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  1. Article: Stress and remodeling of hippocampal spine synapses.

    Hajszan, Tibor

    Vitamins and hormones

    2020  Volume 114, Page(s) 257–279

    Abstract: By nature's original design, stress is a protective mechanism, signaling danger to homeostasis and, as a result, stimulating the brain to initiate coping and adaptive responses, which ultimately increases the chances of survival. On the other hand, ... ...

    Abstract By nature's original design, stress is a protective mechanism, signaling danger to homeostasis and, as a result, stimulating the brain to initiate coping and adaptive responses, which ultimately increases the chances of survival. On the other hand, stress may become a danger to homeostasis itself, when it is so severe or so prolonged that it overpowers cellular reserves. One of the consequences of traumatic stress is loss of hippocampal spine synapses, which is the main topic of this chapter summarizing research findings from the last 10+ years. Loss of spine synapses is thought to be a neuronal defense mechanism against excitotoxic damage, so the subcellular mechanisms of synapse loss are reviewed in the context of glutamatergic insults. One of the main conceptual derivates of stress-induced synaptic alterations is the "synaptogenic" hypothesis of major depressive disorder. The synaptogenic hypothesis postulates an inverse correlation between the number of limbic, mainly prefrontal cortical and hippocampal, spine synapses and the severity of depressive behavior/symptoms. The synaptogenic hypothesis implies that synaptoprotective interventions, that are capable of countering the stress-induced loss of limbic spine synapses, are probably also capable of promoting stress resilience, which may provide the conceptual basis for a preventive approach in antidepressant therapy. Finally, we discuss why electron microscopic stereology is a reliable and highly accurate technique for the quantitative assessment of ultrastructural particulate objects, such as spines and synapses.
    MeSH term(s) Animals ; Depressive Disorder, Major/metabolism ; Depressive Disorder, Major/physiopathology ; Hippocampus/cytology ; Humans ; Neuronal Plasticity ; Neurons/physiology ; Stress, Psychological/physiopathology ; Synapses/physiology
    Language English
    Publishing date 2020-06-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 201161-x
    ISSN 2162-2620 ; 0083-6729
    ISSN (online) 2162-2620
    ISSN 0083-6729
    DOI 10.1016/bs.vh.2020.04.007
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  2. Article ; Online: Stress Resilience is Associated with Hippocampal Synaptoprotection in the Female Rat Learned Helplessness Paradigm.

    Huzian, Orsolya / Baka, Judith / Csakvari, Eszter / Dobos, Nikoletta / Leranth, Csaba / Siklos, Laszlo / Duman, Ronald S / Farkas, Tamas / Hajszan, Tibor

    Neuroscience

    2021  Volume 459, Page(s) 85–103

    Abstract: The synaptogenic hypothesis of major depressive disorder implies that preventing the onset of depressive-like behavior also prevents the loss of hippocampal spine synapses. By applying the psychoactive drugs, diazepam and fluoxetine, we investigated ... ...

    Abstract The synaptogenic hypothesis of major depressive disorder implies that preventing the onset of depressive-like behavior also prevents the loss of hippocampal spine synapses. By applying the psychoactive drugs, diazepam and fluoxetine, we investigated whether blocking the development of helpless behavior by promoting stress resilience in the rat learned helplessness paradigm is associated with a synaptoprotective action in the hippocampus. Adult ovariectomized and intact female Sprague-Dawley rats (n = 297) were treated with either diazepam, fluoxetine, or vehicle, exposed to inescapable footshocks or sham stress, and tested in an active escape task to assess helpless behavior. Escape-evoked corticosterone secretion, as well as remodeling of hippocampal spine synapses at a timepoint representing the onset of escape testing were also analyzed. In ovariectomized females, treatment with diazepam prior to stress exposure prevented helpless behavior, blocked the loss of hippocampal spine synapses, and muted the corticosterone surge evoked by escape testing. Although fluoxetine stimulated escape performance and hippocampal synaptogenesis under non-stressed conditions, almost all responses to fluoxetine were abolished following exposure to inescapable stress. Only a much higher dose of fluoxetine was capable of partly reproducing the strong protective actions of diazepam. Importantly, these protective actions were retained in the presence of ovarian hormones. Our findings indicate that stress resilience is associated with the preservation of spine synapses in the hippocampus, raising the possibility that, besides synaptogenesis, hippocampal synaptoprotection is also implicated in antidepressant therapy.
    MeSH term(s) Animals ; Depressive Disorder, Major ; Disease Models, Animal ; Female ; Fluoxetine/pharmacology ; Helplessness, Learned ; Hippocampus ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Fluoxetine (01K63SUP8D)
    Language English
    Publishing date 2021-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2021.01.029
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  3. Article ; Online: Bisphenol A interferes with synaptic remodeling.

    Hajszan, Tibor / Leranth, Csaba

    Frontiers in neuroendocrinology

    2010  Volume 31, Issue 4, Page(s) 519–530

    Abstract: The potential adverse effects of Bisphenol A (BPA), a synthetic xenoestrogen, have long been debated. Although standard toxicology tests have revealed no harmful effects, recent research highlighted what was missed so far: BPA-induced alterations in the ... ...

    Abstract The potential adverse effects of Bisphenol A (BPA), a synthetic xenoestrogen, have long been debated. Although standard toxicology tests have revealed no harmful effects, recent research highlighted what was missed so far: BPA-induced alterations in the nervous system. Since 2004, our laboratory has been investigating one of the central effects of BPA, which is interference with gonadal steroid-induced synaptogenesis and the resulting loss of spine synapses. We have shown in both rats and nonhuman primates that BPA completely negates the ∼ 70-100% increase in the number of hippocampal and prefrontal spine synapses induced by both estrogens and androgens. Synaptic loss of this magnitude may have significant consequences, potentially causing cognitive decline, depression, and schizophrenia, to mention those that our laboratory has shown to be associated with synaptic loss. Finally, we discuss why children may particularly be vulnerable to BPA, which represents future direction of research in our laboratory.
    MeSH term(s) Androgens/metabolism ; Androgens/pharmacology ; Animals ; Benzhydryl Compounds ; Depression/chemically induced ; Estrogens/metabolism ; Estrogens/pharmacology ; Estrogens, Non-Steroidal/toxicity ; Female ; Hippocampus/drug effects ; Humans ; Male ; Mice ; Neurogenesis/drug effects ; Phenols/blood ; Phenols/metabolism ; Phenols/toxicity ; Prefrontal Cortex/drug effects ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Primates ; Rats ; Synapses/drug effects
    Chemical Substances Androgens ; Benzhydryl Compounds ; Estrogens ; Estrogens, Non-Steroidal ; Phenols ; bisphenol A (MLT3645I99)
    Language English
    Publishing date 2010-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 390985-2
    ISSN 1095-6808 ; 0532-7466 ; 0091-3022
    ISSN (online) 1095-6808
    ISSN 0532-7466 ; 0091-3022
    DOI 10.1016/j.yfrne.2010.06.004
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  4. Article: Extrinsic afferent systems to the dentate gyrus.

    Leranth, Csaba / Hajszan, Tibor

    Progress in brain research

    2007  Volume 163, Page(s) 63–84

    Abstract: The dentate gyrus is the first stage of the intrahippocampal, excitatory, trisynaptic loop, and a primary target of the majority of entorhinal afferents that terminate in a laminar fashion on granule cell dendrites and carry sensory information of ... ...

    Abstract The dentate gyrus is the first stage of the intrahippocampal, excitatory, trisynaptic loop, and a primary target of the majority of entorhinal afferents that terminate in a laminar fashion on granule cell dendrites and carry sensory information of multiple modalities about the external world. The electric activity of the trisynaptic pathway is controlled mainly by different types of local, GABAergic interneurons, and subcortical and commissural afferents. In this chapter we will outline the origin and postsynaptic targets in the dentate gyrus of chemically identified subcortical inputs. These systems are afferents originating from the medial septum/diagonal band of Broca GABAergic and cholinergic neurons, neurochemically distinct types of neurons located in the supramammillary area, serotonergic fibers from the median raphe, noradrenergic afferents from the pontine nucleus, locus ceruleus, dopamine axons originating in the ventral tegmental area, and the commissural projection system. Because of the physiological implications, these afferents are discussed in the context of the glutamatergic innervation of the dentate gyrus. One common feature of the extrinsic dentate afferent systems is that they originate from a relatively small number of neurons. However, the majority of these afferents are able to exert a powerful control over the electrical activity of the hippocampus. This strong influence is due to the fact that the majority of the extrinsic afferents terminate on a relatively small, but specific, populations of neurons that are able to control large areas of the hippocampal formation.
    MeSH term(s) Afferent Pathways/anatomy & histology ; Afferent Pathways/metabolism ; Afferent Pathways/ultrastructure ; Dentate Gyrus/anatomy & histology ; Dopamine/metabolism ; Norepinephrine/metabolism ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances gamma-Aminobutyric Acid (56-12-2) ; Dopamine (VTD58H1Z2X) ; Norepinephrine (X4W3ENH1CV)
    Language English
    Publishing date 2007
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 0079-6123
    ISSN 0079-6123
    DOI 10.1016/S0079-6123(07)63004-0
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  5. Article ; Online: Loss of asymmetric spine synapses in dorsolateral prefrontal cortex of cognitively impaired phencyclidine-treated monkeys.

    Elsworth, John D / Hajszan, Tibor / Leranth, Csaba / Roth, Robert H

    The international journal of neuropsychopharmacology

    2011  Volume 14, Issue 10, Page(s) 1411–1415

    Abstract: Schizophrenia patients, long-term abusers of phencyclidine (PCP), and monkeys treated with PCP all exhibit enduring cognitive deficits. Evidence indicates that loss of prefrontal cortex spine synapses results in cognitive dysfunction, suggesting the ... ...

    Abstract Schizophrenia patients, long-term abusers of phencyclidine (PCP), and monkeys treated with PCP all exhibit enduring cognitive deficits. Evidence indicates that loss of prefrontal cortex spine synapses results in cognitive dysfunction, suggesting the presence of synaptic pathology in the monkey PCP model; however, there is no direct evidence of such changes. In this study we use the monkey PCP model of schizophrenia to investigate at the ultrastructural level whether remodelling of dorsolateral prefrontal cortex (DLPFC) asymmetric spine synapses occurs following PCP. Subchronic PCP treatment resulted in a decrease in the number of asymmetric spine synapses, which was greater in layer II/III than layer V of DLPFC, compared to vehicle-treated controls. This decrease may contribute to PCP-induced cognitive dysfunction in the non-human primate model and perhaps in schizophrenia. Thus, the synapse loss in the PCP model provides a novel target for the development of potential treatments of cognitive dysfunction in this model and in schizophrenia.
    MeSH term(s) Animals ; Chlorocebus aethiops ; Cognition ; Cognition Disorders/chemically induced ; Cognition Disorders/pathology ; Cognition Disorders/psychology ; Dendritic Spines/pathology ; Dendritic Spines/ultrastructure ; Disease Models, Animal ; Male ; Microscopy, Electron, Transmission ; Phencyclidine ; Prefrontal Cortex/pathology ; Prefrontal Cortex/ultrastructure ; Schizophrenia/chemically induced ; Schizophrenia/pathology ; Schizophrenic Psychology ; Synapses/pathology ; Synapses/ultrastructure
    Chemical Substances Phencyclidine (J1DOI7UV76)
    Language English
    Publishing date 2011-06-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1440129-0
    ISSN 1469-5111 ; 1461-1457
    ISSN (online) 1469-5111
    ISSN 1461-1457
    DOI 10.1017/S1461145711000939
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  6. Article ; Online: Stress induces equivalent remodeling of hippocampal spine synapses in a simulated postpartum environment and in a female rat model of major depression.

    Baka, Judith / Csakvari, Eszter / Huzian, Orsolya / Dobos, Nikoletta / Siklos, Laszlo / Leranth, Csaba / MacLusky, Neil J / Duman, Ronald S / Hajszan, Tibor

    Neuroscience

    2016  Volume 343, Page(s) 384–397

    Abstract: Stress and withdrawal of female reproductive hormones are known risk factors of postpartum depression. Although both of these factors are capable of powerfully modulating neuronal plasticity, there is no direct electron microscopic evidence of ... ...

    Abstract Stress and withdrawal of female reproductive hormones are known risk factors of postpartum depression. Although both of these factors are capable of powerfully modulating neuronal plasticity, there is no direct electron microscopic evidence of hippocampal spine synapse remodeling in postpartum depression. To address this issue, hormonal conditions of pregnancy and postpartum period were simulated in ovariectomized adult female Sprague-Dawley rats (n=76). The number of hippocampal spine synapses and the depressive behavior of rats in an active escape task were investigated in untreated control, hormone-withdrawn 'postpartum', simulated proestrus, and hormone-treated 'postpartum' animals. After 'postpartum' withdrawal of gonadal steroids, inescapable stress caused a loss of hippocampal spine synapses, which was related to poor escape performance in hormone-withdrawn 'postpartum' females. These responses were equivalent with the changes observed in untreated controls that is an established animal model of major depression. Maintaining proestrus levels of ovarian hormones during 'postpartum' stress exposure did not affect synaptic and behavioral responses to inescapable stress in simulated proestrus animals. By contrast, maintaining pregnancy levels of estradiol and progesterone during 'postpartum' stress exposure completely prevented the stress-induced loss of hippocampal spine synapses, which was associated with improved escape performance in hormone-treated 'postpartum' females. This protective effect appears to be mediated by a muted stress response as measured by serum corticosterone concentrations. In line with our emerging 'synaptogenic hypothesis' of depression, the loss of hippocampal spine synapses may be a novel perspective both in the pathomechanism and in the clinical management of postpartum affective illness.
    MeSH term(s) Animals ; Corticosterone/blood ; Depression, Postpartum/metabolism ; Depression, Postpartum/pathology ; Depressive Disorder, Major/metabolism ; Depressive Disorder, Major/pathology ; Disease Models, Animal ; Estradiol/administration & dosage ; Estradiol/metabolism ; Female ; Hippocampus/metabolism ; Hippocampus/pathology ; Neuronal Plasticity/physiology ; Ovariectomy ; Postpartum Period ; Proestrus/physiology ; Progesterone/administration & dosage ; Progesterone/metabolism ; Rats, Sprague-Dawley ; Synapses/metabolism ; Synapses/pathology
    Chemical Substances Progesterone (4G7DS2Q64Y) ; Estradiol (4TI98Z838E) ; Corticosterone (W980KJ009P)
    Language English
    Publishing date 2016-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2016.12.021
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  7. Article: Direct catecholaminergic-cholinergic interactions in the basal forebrain. III. Adrenergic innervation of choline acetyltransferase-containing neurons in the rat.

    Hajszán, Tibor / Zaborszky, Laszlo

    The Journal of comparative neurology

    2002  Volume 449, Issue 2, Page(s) 141–157

    Abstract: The central adrenergic neurons have been suggested to play a role in the regulation of arousal and in the neuronal control of the cardiovascular system. To provide morphological evidence that these functions could be mediated via the basal forebrain, we ... ...

    Abstract The central adrenergic neurons have been suggested to play a role in the regulation of arousal and in the neuronal control of the cardiovascular system. To provide morphological evidence that these functions could be mediated via the basal forebrain, we performed correlated light and electron microscopic double-immunolabeling experiments using antibodies against phenylethanolamine N-methyltransferase (PNMT) and choline acetyltransferase, the synthesizing enzymes for adrenaline and acetylcholine, respectively. Most adrenergic/cholinergic appositions were located in the horizontal limb of diagonal band of Broca, within the substantia innominata, and in a narrow band bordering the substantia innominata and the globus pallidus. Quantitative analysis indicated that cholinergic neurons of the substantia innominata receive significantly higher numbers of adrenergic appositions than cholinergic cells in the rest of the basal forebrain. In the majority of cases, the ultrastructural analysis revealed axodendritic asymmetric synapses. By comparing the number and distribution of dopamine beta-hydroxylase (DBH)/cholinergic appositions, described earlier, with those of PNMT/cholinergic interactions in the basal forebrain, it can be concluded that a significant proportion of putative DBH/cholinergic contacts may represent adrenergic input. Our results support the hypothesis that the adrenergic/cholinergic link in the basal forebrain may represent a critical component of a central network coordinating autonomic regulation with cortical activation.
    MeSH term(s) Adrenergic Fibers/enzymology ; Adrenergic Fibers/physiology ; Adrenergic Fibers/ultrastructure ; Animals ; Catecholamines/physiology ; Choline O-Acetyltransferase/physiology ; Cholinergic Fibers/enzymology ; Cholinergic Fibers/physiology ; Cholinergic Fibers/ultrastructure ; Immunohistochemistry ; Male ; Neurons/enzymology ; Neurons/physiology ; Neurons/ultrastructure ; Prosencephalon/enzymology ; Prosencephalon/physiology ; Prosencephalon/ultrastructure ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Catecholamines ; Choline O-Acetyltransferase (EC 2.3.1.6)
    Language English
    Publishing date 2002-07-22
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 3086-7
    ISSN 1096-9861 ; 0021-9967 ; 0092-7317
    ISSN (online) 1096-9861
    ISSN 0021-9967 ; 0092-7317
    DOI 10.1002/cne.10279
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  8. Article: Sex steroids and the dentate gyrus.

    Hajszan, Tibor / Milner, Teresa A / Leranth, Csaba

    Progress in brain research

    2007  Volume 163, Page(s) 399–415

    Abstract: In the late 1980s, the finding that the dentate gyrus contains more granule cells in the male than in the female of certain mouse strains provided the first indication that the dentate gyrus is a significant target for the effects of sex steroids during ... ...

    Abstract In the late 1980s, the finding that the dentate gyrus contains more granule cells in the male than in the female of certain mouse strains provided the first indication that the dentate gyrus is a significant target for the effects of sex steroids during development. Gonadal hormones also play a crucial role in shaping the function and morphology of the adult brain. Besides reproduction-related processes, sex steroids participate in higher brain operations such as cognition and mood, in which the hippocampus is a critical mediator. Being part of the hippocampal formation, the dentate gyrus is naturally involved in these mechanisms and as such, this structure is also a critical target for the activational effects of sex steroids. These activational effects are the results of three major types of steroid-mediated actions. Sex steroids modulate the function of dentate neurons under normal conditions. In addition, recent research suggests that hormone-induced cellular plasticity may play a larger role than previously thought, particularly in the dentate gyrus. Specifically, the regulation of dentate gyrus neurogenesis and synaptic remodeling by sex steroids received increasing attention lately. Finally, the dentate gyrus is influenced by gonadal hormones in the context of cellular injury, and the work in this area demonstrates that gonadal hormones have neuroprotective potential. The expression of estrogen, progestin, and androgen receptors in the dentate gyrus suggests that sex steroids, which could be of gonadal origin and/or synthesized locally in the dentate gyrus, may act directly on dentate cells. In addition, gonadal hormones could also influence the dentate gyrus indirectly, by subcortical hormone-sensitive structures such as the cholinergic septohippocampal system. Importantly, these three sex steroid-related themes, functional effects in the normal dentate gyrus, mechanisms involving neurogenesis and synaptic remodeling, as well as neuroprotection, have substantial implications for understanding normal cognitive function, with clinical importance for epilepsy, Alzheimer's disease and mental disorders.
    MeSH term(s) Animals ; Dentate Gyrus/metabolism ; Gonadal Steroid Hormones/metabolism ; Humans ; Sex Characteristics
    Chemical Substances Gonadal Steroid Hormones
    Language English
    Publishing date 2007
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 0079-6123
    ISSN 0079-6123
    DOI 10.1016/S0079-6123(07)63023-4
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  9. Article: Role of androgens and the androgen receptor in remodeling of spine synapses in limbic brain areas.

    Hajszan, Tibor / MacLusky, Neil J / Leranth, Csaba

    Hormones and behavior

    2007  Volume 53, Issue 5, Page(s) 638–646

    Abstract: Accumulating evidence indicate that structural synaptic plasticity in limbic areas plays a vital role not only in normal brain functions, such as cognition and mood, but also in the development of neurological and mental disorders. We have learned from ... ...

    Abstract Accumulating evidence indicate that structural synaptic plasticity in limbic areas plays a vital role not only in normal brain functions, such as cognition and mood, but also in the development of neurological and mental disorders. We have learned from studies investigating neuronal remodeling that estrogens have an exceptional synaptogenic potential that seems to be specific to limbic areas of the adult female brain. On the other hand, structural synaptic plasticity in the adult male brain and the synaptogenic effect of androgens received relatively little attention. During the last five years, the Leranth laboratory provided conclusive evidence that the hippocampus and prefrontal cortex of adult male rodents and non-human primates retain considerable structural synaptic plasticity similar to the female, and that androgens are capable of inducing spine synapse growth in both the hippocampus and prefrontal cortex similar to estrogens. Our recent work also demonstrates that androgen-induced remodeling of spine synapses in the prefrontal cortex of adult male rats is dependent, at least to some extent, on functional androgen receptors, while being entirely independent of the androgen receptor in the hippocampus. Based on these findings and on their many beneficial effects, we believe that androgens hold a great and undeservingly neglected therapeutic potential that could be employed to reverse synaptic pathology in various neurocognitive and neuropsychiatric disorders.
    MeSH term(s) Androgens/physiology ; Animals ; Brain/physiology ; Female ; Hippocampus/embryology ; Hippocampus/physiology ; Humans ; Limbic System/physiology ; Male ; Prefrontal Cortex/embryology ; Prefrontal Cortex/physiology ; Primates ; Rats ; Receptors, Androgen/genetics ; Receptors, Androgen/physiology ; Spinal Cord/physiology ; Synapses/physiology
    Chemical Substances Androgens ; Receptors, Androgen
    Language English
    Publishing date 2007-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 214409-8
    ISSN 1095-6867 ; 0018-506X
    ISSN (online) 1095-6867
    ISSN 0018-506X
    DOI 10.1016/j.yhbeh.2007.12.007
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  10. Article ; Online: Estimation of the total number of hippocampal CA1 pyramidal neurons: new methodology applied to helpless rats.

    Miettinen, Riitta / Hajszan, Tibor / Riedel, Anett / Szigeti-Buck, Klara / Leranth, Csaba

    Journal of neuroscience methods

    2012  Volume 205, Issue 1, Page(s) 130–138

    Abstract: We have recently reported that in the learned helplessness model of depression, the less hippocampal spine synapses rats have, the more helpless they become. It remains unclear, however, whether the observed synaptic changes are associated with the loss ... ...

    Abstract We have recently reported that in the learned helplessness model of depression, the less hippocampal spine synapses rats have, the more helpless they become. It remains unclear, however, whether the observed synaptic changes are associated with the loss of CA1 pyramidal cells. Cell bodies in the CA1 pyramidal layer are very densely packed, making cell counting difficult in this hippocampal subregion. To address this issue, we developed a new approach that (1) yields excellent preservation of the three-dimensional tissue structure; (2) utilizes osmium tetroxide to unambiguously label nucleoli; and (3) facilitates and accelerates unbiased, reliable counting of densely packed cell bodies. Our method provides an improved tool for studies aiming to evaluate hippocampal atrophy and cell loss, the most characteristic features in many neurodegenerative diseases, such as Alzheimer's disease, temporal lobe epilepsy and ischemia, as well as in several psychiatric disorders. Using this new method, we demonstrated no significant changes in the number of CA1 pyramidal cells in the rat learned helplessness paradigm. In addition, volumes of the CA1 pyramidal cell layer and the entire CA1 subfield remained unchanged among treatment groups. We conclude that previously observed synaptic alterations in helpless rats are not associated with CA1 pyramidal cell loss. This finding suggests that behavioral outcome in the learned helplessness paradigm is related to plastic events at the synaptic level, rather than at the level of principal cells.
    MeSH term(s) Algorithms ; Animals ; CA1 Region, Hippocampal/cytology ; Calbindins ; Cell Count/methods ; Electroshock ; Epoxy Resins ; Helplessness, Learned ; Immunohistochemistry ; Male ; Microscopy, Electron ; Osmium Tetroxide ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein G/metabolism ; Tissue Embedding ; Tissue Fixation
    Chemical Substances Calbindins ; Epoxy Resins ; S100 Calcium Binding Protein G ; Durcupan ACM (37187-52-3) ; Osmium Tetroxide (P40W033BGM)
    Language English
    Publishing date 2012-03-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 282721-9
    ISSN 1872-678X ; 0165-0270
    ISSN (online) 1872-678X
    ISSN 0165-0270
    DOI 10.1016/j.jneumeth.2011.12.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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