Neurogenic and angiogenic actions of electroconvulsive seizures in adult rat brain

Johan Hellsten

Neurogenic and angiogenic actions of electroconvulsive seizures in adult rat brain

Johan Hellsten

Psychiatric Neuromodulation Unit (PNU)

Research output: Thesis › Doctoral Thesis (compilation)

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Abstract

In the current thesis, the neurogenic and angiogenic response to electroconvulsive seizure (ECS)-treatment was investigated in the adult rat brain. ECS-treatment is an animal model for the antidepressant treatment electroconvulsive therapy (ECT), which is considered to be the most effective antidepressant treatment modality today, however with not yet fully understood modes of action. Depression, which is a common and devastating illness has recently been proposed to be caused by a decreased hippocampal neurogenesis and cellular plasticity in general, possibly due to elevated levels of the stress hormone cortisol, manifesting itself as a reduction in hippocampal volume. In the current thesis, ECS-treatment was shown to be able to oppose stress hormone-induced decrease in hippocampal neurogenesis and also induce proliferation of non-neuronal cells. A large majority of these cells were identified as being endothelial cells, and neurogenesis and angiogenesis in response to ECS-treatment seemingly occurred in concert. In addition to neurogenesis, ECS-treatment induced strong neuronal activation in the hypothalamus, co-localising with a strong angiogenic response. Endothelial cells have been shown to influence neuronal and glial function and we hypothesise that the increase in hypothalamic endothelial cell proliferation could for example influence neuroendocrine signaling. Besides possibly influencing neuronal and glial function, endothelial cells are building blocks of blood vessels. We detect a strong angiogenic response in the hippocampus, which in fact results in a 16% increase in vessel length in the molecular layer of the dentate gyrus. This finding has important implications for the trophic actions of ECS-treatment. In addition to counteracting decreases in neurogenesis, ECS-treatment increase the vascularization of a structure that has been shown to be vulnerable to stress and decrease in size in depressed patients. Understanding this angiogenic response and possibly being able to stimulate it by other means than ECS-treatment could possibly lead to the development of new and more effective antidepressant treatments.

Original language	English
Qualification	Doctor
Awarding Institution	Psychiatric Neuromodulation Unit (PNU)
Supervisors/Advisors	Träskman Bendz, Lil, Supervisor Tingström, Anders, Supervisor
Award date	2005 Sept 29
Publisher	Molecular Psychiatry Unit
ISBN (Print)	91-628-6592-7
Publication status	Published - 2005

Bibliographical note

Defence details

Date: 2005-09-29
Time: 09:00
Place: Segerfalksalen Wallenberg Neuroscience Center BMC A10 22184 Lund Sweden

External reviewer(s)

Name: Reid, Ian
Title: Professor
Affiliation: University of Aberdeen

---

<div class="article_info">Johan Hellsten, Malin Wennström, Paul Mohapel, Christine T. Ekdahl, Johan Bengzon and Anders Tingström. <span class="article_issue_date">2002</span>. <a href="javascript:downloadFile(545308)" class="article_link">Electroconvulsive seizures increase hippocampal neurogenesis after chronic corticosterone treatment</a> <span class="journal_series_title">Eur J Neurosci</span>, <span class="journal_volume">vol 16</span> <span class="journal_pages">pp 283-290</span>. <span class="journal_distributor">Blackwell</span></div>
<div class="article_info">J. Hellsten, M. Wennström, J. Bengzon, P. Mohapel and A. Tingström. <span class="article_issue_date">2004</span>. <a href="javascript:downloadFile(545309)" class="article_link">Electroconvulsive seizures induce endothelial cell proliferation in adult rat hippocampus</a> <span class="journal_series_title">Biological Psychiatry</span>, <span class="journal_volume">vol 55</span> <span class="journal_pages">pp 420-427</span>. <span class="journal_distributor">Elsevier</span></div>
<div class="article_info">J. Ekstrand, J. Hellsten, M. Wennström and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Inhibition of endothelial cell proliferation does not prevent electroconvulsive seizure-induced neural precursor proliferation in adult rat hippocampus.</span> (manuscript)</div>
<div class="article_info">J. Hellsten, M.J. West, A. Arvidsson, J. Ekstrand, L. Jansson, M. Wennström and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Electroconvulsive seizures induce angiogenesis in adult rat hippocampus</span> <span class="journal_series_title">Biol Psychiatry</span>, (inpress)</div>
<div class="article_info">L. Jansson, J. Hellsten and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Region specific hypothalamic neuronal activation and endothelial cell proliferation in response to electroconvulsive seizures</span> (submitted)</div>

Subject classification (UKÄ)

Psychiatry

Free keywords

vävnadskultur
Psychiatry
clinical psychology
psychosomatics
klinisk psykologi
psykosomatik
histokemi
cytokemi
Histologi
tissue culture
histochemistry
cytochemistry
Histology
Biology
Biologi
electroconvulsive seizures
hippocampus
depression
angiogenesis
neurogenesis
Psykiatri

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Cite this

@phdthesis{4c151ea778924418819975ed22437b22,

title = "Neurogenic and angiogenic actions of electroconvulsive seizures in adult rat brain",

abstract = "In the current thesis, the neurogenic and angiogenic response to electroconvulsive seizure (ECS)-treatment was investigated in the adult rat brain. ECS-treatment is an animal model for the antidepressant treatment electroconvulsive therapy (ECT), which is considered to be the most effective antidepressant treatment modality today, however with not yet fully understood modes of action. Depression, which is a common and devastating illness has recently been proposed to be caused by a decreased hippocampal neurogenesis and cellular plasticity in general, possibly due to elevated levels of the stress hormone cortisol, manifesting itself as a reduction in hippocampal volume. In the current thesis, ECS-treatment was shown to be able to oppose stress hormone-induced decrease in hippocampal neurogenesis and also induce proliferation of non-neuronal cells. A large majority of these cells were identified as being endothelial cells, and neurogenesis and angiogenesis in response to ECS-treatment seemingly occurred in concert. In addition to neurogenesis, ECS-treatment induced strong neuronal activation in the hypothalamus, co-localising with a strong angiogenic response. Endothelial cells have been shown to influence neuronal and glial function and we hypothesise that the increase in hypothalamic endothelial cell proliferation could for example influence neuroendocrine signaling. Besides possibly influencing neuronal and glial function, endothelial cells are building blocks of blood vessels. We detect a strong angiogenic response in the hippocampus, which in fact results in a 16% increase in vessel length in the molecular layer of the dentate gyrus. This finding has important implications for the trophic actions of ECS-treatment. In addition to counteracting decreases in neurogenesis, ECS-treatment increase the vascularization of a structure that has been shown to be vulnerable to stress and decrease in size in depressed patients. Understanding this angiogenic response and possibly being able to stimulate it by other means than ECS-treatment could possibly lead to the development of new and more effective antidepressant treatments.",

keywords = "v{\"a}vnadskultur, Psychiatry, clinical psychology, psychosomatics, klinisk psykologi, psykosomatik, histokemi, cytokemi, Histologi, tissue culture, histochemistry, cytochemistry, Histology, Biology, Biologi, electroconvulsive seizures, hippocampus, depression, angiogenesis, neurogenesis, Psykiatri",

author = "Johan Hellsten",

note = "Defence details Date: 2005-09-29 Time: 09:00 Place: Segerfalksalen Wallenberg Neuroscience Center BMC A10 22184 Lund Sweden External reviewer(s) Name: Reid, Ian Title: Professor Affiliation: University of Aberdeen --- <div class={"}article_info{"}>Johan Hellsten, Malin Wennstr{\"o}m, Paul Mohapel, Christine T. Ekdahl, Johan Bengzon and Anders Tingstr{\"o}m. <span class={"}article_issue_date{"}>2002</span>. <a href={"}javascript:downloadFile(545308){"} class={"}article_link{"}>Electroconvulsive seizures increase hippocampal neurogenesis after chronic corticosterone treatment</a> <span class={"}journal_series_title{"}>Eur J Neurosci</span>, <span class={"}journal_volume{"}>vol 16</span> <span class={"}journal_pages{"}>pp 283-290</span>. <span class={"}journal_distributor{"}>Blackwell</span></div> <div class={"}article_info{"}>J. Hellsten, M. Wennstr{\"o}m, J. Bengzon, P. Mohapel and A. Tingstr{\"o}m. <span class={"}article_issue_date{"}>2004</span>. <a href={"}javascript:downloadFile(545309){"} class={"}article_link{"}>Electroconvulsive seizures induce endothelial cell proliferation in adult rat hippocampus</a> <span class={"}journal_series_title{"}>Biological Psychiatry</span>, <span class={"}journal_volume{"}>vol 55</span> <span class={"}journal_pages{"}>pp 420-427</span>. <span class={"}journal_distributor{"}>Elsevier</span></div> <div class={"}article_info{"}>J. Ekstrand, J. Hellsten, M. Wennstr{\"o}m and A. Tingstr{\"o}m. <span class={"}article_issue_date{"}>2005</span>. <span class={"}article_title{"}>Inhibition of endothelial cell proliferation does not prevent electroconvulsive seizure-induced neural precursor proliferation in adult rat hippocampus.</span> (manuscript)</div> <div class={"}article_info{"}>J. Hellsten, M.J. West, A. Arvidsson, J. Ekstrand, L. Jansson, M. Wennstr{\"o}m and A. Tingstr{\"o}m. <span class={"}article_issue_date{"}>2005</span>. <span class={"}article_title{"}>Electroconvulsive seizures induce angiogenesis in adult rat hippocampus</span> <span class={"}journal_series_title{"}>Biol Psychiatry</span>, (inpress)</div> <div class={"}article_info{"}>L. Jansson, J. Hellsten and A. Tingstr{\"o}m. <span class={"}article_issue_date{"}>2005</span>. <span class={"}article_title{"}>Region specific hypothalamic neuronal activation and endothelial cell proliferation in response to electroconvulsive seizures</span> (submitted)</div>",

year = "2005",

language = "English",

isbn = "91-628-6592-7",

series = "Lund University Faculty of Medicine Doctoral Dissertation Series ",

publisher = "Molecular Psychiatry Unit",

type = "Doctoral Thesis (compilation)",

school = "Psychiatric Neuromodulation Unit (PNU)",

}

TY - THES

T1 - Neurogenic and angiogenic actions of electroconvulsive seizures in adult rat brain

AU - Hellsten, Johan

N1 - Defence details Date: 2005-09-29 Time: 09:00 Place: Segerfalksalen Wallenberg Neuroscience Center BMC A10 22184 Lund Sweden External reviewer(s) Name: Reid, Ian Title: Professor Affiliation: University of Aberdeen --- <div class="article_info">Johan Hellsten, Malin Wennström, Paul Mohapel, Christine T. Ekdahl, Johan Bengzon and Anders Tingström. <span class="article_issue_date">2002</span>. <a href="javascript:downloadFile(545308)" class="article_link">Electroconvulsive seizures increase hippocampal neurogenesis after chronic corticosterone treatment</a> <span class="journal_series_title">Eur J Neurosci</span>, <span class="journal_volume">vol 16</span> <span class="journal_pages">pp 283-290</span>. <span class="journal_distributor">Blackwell</span></div> <div class="article_info">J. Hellsten, M. Wennström, J. Bengzon, P. Mohapel and A. Tingström. <span class="article_issue_date">2004</span>. <a href="javascript:downloadFile(545309)" class="article_link">Electroconvulsive seizures induce endothelial cell proliferation in adult rat hippocampus</a> <span class="journal_series_title">Biological Psychiatry</span>, <span class="journal_volume">vol 55</span> <span class="journal_pages">pp 420-427</span>. <span class="journal_distributor">Elsevier</span></div> <div class="article_info">J. Ekstrand, J. Hellsten, M. Wennström and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Inhibition of endothelial cell proliferation does not prevent electroconvulsive seizure-induced neural precursor proliferation in adult rat hippocampus.</span> (manuscript)</div> <div class="article_info">J. Hellsten, M.J. West, A. Arvidsson, J. Ekstrand, L. Jansson, M. Wennström and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Electroconvulsive seizures induce angiogenesis in adult rat hippocampus</span> <span class="journal_series_title">Biol Psychiatry</span>, (inpress)</div> <div class="article_info">L. Jansson, J. Hellsten and A. Tingström. <span class="article_issue_date">2005</span>. <span class="article_title">Region specific hypothalamic neuronal activation and endothelial cell proliferation in response to electroconvulsive seizures</span> (submitted)</div>

PY - 2005

Y1 - 2005

N2 - In the current thesis, the neurogenic and angiogenic response to electroconvulsive seizure (ECS)-treatment was investigated in the adult rat brain. ECS-treatment is an animal model for the antidepressant treatment electroconvulsive therapy (ECT), which is considered to be the most effective antidepressant treatment modality today, however with not yet fully understood modes of action. Depression, which is a common and devastating illness has recently been proposed to be caused by a decreased hippocampal neurogenesis and cellular plasticity in general, possibly due to elevated levels of the stress hormone cortisol, manifesting itself as a reduction in hippocampal volume. In the current thesis, ECS-treatment was shown to be able to oppose stress hormone-induced decrease in hippocampal neurogenesis and also induce proliferation of non-neuronal cells. A large majority of these cells were identified as being endothelial cells, and neurogenesis and angiogenesis in response to ECS-treatment seemingly occurred in concert. In addition to neurogenesis, ECS-treatment induced strong neuronal activation in the hypothalamus, co-localising with a strong angiogenic response. Endothelial cells have been shown to influence neuronal and glial function and we hypothesise that the increase in hypothalamic endothelial cell proliferation could for example influence neuroendocrine signaling. Besides possibly influencing neuronal and glial function, endothelial cells are building blocks of blood vessels. We detect a strong angiogenic response in the hippocampus, which in fact results in a 16% increase in vessel length in the molecular layer of the dentate gyrus. This finding has important implications for the trophic actions of ECS-treatment. In addition to counteracting decreases in neurogenesis, ECS-treatment increase the vascularization of a structure that has been shown to be vulnerable to stress and decrease in size in depressed patients. Understanding this angiogenic response and possibly being able to stimulate it by other means than ECS-treatment could possibly lead to the development of new and more effective antidepressant treatments.

AB - In the current thesis, the neurogenic and angiogenic response to electroconvulsive seizure (ECS)-treatment was investigated in the adult rat brain. ECS-treatment is an animal model for the antidepressant treatment electroconvulsive therapy (ECT), which is considered to be the most effective antidepressant treatment modality today, however with not yet fully understood modes of action. Depression, which is a common and devastating illness has recently been proposed to be caused by a decreased hippocampal neurogenesis and cellular plasticity in general, possibly due to elevated levels of the stress hormone cortisol, manifesting itself as a reduction in hippocampal volume. In the current thesis, ECS-treatment was shown to be able to oppose stress hormone-induced decrease in hippocampal neurogenesis and also induce proliferation of non-neuronal cells. A large majority of these cells were identified as being endothelial cells, and neurogenesis and angiogenesis in response to ECS-treatment seemingly occurred in concert. In addition to neurogenesis, ECS-treatment induced strong neuronal activation in the hypothalamus, co-localising with a strong angiogenic response. Endothelial cells have been shown to influence neuronal and glial function and we hypothesise that the increase in hypothalamic endothelial cell proliferation could for example influence neuroendocrine signaling. Besides possibly influencing neuronal and glial function, endothelial cells are building blocks of blood vessels. We detect a strong angiogenic response in the hippocampus, which in fact results in a 16% increase in vessel length in the molecular layer of the dentate gyrus. This finding has important implications for the trophic actions of ECS-treatment. In addition to counteracting decreases in neurogenesis, ECS-treatment increase the vascularization of a structure that has been shown to be vulnerable to stress and decrease in size in depressed patients. Understanding this angiogenic response and possibly being able to stimulate it by other means than ECS-treatment could possibly lead to the development of new and more effective antidepressant treatments.

KW - vävnadskultur

KW - Psychiatry

KW - clinical psychology

KW - psychosomatics

KW - klinisk psykologi

KW - psykosomatik

KW - histokemi

KW - cytokemi

KW - Histologi

KW - tissue culture

KW - histochemistry

KW - cytochemistry

KW - Histology

KW - Biology

KW - Biologi

KW - electroconvulsive seizures

KW - hippocampus

KW - depression

KW - angiogenesis

KW - neurogenesis

KW - Psykiatri

M3 - Doctoral Thesis (compilation)

SN - 91-628-6592-7

T3 - Lund University Faculty of Medicine Doctoral Dissertation Series

PB - Molecular Psychiatry Unit

ER -

Neurogenic and angiogenic actions of electroconvulsive seizures in adult rat brain

Abstract

Bibliographical note

Subject classification (UKÄ)

Free keywords

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