Modulation of adult-born neurons in the inflamed hippocampus

Abstract

Throughout life new neurons are continuously added to the hippocampal circuitry involved with spatial learning and memory. These new cells originate from neural precursors in the subgranular zone of the dentate gyrus, migrate into the granule cell layer, and integrate into neural networks encoding spatial and contextual information. This process can be influenced by several environmental and endogenous factors and is modified in different animal models of neurological disorders. Neuroinflammation, as defined by the presence of activated microglia, is a common key factor to the progression of neurological disorders. Analysis of the literature shows that microglial activation impacts not only the production, but also the migration and the recruitment of new neurons. The impact of microglia on adult-born neurons appears much more multifaceted than ever envisioned before, combining both supportive and detrimental effects that are dependent upon the activation phenotype and the factors being released. The development of strategies aimed to change microglia toward states that promote functional neurogenesis could therefore offer novel therapeutic opportunities against neurological disorders associated with cognitive deficits and neuroinflammation. The present review summarizes the current knowledge on how production, distribution, and recruitment of new neurons into behaviorally relevant neural networks are modified in the inflamed hippocampus.

Systemic lipopolysaccharide administration impairs retrieval of context–object discrimination, but not spatial, memory: Evidence for selective disruption of specific hippocampus-dependent memory functions during acute neuroinflammation

“…In this regard, we were able to specifically test whether acute neuroinflammation affects recognizing a familiar object vs. retrieving a context-object association. Consistent with previous reports, systemic LPS administration 6 h prior to testing did not affect NOR (Hauss-Wegrzyniak et al, 2000; Belarbi and Rosi, 2013). However, there have also been reports that acute LPS administration, whether i.p.…”

Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus

“…Classic activation of microglia was reported to suppress neurogenesis by expressing pro-inflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor a, while with alternative activation, microglia release anti-inflammatory cytokines (i.e., IL-4, IGF-1 and transforming growth factor b), and promote neurogenesis). 44 In our case, subtype identification of microglia was not performed, whereas the elevated microglia proportion in the hilus is likely one of the mechanisms regulating neurogenesis, although no clear clue refers whether they are supportive or detrimental to neurogenesis.…”

Robust increase of microglia proliferation in the fornix of hippocampal axonal pathway after a single LPS stimulation

“…MBP is important in the process of myelination of nerves in the nervous system and its decline is associated with disorder of oligodendrocytic myelin sheath. Thus, detectable cellular damages were not detected by a single administration of 1 mg/kg LPS, but activated microglia produce pivotal factors to eliminate pathogens and toxic factors as well as apoptotic cell debris to maintain tissue homeostasis (Lalancette-Hébert et al, 2007;Belarbi and Rosi, 2013). Preconditioning of peripheral administration of 0.05-1.0 mg/kg LPS can cause transient neuroprotective responses against ischemia, stroke, and more destructive LPS treatments (Kitamura et al, 2004;Glezer et al, 2007;Imai et al, 2007;Shpargel et al, 2008).…”