Hippocampal Neurogenesis

Catlow, Briony J.; Jalloh, Ahmad; Sanchez‐Ramos, Juan

doi:10.1016/b978-0-12-800212-4.00077-7

Cited by 14 publications

(5 citation statements)

References 63 publications

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“…In another study by the same group, mice were administered onceweekly doses of psilocybin for 4 weeks; they showed that compared with administration of saline, chronic administration of psilocybin (1.5 mg/kg) led to a significantly increased number of BrdU-positive cells. [45] Our DCX and BrdU immunofluorescence staining results further supported the hypothesis that the promotion of hippocampal neuroplasticity may be the mechanism underlying psilocybin-induced facilitation of fear extinction. Malberg et al [46] showed that cell proliferation in the adult hippocampus is decreased by an inescapable stress, ie, foot shock.…”

Section: Discussionsupporting

confidence: 78%

Psilocybin facilitates fear extinction in mice by promoting hippocampal neuroplasticity

Zhao

et al. 2023

Chinese Medical Journal

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Background: Posttraumatic stress disorder (PTSD) and depression are highly comorbid. Psilocybin exerts substantial therapeutic effects on depression by promoting neuroplasticity. Fear extinction is a key process in the mechanism of first-line exposurebased therapies for PTSD. We hypothesized that psilocybin would facilitate fear extinction by promoting hippocampal neuroplasticity. Methods: First, we assessed the effects of psilocybin on percentage of freezing time in an auditory cued fear conditioning (FC) and fear extinction paradigm in mice. Psilocybin was administered 30 min before extinction training. Fear extinction testing was performed on the first day; fear extinction retrieval and fear renewal were tested on the sixth and seventh days, respectively. Furthermore, we verified the effect of psilocybin on hippocampal neuroplasticity using Golgi staining for the dendritic complexity and spine density, Western blotting for the protein levels of brain derived neurotrophic factor (BDNF) and mechanistic target of rapamycin (mTOR), and immunofluorescence staining for the numbers of doublecortin (DCX)-and bromodeoxyuridine (BrdU)-positive cells. Results: A single dose of psilocybin (2.5 mg/kg, i.p.) reduced the increase in the percentage of freezing time induced by FC at 24 h, 6th day and 7th day after administration. In terms of structural neuroplasticity, psilocybin rescued the decrease in hippocampal dendritic complexity and spine density induced by FC; in terms of neuroplasticity related proteins, psilocybin rescued the decrease in the protein levels of hippocampal BDNF and mTOR induced by FC; in terms of neurogenesis, psilocybin rescued the decrease in the numbers of DCX-and BrdU-positive cells in the hippocampal dentate gyrus induced by FC. Conclusions: A single dose of psilocybin facilitated rapid and sustained fear extinction; this effect might be partially mediated by the promotion of hippocampal neuroplasticity. This study indicates that psilocybin may be a useful adjunct to exposurebased therapies for PTSD and other mental disorders characterized by failure of fear extinction.

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Section: Discussionsupporting

confidence: 78%

Psilocybin facilitates fear extinction in mice by promoting hippocampal neuroplasticity

Zhao

et al. 2023

Chinese Medical Journal

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“…However, its outstanding sensitivity and rapid activation of host immune responses provide a severe limitation when using cell therapy based on brain grafts or transplants (Hoornaert et al, 2017). Therefore, the observed decrease in the CD80 protein expression after psilocin and DMT treatment, together with their reported activity towards induction of neurogenesis and neuroplasticity, is promising (Catlow et al, 2016; Ly et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

The DMT and Psilocin Treatment Changes CD11b+ Activated Microglia Immunological Phenotype

Kozlowska

Klimczak

Wiatr

et al. 2021

Preprint

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Psychedelics are new, promising candidate molecules for clinical use in psychiatric disorders such as Treatment-Resistant Depression (TRD) and Post Traumatic Stress Disorder (PTSD). They were recently also proposed as molecules supporting neural tissue repair by anti-inflammatory properties. Here we reported that two classic psychedelics, DMT and psilocin, can influence microglial functions by reducing the level of TLR4, p65, CD80 proteins, which are markers of the immune response, and upregulat TREM2 neuroprotective receptor. Psilocin also secured neuronal survival in the neuron-microglia co-culture model by attenuating the phagocytic function of microglia. We conclude that DMT and psilocin regulate the immunomodulatory potential of microglia. Of note, psychedelics were previously reported as a relatively safe treatment approach. The demonstrated regulation of inflammatory molecules and microglia phagocytosis suggests that psychedelics or their analogs are candidates in the therapy of neurological disorders where microglia and inflammation significantly contribute to pathogenic disease mechanisms.

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“…Exercise relieves stress and anxiety and thus augments mental and physical health 3,11 (2008) demonstrated that treadmill running increases the BDNF level 1 . BDNF signaling is probably the key mechanism for triggering brain neuroplasticity 16,17 and anti-apoptotic cell death that leads to the improvement of cognitive function 4,16 .…”

Section: Discussionmentioning

confidence: 99%

Swimming Improves Memory Function and Decreases N-Methyl-D-Aspartate in Ageing Rats

Hanik Badriyah Hidayati,

Purwo Sri Rejeki,

Lilik Herawati

et al. 2021

Indian Journal of Forensic Medicine & Toxicology

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A single Memory impairment substantially reduces the quality of life in the elderly. It is associated with the alteration of neurotrophic (NT) factors, such as brain-derived neurotrophic factor (BDNF) and glutamate receptor N-methyl-D-aspartate (NMDA). Exercise is often used to reduce cognitive impairment. Previous studies show that the benefits of aerobic exercises on such impairments are correlated with increasing BDNF and preventing the production of NMDA. However, some results remain controversial. Thus, the association between exercise and Memory was addressed by examining increases in BDNF and the reduction of NMDA in ageing rats. The study used a randomized, post-test-only controlled group of 30 male one-year-old ageing Rattus norvegicus divided into three groups, namely, K0 (control) and K1 and K2 (aerobic swimming exercise). K1 and K2 animals differed in the frequency of exercise, which is three and four sessions per week, respectively. Memory was assessed using Y-maze performance. BDNF and NMDA were analyzed using enzyme-linked immunosorbent assays. A significant improvement in memory function and reduction in the NMDA level were observed in K1 and K2 group rats (p = 0.001; p = 0.041). No significant impact on the BDNF levels was observed (p = 0.387). Swimming may boost Memory by reducing the NMDA level but not by increasing BDNF. Swimming is a promising method for preventing or delaying memory loss in degenerative brain diseases. Further investigation is needed to fully understand underlying mechanisms.

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Hippocampal Neurogenesis

Cited by 14 publications

References 63 publications

Psilocybin facilitates fear extinction in mice by promoting hippocampal neuroplasticity

Psilocybin facilitates fear extinction in mice by promoting hippocampal neuroplasticity

The DMT and Psilocin Treatment Changes CD11b+ Activated Microglia Immunological Phenotype

Swimming Improves Memory Function and Decreases N-Methyl-D-Aspartate in Ageing Rats

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