{"title":"28 Neurogenesis in the Adult Songbird: A Model for Inducible Striatal Neuronal Addition","authors":"S. Goldman","doi":"10.1101/087969784.52.593","DOIUrl":null,"url":null,"abstract":"The damaged brain has traditionally been thought to exhibit little significant structural repair after injury. In part, this appears to reflect the failure of the mature forebrain to generate new neurons, except for a few discrete, relatively archaic regions of the brain, the hippocampus and olfactory bulb (OB) (Altman and Das 1966; Bayer et al. 1982; for review, see Goldman 1998; Alvarez-Buylla and Garcia-Verdugo 2002; Gage 2002). The limitation on neuronal addition to the adult brain has clearly been selected, and thus comprises an adaptation of likely, if unclear, evolutionary benefit. Among other possibilities, the lack of persistent neurogenesis in most regions of the adult mammalian brain may be associated with the need to stabilize the retention of long-term memories and entrained behaviors (Rakic 2002). Perhaps as a result, the adult mammalian neocortex exhibits no constitutive neuronal addition, and little or none after injury, except for discrete experimental lesions of defined neuronal populations (Magavi et al. 2000). In contrast, the subcortical neostriatum retains the capacity to regenerate neurons after stroke and major traumatic injury (Arvidsson et al. 2002; Parent et al. 2002; Jin et al. 2003a; Parent 2003). However, the numbers of striatal neurons generated in response to stroke have thus far been described as comprising only a small fraction of the population lost to the ischemic insult and have not yet been demonstrated to contribute to functional recovery. In general terms, the lack of compensatory neuronal replacement in most adult brain regions has impeded not only the recovery of...","PeriodicalId":10493,"journal":{"name":"Cold Spring Harbor Monograph Archive","volume":"75 1","pages":"593-617"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cold Spring Harbor Monograph Archive","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/087969784.52.593","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3
Abstract
The damaged brain has traditionally been thought to exhibit little significant structural repair after injury. In part, this appears to reflect the failure of the mature forebrain to generate new neurons, except for a few discrete, relatively archaic regions of the brain, the hippocampus and olfactory bulb (OB) (Altman and Das 1966; Bayer et al. 1982; for review, see Goldman 1998; Alvarez-Buylla and Garcia-Verdugo 2002; Gage 2002). The limitation on neuronal addition to the adult brain has clearly been selected, and thus comprises an adaptation of likely, if unclear, evolutionary benefit. Among other possibilities, the lack of persistent neurogenesis in most regions of the adult mammalian brain may be associated with the need to stabilize the retention of long-term memories and entrained behaviors (Rakic 2002). Perhaps as a result, the adult mammalian neocortex exhibits no constitutive neuronal addition, and little or none after injury, except for discrete experimental lesions of defined neuronal populations (Magavi et al. 2000). In contrast, the subcortical neostriatum retains the capacity to regenerate neurons after stroke and major traumatic injury (Arvidsson et al. 2002; Parent et al. 2002; Jin et al. 2003a; Parent 2003). However, the numbers of striatal neurons generated in response to stroke have thus far been described as comprising only a small fraction of the population lost to the ischemic insult and have not yet been demonstrated to contribute to functional recovery. In general terms, the lack of compensatory neuronal replacement in most adult brain regions has impeded not only the recovery of...
传统上认为,受损的大脑在受伤后几乎没有明显的结构修复。在某种程度上,这似乎反映了成熟的前脑不能产生新的神经元,除了大脑中一些离散的、相对古老的区域,海马体和嗅球(OB) (Altman and Das 1966;Bayer et al. 1982;回顾,见Goldman 1998;Alvarez-Buylla和Garcia-Verdugo 2002;计2002)。对成年大脑神经元添加的限制显然是被选择的,因此包含了一种可能的(如果不清楚的话)进化益处的适应。在其他可能性中,在成年哺乳动物大脑的大多数区域缺乏持续的神经发生可能与需要稳定长期记忆的保留和被训练的行为有关(Rakic 2002)。也许正因为如此,成年哺乳动物的新皮层在损伤后没有出现构成性神经元的增加,除了特定神经元群的离散实验损伤外,几乎没有神经元的增加(Magavi et al. 2000)。相反,皮层下新纹状体在中风和重大创伤性损伤后仍保留再生神经元的能力(Arvidsson等,2002;Parent等人,2002;Jin et al. 2003a;父母2003年)。然而,迄今为止,对中风产生的纹状体神经元的数量被描述为仅占缺血性损伤损失的一小部分,尚未被证明有助于功能恢复。一般来说,大多数成人大脑区域缺乏代偿性神经元替代不仅阻碍了…