Hippocampal spine changes across the sleep-wake cycle: corticosterone and kinases

Ikeda, Motoko; Hojo, Yasushi; Komatsuzaki, Yoshimasa; Okamoto, Masahiro; Kato, Asami; Takeda, Taishi; Kawato, Suguru

doi:10.1530/endoabs.44.ja2

Cited by 3 publications

(6 citation statements)

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“…LIMK and cofilin are good candidates for signal proteins in the neurosteroid‐induced actin reassembly leading to spinogenesis via the pathway: LIMK → phosphorylation of cofilin → actin polymerisation → spine increase . In addition to cofilin, MAPK and cortactin cascade may couple with PKA and PKC via the pathway of PKC → Raf1 → MAPK, PKA → B‐Raf → MAPK → phosphorylation of cortactin → actin polymerisation → spine increase.…”

Section: Mechanisms Of the Rapid Spine Increase Depending On Protein mentioning

confidence: 99%

“…Although rapid E 2 effects (in vitro and in vivo) have been extensively studied and well clarified, the rapid effects of androgens and stress steroids need much more investigation to enable a deeper understanding of the common or differing molecular mechanisms of these neurosteroidal actions. As one additional example of the CORT effect, circadian cycle‐dependent oscillation of CORT (3‐30 nmol L ‐1 ) induced the cyclic rise and fall of spine density and these changes were a result of kinase‐dependent signalling, including MAPK, LIMK, PKA and PKC …”

Section: Summary and Future Directionsmentioning

confidence: 99%

“…As one additional example of the CORT effect, circadian cycle-dependent oscillation of CORT (3-30 nmol L -1 ) induced the cyclic rise and fall of spine density and these changes were a result of kinase-dependent signalling, including MAPK, LIMK, PKA and PKC. 48 The interactions between rapid/nongenomic signalling and slow/ genomic signalling via classic steroid receptors comprise another interesting topic for investigation. 12…”

Section: Summary and Future Directionsmentioning

confidence: 99%

“…The involvement of many kinases was demonstrated, including LIMK, extracellular signal-regulated kinase (Erk) MAPK, p38 MAPK, PKA, PKC and PI3K, in the rapid spinogenesis induced by neurosteroids, such as androgen, oestrogen and corticosteroid in the hippocampal CA1 region 5,10,15,30. LIMK and cofilin are good candidates for signal proteins in the neurosteroid-induced actin reassembly leading to spinogenesis via the pathway: LIMK → phosphorylation of cofilin → actin polymerisation → spine increase 15,[47][48][49]. In addition to cofilin, MAPK and cort-actin cascade may couple with PKA and PKC via the pathway of PKC → Raf1 → MAPK, PKA → B-Raf → MAPK → phosphorylation of cortactin → actin polymerisation → spine increase.…”

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confidence: 99%

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Rapid nongenomic modulation by neurosteroids of dendritic spines in the hippocampus: Androgen, oestrogen and corticosteroid

Murakami

Hojo

Kato

et al. 2018

J Neuroendocrinology

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Memories are stored in synapses that consist of axon terminals and dendritic spines.Dendritic spines are postsynaptic structures of synapses and are essential for synaptic plasticity and cognition. Therefore, extensive investigations concerning the functions and structures of spines have been performed. Sex steroids and stress steroids have been shown to modulate hippocampal synapses. Although the rapid modulatory action of sex steroids on synapses has been studied in hippocampal neurones over several decades, the essential molecular mechanisms have not been fully understood.Here, a description of kinase-dependent signalling mechanisms is provided that can explain the rapid nongenomic modulation of dendritic spinogenesis in rat and mouse hippocampal slices by the application of sex steroids, including dihydrotestosterone, testosterone, oestradiol and progesterone. We also indicate the role of synaptic (classic) sex steroid receptors that trigger these rapid synaptic modulations. Moreover, we describe rapid nongenomic spine modulation by applying corticosterone, which is an acute stress model of the hippocampus. The explanations for the results obtained are mainly based on the optical imaging of dendritic spines. Comparisons are also performed with results obtained from other types of imaging, including electron microscopic imaging. Relationships between spine modulation and modulation of cognition are discussed. We recognise that most of rapid effects of exogenously applied oestrogen and androgen were observed in steroid-depleted conditions, including acute slices of the hippocampus, castrated male animals and ovariectomised female animals. Therefore, the previously observed effects can be considered as a type of recovery event, which may be essentially similar to hormone replacement therapy under hormone-decreased conditions. On the other hand, in gonadally intact young animals with high levels of endogenous sex hormones, further supplementation of sex hormones might not be effective, whereas the infusion of blockers for steroid receptors or kinases may be effective, with respect to suppressing sex hormone functions, thus providing useful information regarding molecular mechanisms. K E Y W O R D Sandrogens, cortisol/corticosterone, glucocorticoids, membrane/nuclear receptors, neuroactive steroids, oestrogens, steroids

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Section: Mechanisms Of the Rapid Spine Increase Depending On Protein mentioning

confidence: 99%

Section: Summary and Future Directionsmentioning

confidence: 99%

Section: Summary and Future Directionsmentioning

confidence: 99%

mentioning

confidence: 99%

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Rapid nongenomic modulation by neurosteroids of dendritic spines in the hippocampus: Androgen, oestrogen and corticosteroid

Murakami

Hojo

Kato

et al. 2018

J Neuroendocrinology

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“…Studies utilizing other methods of repeated B administration that likely enhance circadian peaks of B have also observed similar effects on structural plasticity (Liu and Aghajanian, 2008;Liston and Gan, 2011;Gourley et al, 2013;Swanson et al, 2013), although information is not yet forthcoming regarding the precise morphological differences in spine volume and subtype under these varying regimens of glucocorticoid treatment. Several recent studies have linked glucocorticoid circadian rhythmicity to natural variations in spine formation and elimination (i.e., in somatosensory cortex and hippocampus) (Liston et al, 2013;Ikeda et al, 2015). In two other reports, disruption of the circadian photoperiod induced regressive structural changes in hippocampal and mPFC, along with corresponding cognitive impairments (Pyter et al, 2005;Karatsoreos et al, 2011).…”

Section: Role Of Disruptions In the Adrenocortical Rhythmmentioning

confidence: 99%

Prolonged corticosterone exposure induces dendritic spine remodeling and attrition in the rat medial prefrontal cortex

et al. 2016

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The stress-responsive hypothalamo-pituitary-adrenal (HPA) axis plays a central role in promoting adaptations acutely, while adverse effects on physiology and behavior following chronic challenges may result from over-activity of this system. Elevations in glucocorticoids, the endproducts of HPA activation, play roles in adaptive and maladaptive processes by targeting cognate receptors throughout neurons in limbic cortical networks to alter synaptic functioning. Since previous work has shown that chronic stress leads to functionally relevant regressive alterations in dendritic spine shape and number in pyramidal neurons in medial prefrontal cortex (mPFC), here we examine the capacity of sustained increases in circulating corticosterone alone to alter dendritic spine morphology and density in this region. Rats were implanted with subcutaneous corticosterone pellets to provide continuous exposure to levels approximating the circadian mean or peak of the steroid for 1, 2, or 3 weeks. Pyramidal neurons in prelimbic area of mPFC were selected for intracellular fluorescent dye-filling, followed by high-resolution 3D imaging and analysis of dendritic arborization and spine morphometry. Two or more weeks of corticosterone exposure decreased dendritic spine volume in mPFC, whereas higher dose exposure of the steroid resulted in apical dendritic retraction and spine loss in the same cell population, with thin spine subtypes showing the greatest degree of attrition. Finally, these structural alterations were noted to persist following a 3-week washout period and corresponding restoration of circadian HPA rhythmicity. These studies suggest that prolonged disruptions in adrenocortical functioning may be sufficient to induce enduring regressive structural and functional alterations in mPFC. Graphical abstractUsing high-resolution confocal laser-scanning microscopy, the authors show that prolonged elevations in corticosterone induce persistent alterations in dendritic spine morphology and decreased density in rat medial prefrontal cortex. This darkfield image shows layer 2/3 prefrontal pyramidal neurons selected for intracellular dye-filling with Lucifer Yellow (cyan).

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Prolonged corticosterone exposure induces dendritic spine remodeling and attrition in the rat medial prefrontal cortex

Anderson

Glanz

Johnson

et al. 2016

J of Comparative Neurology

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The stress-responsive hypothalamo-pituitary-adrenal (HPA) axis plays a central role in promoting adaptations acutely, while adverse effects on physiology and behavior following chronic challenges may result from over-activity of this system. Elevations in glucocorticoids, the end-products of HPA activation, play roles in adaptive and maladaptive processes by targeting cognate receptors throughout neurons in limbic cortical networks to alter synaptic functioning. Since previous work has shown that chronic stress leads to functionally relevant regressive alterations in dendritic spine shape and number in pyramidal neurons in medial prefrontal cortex (mPFC), here we examine the capacity of sustained increases in circulating corticosterone alone to alter dendritic spine morphology and density in this region. Rats were implanted with subcutaneous corticosterone pellets to provide continuous exposure to levels approximating the circadian mean or peak of the steroid for 1, 2, or 3 weeks. Pyramidal neurons in prelimbic area of mPFC were selected for intracellular fluorescent dye-filling, followed by high-resolution 3D imaging and analysis of dendritic arborization and spine morphometry. Two or more weeks of corticosterone exposure decreased dendritic spine volume in mPFC, whereas higher dose exposure of the steroid resulted in apical dendritic retraction and spine loss in the same cell population, with thin spine subtypes showing the greatest degree of attrition. Finally, these structural alterations were noted to persist following a 3-week washout period and corresponding restoration of circadian HPA rhythmicity. These studies suggest that prolonged disruptions in adrenocortical functioning may be sufficient to induce enduring regressive structural and functional alterations in mPFC.

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Hippocampal spine changes across the sleep-wake cycle: corticosterone and kinases

Cited by 3 publications

References 0 publications

Rapid nongenomic modulation by neurosteroids of dendritic spines in the hippocampus: Androgen, oestrogen and corticosteroid

Rapid nongenomic modulation by neurosteroids of dendritic spines in the hippocampus: Androgen, oestrogen and corticosteroid

Prolonged corticosterone exposure induces dendritic spine remodeling and attrition in the rat medial prefrontal cortex

Prolonged corticosterone exposure induces dendritic spine remodeling and attrition in the rat medial prefrontal cortex

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