166
Letters to the Editor / Brain Stimulation 8 (2014) 160e167
This research was supported by the National Natural Science Foundation of China (61025019, 61273063), and the Applied Basic Research Projects in Hebei Province.
Jing Wang Department of Neurobiology and Beijing Institute for Brain Disorders, School of Basic Medical Sciences, Capital Medical University, Beijing, PR China Yun Wei Institute of Electrical Engineering Yanshan University Qinhuangdao 066004, PR China Jianbin Wen Xiaoli Li* State Key Laboratory of Cognitive Neuroscience and Learning & IDG/McGovern Institute for Brain Research, Beijing Normal University, Beijing 100875, PR China Center for Collaboration and Innovation in Brain and Learning Sciences, Beijing Normal University, Beijing 100875, PR China * Corresponding author. Beijing Normal University, McGovern Institute for Brain Research, State Key Laboratory of Cognitive Neuroscience and Learning & IDG, Beijing 100875, PR China. E-mail addresses: [email protected], [email protected] (X. Li)
Received 12 August 2014 Available online 22 November 2014 http://dx.doi.org/10.1016/j.brs.2014.10.015
References [1] Auvichayapat P, Auvichayapat N. Basic knowledge of transcranial direct current stimulation. J Med Assoc Thai 2011;94:518e27. [2] Nitsche MA, Cohen LG, Wassermann EM, et al. Transcranial direct current stimulation: State of the art 2008. Brain Stimul 2008;1:206e23. [3] Brunoni AR, Nitsche MA, Bolognini N, et al. Clinical research with transcranial direct current stimulation (tDCS): challenges and future directions. Brain Stimul 2012;5:175e95. [4] Nitsche MA, Paulus W. Transcranial direct current stimulation e update 2011. Restor Neurol Neurosci 2011;29:463e92. [5] Poreisz C, Boros K, Antal A, Paulus W. Safety aspects of transcranial direct current stimulation concerning healthy subjects and patients. Brain Res Bull 2007; 72:208e14. [6] Palm U, Keeser D, Schiller C, et al. Skin lesions after treatment with transcranial direct current stimulation (tDCS). Brain Stimul 2008;1:386e7. [7] Rodríguez Neus, Opisso Eloy. Skin lesions induced by transcranial direct current stimulation (tDCS). Brain Stimul 2014;7:765e7. [8] Frank E, Wilfurth S, Landgrebe M, Eichhammer P, Hajak G, Langguth B. Anodal skin lesions after treatment with transcranial direct current stimulation. Brain Stimul 2010;3:58e9. [9] Russo R, Wallace D, Fitzgerald PB, Cooper NR. Perception of comfort during active and sham transcranial direct current stimulation: a double blind study. Brain Stimul 2013;6:946e51.
mediated by adult neurogenesis, could represent one way by which ECT evokes antidepressant effects. This notion is supported by the role of adult hippocampal neurogenesis in the therapeutic effect of antidepressant drugs [1]. ECT also strongly stimulates hippocampal neurogenesis, more than any other antidepressant therapy, an effect observed not only in rodents [2], but also in non-human primates [3]. Nevertheless, adult neurogenesis is not restricted to the dentate gyrus of the hippocampus. In fact, the subventricular zone (SVZ) in the wall of the lateral ventricles is the main site of adult neurogenesis in rodents, generating throughout life neuroblasts that migrate to the olfactory bulb, where they differentiate mainly into calretinin-positive GABAergic granule cells. Importantly, also in humans, cell proliferation in the adult SVZ is much more extensive than in the dentate gyrus of the hippocampus [4]. A recent radiocarbon-14 dating study demonstrated in humans a lack of adult neurogenesis in the olfactory bulb, but robust ongoing neurogenesis in the striatum [5]. This technique takes advantage of the worldwide incorporation of C-14 during atomic weapons experiments in the 1950s and represents a real methodological improvement in detecting adult neurogenesis in human samples. Surprisingly, Ernst and colleagues found a significant high level of striatal neurogenesis in humans (2.7% cell replacement/year). Importantly for the potential translational value of these findings is the fact that striatal neurogenesis in humans appears to generate the same subtype of calretinin-positive GABAergic interneurons as reported to be continuously generated in the postnatal and adult rodent striatum [6,7]. The functional significance of this process in humans is yet unknown. Nevertheless, these results suggest that there is a switch in SVZ adult neurogenesis from olfactory bulb in rodents to the striatum in humans. A logical consequence would be that SVZ neurogenesis may not serve olfactory functions in humans as in rodents, but may provide a high degree of plasticity to striatal circuits. We demonstrated recently in a model of ECT in rats that repeated external electrical brain stimulation for one week boosted cell proliferation in the SVZ, followed by migration and accumulation of calretinin-positive interneurons in the medial striatum adjacent to the SVZ [8]. Newborn interneurons induced by ECT showed morphological features of granule cells, similar to those described in the olfactory bulb and dentate gyrus. At the present time point, we cannot estimate yet the functional significance and the impact of these newborn GABAergic interneurons on local striatal networks. However, it seems of particular importance that enhanced GABAergic transmission was proposed to play a major role in the beneficial effects of ECT [9]. On the other side, it should be noticed that most newborn neurons were found in the medial striatum, which is part of the limbic system. This area is tightly interconnected with the prefrontal cortex and the amygdala [10], therefore its altered plasticity generated by neurogenesis may impact on mechanisms associated with the regulation of mood and anxiety. Future studies may further unravel the function of newborn striatal calretinin-positive interneurons and the functional significance of the stimulatory effect of ECT on their number.
ECT and Striatal Plasticity
Grant sponsor: Deutsche Forschungsgemeinschaft; Grant number: GA427/11-1 and the Collaborative Research Center (Sonderforschungsbereich) 636 of the University of Heidelberg.
Electroconvulsive therapy (ECT) represents by far the most effective therapy of treatment-resistant depression as well as of other severe psychiatric disorders. However, the neurobiological mechanism of action by which ECT achieves these therapeutic effects is not yet clear. Changes of neuronal plasticity, in particular
Dragos Inta* Peter Gass Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, J5, 68159, Mannheim, Germany
Letters to the Editor / Brain Stimulation 8 (2014) 160e167
author. Tel.: þ49 (0)621 1703 2933; fax: þ49 (0) 621 1703 6205. E-mail address: [email protected] (D. Inta)
* Corresponding
Received 10 November 2014 Available online 2 December 2014
http://dx.doi.org/10.1016/j.brs.2014.11.007
References [1] Santarelli L, Saxe M, Gross C, et al. Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science 2003;301:805e9. [2] Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci 2000;20: 9104e10.
167
[3] Perera TD, Coplan JD, Lisanby SH, et al. Antidepressant-induced neurogenesis in the hippocampus of adult nonhuman primates. J Neurosci 2007;27: 4894e901. [4] Curtis MA, Low VF, Faull RL. Neurogenesis and progenitor cells in the adult human brain: a comparison between hippocampal and subventricular progenitor proliferation. Dev Neurobiol 2012;72:990e1005. [5] Ernst A, Alkass K, Bernard S, et al. Neurogenesis in the striatum of the adult human brain. Cell 2014;156:1072e83. [6] Inta D, Alfonso J, von Engelhardt J, et al. Neurogenesis and widespread forebrain migration of distinct GABAergic neurons from the postnatal subventricular zone. Proc Natl Acad Sci U S A 2008;105:20994e9. [7] Dayer AG, Cleaver KM, Abouantoun T, Cameron HA. New GABAergic interneurons in the adult neocortex and striatum are generated from different precursors. J Cell Biol 2005;168:415e27. [8] Inta D, Lima-Ojeda JM, Lau T, et al. Electroconvulsive therapy induces neurogenesis in frontal rat brain areas. PLoS One 2013;8:e69869. [9] Sackeim HA, Decina P, Prohovnik I, Malitz S, Resor SR. Anticonvulsant and antidepressant properties of electroconvulsive therapy: a proposed mechanism of action. Biol Psychiatry 1983;18:1301e10. [10] McGeorge AJ, Faull RL. The organization of the projection from the cerebral cortex to the striatum in the rat. Neuroscience 1989;29:503e37.
Letters to the Editor / Brain Stimulation 8 (2014) 160e167
This research was supported by the National Natural Science Foundation of China (61025019, 61273063), and the Applied Basic Research Projects in Hebei Province.
Jing Wang Department of Neurobiology and Beijing Institute for Brain Disorders, School of Basic Medical Sciences, Capital Medical University, Beijing, PR China Yun Wei Institute of Electrical Engineering Yanshan University Qinhuangdao 066004, PR China Jianbin Wen Xiaoli Li* State Key Laboratory of Cognitive Neuroscience and Learning & IDG/McGovern Institute for Brain Research, Beijing Normal University, Beijing 100875, PR China Center for Collaboration and Innovation in Brain and Learning Sciences, Beijing Normal University, Beijing 100875, PR China * Corresponding author. Beijing Normal University, McGovern Institute for Brain Research, State Key Laboratory of Cognitive Neuroscience and Learning & IDG, Beijing 100875, PR China. E-mail addresses: [email protected], [email protected] (X. Li)
Received 12 August 2014 Available online 22 November 2014 http://dx.doi.org/10.1016/j.brs.2014.10.015
References [1] Auvichayapat P, Auvichayapat N. Basic knowledge of transcranial direct current stimulation. J Med Assoc Thai 2011;94:518e27. [2] Nitsche MA, Cohen LG, Wassermann EM, et al. Transcranial direct current stimulation: State of the art 2008. Brain Stimul 2008;1:206e23. [3] Brunoni AR, Nitsche MA, Bolognini N, et al. Clinical research with transcranial direct current stimulation (tDCS): challenges and future directions. Brain Stimul 2012;5:175e95. [4] Nitsche MA, Paulus W. Transcranial direct current stimulation e update 2011. Restor Neurol Neurosci 2011;29:463e92. [5] Poreisz C, Boros K, Antal A, Paulus W. Safety aspects of transcranial direct current stimulation concerning healthy subjects and patients. Brain Res Bull 2007; 72:208e14. [6] Palm U, Keeser D, Schiller C, et al. Skin lesions after treatment with transcranial direct current stimulation (tDCS). Brain Stimul 2008;1:386e7. [7] Rodríguez Neus, Opisso Eloy. Skin lesions induced by transcranial direct current stimulation (tDCS). Brain Stimul 2014;7:765e7. [8] Frank E, Wilfurth S, Landgrebe M, Eichhammer P, Hajak G, Langguth B. Anodal skin lesions after treatment with transcranial direct current stimulation. Brain Stimul 2010;3:58e9. [9] Russo R, Wallace D, Fitzgerald PB, Cooper NR. Perception of comfort during active and sham transcranial direct current stimulation: a double blind study. Brain Stimul 2013;6:946e51.
mediated by adult neurogenesis, could represent one way by which ECT evokes antidepressant effects. This notion is supported by the role of adult hippocampal neurogenesis in the therapeutic effect of antidepressant drugs [1]. ECT also strongly stimulates hippocampal neurogenesis, more than any other antidepressant therapy, an effect observed not only in rodents [2], but also in non-human primates [3]. Nevertheless, adult neurogenesis is not restricted to the dentate gyrus of the hippocampus. In fact, the subventricular zone (SVZ) in the wall of the lateral ventricles is the main site of adult neurogenesis in rodents, generating throughout life neuroblasts that migrate to the olfactory bulb, where they differentiate mainly into calretinin-positive GABAergic granule cells. Importantly, also in humans, cell proliferation in the adult SVZ is much more extensive than in the dentate gyrus of the hippocampus [4]. A recent radiocarbon-14 dating study demonstrated in humans a lack of adult neurogenesis in the olfactory bulb, but robust ongoing neurogenesis in the striatum [5]. This technique takes advantage of the worldwide incorporation of C-14 during atomic weapons experiments in the 1950s and represents a real methodological improvement in detecting adult neurogenesis in human samples. Surprisingly, Ernst and colleagues found a significant high level of striatal neurogenesis in humans (2.7% cell replacement/year). Importantly for the potential translational value of these findings is the fact that striatal neurogenesis in humans appears to generate the same subtype of calretinin-positive GABAergic interneurons as reported to be continuously generated in the postnatal and adult rodent striatum [6,7]. The functional significance of this process in humans is yet unknown. Nevertheless, these results suggest that there is a switch in SVZ adult neurogenesis from olfactory bulb in rodents to the striatum in humans. A logical consequence would be that SVZ neurogenesis may not serve olfactory functions in humans as in rodents, but may provide a high degree of plasticity to striatal circuits. We demonstrated recently in a model of ECT in rats that repeated external electrical brain stimulation for one week boosted cell proliferation in the SVZ, followed by migration and accumulation of calretinin-positive interneurons in the medial striatum adjacent to the SVZ [8]. Newborn interneurons induced by ECT showed morphological features of granule cells, similar to those described in the olfactory bulb and dentate gyrus. At the present time point, we cannot estimate yet the functional significance and the impact of these newborn GABAergic interneurons on local striatal networks. However, it seems of particular importance that enhanced GABAergic transmission was proposed to play a major role in the beneficial effects of ECT [9]. On the other side, it should be noticed that most newborn neurons were found in the medial striatum, which is part of the limbic system. This area is tightly interconnected with the prefrontal cortex and the amygdala [10], therefore its altered plasticity generated by neurogenesis may impact on mechanisms associated with the regulation of mood and anxiety. Future studies may further unravel the function of newborn striatal calretinin-positive interneurons and the functional significance of the stimulatory effect of ECT on their number.
ECT and Striatal Plasticity
Grant sponsor: Deutsche Forschungsgemeinschaft; Grant number: GA427/11-1 and the Collaborative Research Center (Sonderforschungsbereich) 636 of the University of Heidelberg.
Electroconvulsive therapy (ECT) represents by far the most effective therapy of treatment-resistant depression as well as of other severe psychiatric disorders. However, the neurobiological mechanism of action by which ECT achieves these therapeutic effects is not yet clear. Changes of neuronal plasticity, in particular
Dragos Inta* Peter Gass Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, J5, 68159, Mannheim, Germany
Letters to the Editor / Brain Stimulation 8 (2014) 160e167
author. Tel.: þ49 (0)621 1703 2933; fax: þ49 (0) 621 1703 6205. E-mail address: [email protected] (D. Inta)
* Corresponding
Received 10 November 2014 Available online 2 December 2014
http://dx.doi.org/10.1016/j.brs.2014.11.007
References [1] Santarelli L, Saxe M, Gross C, et al. Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science 2003;301:805e9. [2] Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci 2000;20: 9104e10.
167
[3] Perera TD, Coplan JD, Lisanby SH, et al. Antidepressant-induced neurogenesis in the hippocampus of adult nonhuman primates. J Neurosci 2007;27: 4894e901. [4] Curtis MA, Low VF, Faull RL. Neurogenesis and progenitor cells in the adult human brain: a comparison between hippocampal and subventricular progenitor proliferation. Dev Neurobiol 2012;72:990e1005. [5] Ernst A, Alkass K, Bernard S, et al. Neurogenesis in the striatum of the adult human brain. Cell 2014;156:1072e83. [6] Inta D, Alfonso J, von Engelhardt J, et al. Neurogenesis and widespread forebrain migration of distinct GABAergic neurons from the postnatal subventricular zone. Proc Natl Acad Sci U S A 2008;105:20994e9. [7] Dayer AG, Cleaver KM, Abouantoun T, Cameron HA. New GABAergic interneurons in the adult neocortex and striatum are generated from different precursors. J Cell Biol 2005;168:415e27. [8] Inta D, Lima-Ojeda JM, Lau T, et al. Electroconvulsive therapy induces neurogenesis in frontal rat brain areas. PLoS One 2013;8:e69869. [9] Sackeim HA, Decina P, Prohovnik I, Malitz S, Resor SR. Anticonvulsant and antidepressant properties of electroconvulsive therapy: a proposed mechanism of action. Biol Psychiatry 1983;18:1301e10. [10] McGeorge AJ, Faull RL. The organization of the projection from the cerebral cortex to the striatum in the rat. Neuroscience 1989;29:503e37.
