny neurons (MSNs) and certain interneurons, but far less consistently to embryonic, progenitor or glial Cells. These enrichments were due to sets of genes that were specifically expressed in each of these Cell types. We also found that many of the diverse gene sets previously associated with schizophrenia (genes involved in synaptic function, those encoding mRNAs that interact with FMRP, antipsychotic targets, etc.) generally implicated the same Brain Cell types. Our results suggest a parsimonious explanation: the common-variant genetic results for schizophrenia point at a limited set of neurons, and the gene sets point to the same Cells. The genetic risk associated with MSNs did not overlap with that of glutamatergic pyramidal Cells and interneurons, suggesting that different Cell types have biologically distinct roles in schizophrenia.
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genetic identification of Brain Cell types underlying schizophrenia
bioRxiv, 2017Co-Authors: Nathan G Skene, Helena Gaspar, Paola Giustirodriguez, Trygve E Bakken, Julien Bryois, James J Crowley, Gerome Breen, Rebecca D Hodge, Jeremy A Miller, Ana B MunozmanchadoAbstract:With few exceptions, the marked advances in knowledge about the genetic basis for schizophrenia have not converged on findings that can be confidently used for precise experimental modeling. Applying knowledge of the Cellular taxonomy of the Brain from single-Cell RNA-sequencing, we evaluated whether the genomic loci implicated in schizophrenia map onto specific Brain Cell types. The common variant genomic results consistently mapped to pyramidal Cells, medium spiny neurons, and certain interneurons but far less consistently to embryonic, progenitor, or glial Cells. These enrichments were due to distinct sets of genes specifically expressed in each of these Cell types. Many of the diverse gene sets associated with schizophrenia (including antipsychotic targets) implicate the same Brain Cell types. Our results provide a parsimonious explanation: the common-variant genetic results for schizophrenia point at a limited set of neurons, and the gene sets point to the same Cells. While some of the genetic risk is associated with GABAergic interneurons, this risk largely does not overlap with that from projecting Cells.
Vielka L. Salazar - One of the best experts on this subject based on the ideXlab platform.
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simulated predator stimuli reduce Brain Cell proliferation in two electric fish species brachyhypopomus gauderio and apteronotus leptorhynchus
The Journal of Experimental Biology, 2017Co-Authors: Kent D Dunlap, Michael Ragazzi, Geoffrey Keane, Elise Lasky, Vielka L. SalazarAbstract:ABSTRACT The Brain structure of many animals is influenced by their predators, but the Cellular processes underlying this Brain plasticity are not well understood. Previous studies showed that electric fish (Brachyhypopomus occidentalis) naturally exposed to high predator (Rhamdia quelen) density and tail injury had reduced Brain Cell proliferation compared with individuals facing few predators and those with intact tails. However, these field studies described only correlations between predator exposure and Cell proliferation. Here, we used a congener Brachyhypopomus gauderio and another electric fish Apteronotus leptorhynchus to experimentally test the hypothesis that exposure to a predator stimulus and tail injury causes alterations in Brain Cell proliferation. To simulate predator exposure, we either amputated the tail followed by short-term (1 day) or long-term (17–18 days) recovery or repeatedly chased intact fish with a plastic rod over a 7 day period. We measured Cell proliferation (PCNA+ Cell density) in the telencephalon and diencephalon, and plasma cortisol, which commonly mediates stress-induced changes in Brain Cell proliferation. In both species, either tail amputation or simulated predator chase decreased Cell proliferation in the telencephalon in a manner resembling the effect of predators in the field. In A. leptorhynchus, Cell proliferation decreased drastically in the short term after tail amputation and partially rebounded after long-term recovery. In B. gauderio, tail amputation elevated cortisol levels, but repeated chasing had no effect. In A. leptorhynchus, tail amputation elevated cortisol levels in the short term but not in the long term. Thus, predator stimuli can cause reductions in Brain Cell proliferation, but the role of cortisol is not clear.
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predators inhibit Brain Cell proliferation in natural populations of electric fish brachyhypopomus occidentalis
Proceedings of The Royal Society B: Biological Sciences, 2016Co-Authors: Kent D Dunlap, Michael Ragazzi, Alex Tran, Rudiger Krahe, Vielka L. SalazarAbstract:Compared with laboratory environments, complex natural environments promote Brain Cell proliferation and neurogenesis. Predators are one important feature of many natural environments, but, in the ...