Adult hippocampal neurogenesis and antidepressants effects

Planchez, Barbara; Surget, Alexandre; Belzung, Catherine

doi:10.1016/j.coph.2019.11.009

Cited by 48 publications

(34 citation statements)

References 57 publications

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“…These findings suggest that PEA could modulate the overall synaptic function and influence neuronal activity and cellular mechanisms underlying depression and memory formation, possibly improving LTP, dendritic spine remodelling, associated with improved cognitive tasks affected by HFD. It should be noted that neuronal projections extending from the CA1 region of the hippocampus to the PFC are involved in aspects of cognition related to executive function and emotional regulation and potentially crucial elements in the pathophysiology of several neuropsychiatric diseases, including depression (Planchez, Surget, & Belzung, 2019).…”

Section: Discussionmentioning

confidence: 99%

Palmitoylethanolamide counteracts brain fog improving depressive‐like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis

Lama

Pirozzi

Annunziata

et al. 2020

British J Pharmacology

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Background and Purpose High‐fat diet (HFD)‐induced obesity is accompanied by metabolic and neurochemical changes that have been associated with depression. Recent studies indicate that palmitoylethanolamide (PEA) exerts metabolic effects and holds neuroprotective potential. However, studies on HFD exposure in mice which investigate the effects of PEA on monoamine system and synaptic plasticity are limited. Experimental Approach In C57Bl/6J male mice, obesity was established by HFD feeding for 12 weeks. Then, mice were treated with ultra‐micronized PEA (30 mg·kg−1 daily p.o.) or vehicle for 7 weeks along with HFD. Mice receiving chow diet and vehicle served as controls. Thereafter, depressive‐, anhedonic‐like behaviour and cognitive performance were measured. Monoamine analyses were performed on brain areas (nucleus accumbens, Nac; prefrontal cortex, PFC; hippocampus), and markers of synaptic plasticity and neurogenesis were evaluated in hippocampus. Key Results PEA limited depressive‐ and anhedonic‐like behaviour, and cognitive deficits induced by HFD. PEA induced an increase in 5‐HT levels in PFC, and a reduction of dopamine and 5‐HT turnover in Nac and PFC, respectively. Moreover, PEA increased dopamine levels in the hippocampus and PFC. At a molecular level, PEA restored brain‐derived neurotrophic factor signalling pathway in hippocampus and PFC, indicating an improvement of synaptic plasticity. In particular, PEA counteracted the reduction of glutamatergic synaptic density induced by HFD in the stratum radiatum of the CA1 of the hippocampus, where it also exhibited neurogenesis‐promoting abilities. Conclusion and Implications PEA may represent an adjuvant therapy to limit depressive‐like behaviours and memory deficit, affecting monoamine homeostasis, synaptic plasticity and neurogenesis. LINKED ARTICLES This article is part of a themed issue on Neurochemistry in Japan. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.4/issuetoc

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Section: Discussionmentioning

confidence: 99%

Palmitoylethanolamide counteracts brain fog improving depressive‐like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis

Lama

Pirozzi

Annunziata

et al. 2020

British J Pharmacology

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“…NSC grafting promoted higher levels of normal hippocampal neurogenesis with reduced aberrant neurogenesis even at nine months post-SE. Such effects could facilitate better cognitive and mood function because of the involvement of hippocampal neurogenesis in the formation and/or retrieval of different types of memories [84][85][86][87][88] and mood function [89]. Evidence supporting the involvement of normal neurogenesis in mood function includes observations that neurogenesis deficiency leads to increased depressive-like behavior [90] and selective ablation of neurogenesis blocks behavioral responses to chronic antidepressant treatment [91][92].…”

Section: Prospective Mechanisms Of Better Cognitive and Mood Functionmentioning

confidence: 99%

Hippocampal Neural Stem Cell Grafting after Status Epilepticus Alleviates Chronic Epilepsy and Abnormal Plasticity, and Maintains Better Memory and Mood Function

Hattiangady¹,

Kuruba²,

Shuai³

et al. 2020

Aging and disease

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Hippocampal damage after status epilepticus (SE) leads to multiple epileptogenic changes, which lead to chronic temporal lobe epilepsy (TLE). Morbidities such as spontaneous recurrent seizures (SRS) and memory and mood impairments are seen in a significant fraction of SE survivors despite the administration of antiepileptic drugs after SE. We examined the efficacy of bilateral intra-hippocampal grafting of neural stem/progenitor cells (NSCs) derived from the embryonic day 19 rat hippocampi, six days after SE for restraining SE-induced SRS, memory, and mood impairments in the chronic phase. Grafting of NSCs curtailed the progression of SRS at 3-5 months post-SE and reduced the frequency and severity of SRS activity when examined at eight months post-SE. Reduced SRS activity was also associated with improved memory function. Graft-derived cells migrated into different hippocampal cell layers, differentiated into GABA-ergic interneurons, astrocytes, and oligodendrocytes. Significant percentages of graft-derived cells also expressed beneficial neurotrophic factors such as the fibroblast growth factor-2, brain-derived neurotrophic factor, insulin-like growth factor-1 and glial cell line-derived neurotrophic factor. NSC grafting protected neuropeptide Y-and parvalbumin-positive host interneurons, diminished the abnormal migration of newly born neurons, and rescued the reelin+ interneurons in the dentate gyrus. Besides, grafting led to the maintenance of a higher level of normal neurogenesis in the chronic phase after SE and diminished aberrant mossy fiber sprouting in the dentate gyrus. Thus, intrahippocampal grafting of hippocampal NSCs shortly after SE considerably curbed the progression of epileptogenic processes and SRS, which eventually resulted in less severe chronic epilepsy devoid of significant cognitive and mood impairments.

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“…For years now, there have been controversial links between systemic TH status and the pace of human hippocampal neurogenesis. Adult-onset hypothyroidism, the secondmost common human endocrine disorder, associates with depression, and shares the hallmarks of reduced AHN and decreased hippocampal volume with AD, as well as memory impairments and emotional alterations (Cooke et al, 2014;Planchez et al, 2020). T 4 treatment in (sub)clinical hypothyroid patients reversed underperformance on several cognitive tests specifically designed for assessing hippocampal function (Correia et al, 2009).…”

Section: The Link Between Thyroid Hormone Hippocampal Neurogenesis Amentioning

confidence: 99%

Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury

Vancamp¹,

Butruille²,

Demeneix³

et al. 2020

Front. Neurosci.

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Neurodegenerative diseases are characterized by chronic neuronal and/or glial cell loss, while traumatic injury is often accompanied by the acute loss of both. Multipotent neural stem cells (NSCs) in the adult mammalian brain spontaneously proliferate, forming neuronal and glial progenitors that migrate toward lesion sites upon injury. However, they fail to replace neurons and glial cells due to molecular inhibition and the lack of pro-regenerative cues. A major challenge in regenerative biology therefore is to unveil signaling pathways that could override molecular brakes and boost endogenous repair. In physiological conditions, thyroid hormone (TH) acts on NSC commitment in the subventricular zone, and the subgranular zone, the two largest NSC niches in mammals, including humans. Here, we discuss whether TH could have beneficial actions in various pathological contexts too, by evaluating recent data obtained in mammalian models of multiple sclerosis (MS; loss of oligodendroglial cells), Alzheimer's disease (loss of neuronal cells), stroke and spinal cord injury (neuroglial cell loss). So far, TH has shown promising effects as a stimulator of remyelination in MS models, while its role in NSC-mediated repair in other diseases remains elusive. Disentangling the spatiotemporal aspects of the injury-driven repair response as well as the molecular and cellular mechanisms by which TH acts, could unveil new ways to further exploit its proregenerative potential, while TH (ant)agonists with cell type-specific action could provide safer and more target-directed approaches that translate easier to clinical settings.

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Adult hippocampal neurogenesis and antidepressants effects

Cited by 48 publications

References 57 publications

Palmitoylethanolamide counteracts brain fog improving depressive‐like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis

Palmitoylethanolamide counteracts brain fog improving depressive‐like behaviour in obese mice: Possible role of synaptic plasticity and neurogenesis

Hippocampal Neural Stem Cell Grafting after Status Epilepticus Alleviates Chronic Epilepsy and Abnormal Plasticity, and Maintains Better Memory and Mood Function

Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury

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