Altered trkB neurotrophin receptor activation does not influence the N-methyl-d-aspartate receptor antagonist-mediated neurotoxicity in mouse posterior cingulate cortex

Väisänen, Jussi; Saarelainen, Tommi; Koponen, Eija; Ċastrén, Eero

doi:10.1016/s0304-3940(03)00744-4

Cited by 5 publications

(2 citation statements)

References 16 publications

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“…For these reasons, individuals who are 50 years old may start to experience manifestations of imbalance5 and body instability 6. Therefore, simple activities like standing up or rising from a chair may become limited or even dangerous, because they are dependent on both gait and balance 2…”

Section: Introductionmentioning

confidence: 99%

Functional mobility and balance in community-dwelling elderly submitted to multisensory versus strength exercises

Alfieri¹

2010

CIA

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It is well documented that aging impairs balance and functional mobility. The objective of this study was to compare the efficacy of multisensory versus strength exercises on these parameters. We performed a simple blinded randomized controlled trial with 46 community-dwelling elderly allocated to strength ([GST], N = 23, 70.2-years-old ± 4.8 years) or multisensory ([GMS], N = 23, 68.8-years-old ± 5.9 years) exercises twice a week for 12 weeks. Subjects were evaluated by blinded raters using the timed ‘up and go’ test (TUG), the Guralnik test battery, and a force platform. By the end of the treatment, the GMS group showed a significant improvement in TUG (9.1 ± 1.9 seconds (s) to 8.0 ± 1.0 s, P = 0.002); Guralnik test battery (10.6 ± 1.2 to 11.3 ± 0.8 P = 0.009); lateromedial (6.1 ± 11.7 cm to 3.1 ± 1.6 cm, P = 0.02) and anteroposterior displacement (4.7 ± 4.2 cm to 3.4 ± 1.0 cm, P = 0.03), which were not observed in the GST group. These results reproduce previous findings in the literature and mean that the stimulus to sensibility results in better achievements for the control of balance and dynamic activities. Multisensory exercises were shown to be more efficacious than strength exercises to improve functional mobility.

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Section: Introductionmentioning

confidence: 99%

Functional mobility and balance in community-dwelling elderly submitted to multisensory versus strength exercises

Alfieri¹

2010

CIA

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“…BDNF has also been shown to prevent MK801-induced death in cultured cortical neurons, though the precise mechanisms were not investigated (Hansen et al, 2004). However, using HSP-70 expression as an indicator of toxicity, it was reported that activation of the BDNF receptor, TrkB, had no influence on MK-801-induced neurotoxicity in the posterior cingulate cortex of mouse brain (Väisänen et al, 2003). This inconsistency prompted us to investigate the effect of BDNF on PCP-induced neuronal death in organotypic corticostriatal cultures, using caspase-3 activation and DNA fragmentation as two indices for neuronal apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Brain-derived neurotrophic factor prevents phencyclidine-induced apoptosis in developing brain by parallel activation of both the ERK and PI-3K/Akt pathways

et al. 2010

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SummaryPhencyclidine is an N-methyl D-aspartate receptor (NMDAR) blocker that has been reported to induce neuronal apoptosis during development and schizophrenia-like behaviors in rats later in life. Brain derived neurotrophic factor (BDNF) has been shown to prevent neuronal death caused by NMDAR blockade, but the precise mechanism is unknown. This study examined the role of the phosphatidylinositol-3 kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) pathways in BDNF protection of PCP-induced apoptosis in corticostriatal organotypic cultures. It was observed that BDNF inhibited PCP-induced apoptosis in a concentration dependent fashion. BDNF effectively prevented PCP-induced inhibition of the ERK and PI-3K/Akt pathways and suppressed GSK-3β activation. Blockade of either PI-3K/Akt or ERK activation abolished BDNF protection. Western blot analysis revealed that the PI-3K inhibitor LY294002 prevented the stimulating effect of BDNF on the PI-3K/Akt pathway, but had no effect on the ERK pathway. Similarly, the ERK inhibitor PD98059 prevented the stimulating effect of BDNF on the ERK pathway, but not the PI-3K/Akt pathway. Co-application of LY294002 and PD98059 had no additional effect on BDNF-evoked activation of Akt or ERK. However, concurrent exposure to PD98059 and LY294002 caused much greater inhibition of BDNF-evoked phosphorylation of GSK-3β at serine 9 than did LY294002 alone. Finally, either BDNF or GSK-3β inhibition prevented PCP-induced suppression of cyclic-AMP response element binding protein (CREB) phosphorylation. These data demonstrate that the protective effect of BDNF against PCP-induced apoptosis is mediated by parallel activation of the PI-3K/Akt and ERK pathways, most likely involves inhibition of GSK-3β and activation of CREB. KeywordsPCP (phencyclidine); NMDAR (N-methyl-D-aspartate receptor); BDNF (brain-derived neurotrophic factor); PI-3K (phosphoinositide-3 kinase); ERK (extracellular signal-regulated kinase); GSK-3β (Glycogen Synthase Kinase 3 β);

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Neurotrophins and Psychiatric Disorders

Ċastrén

2014

Neurotrophic Factors

123

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Increasing number of studies has during the last decade linked neurotrophic factors with the pathophysiology of neuropsychiatric disorders and with the mechanisms of action of drugs used for the treatment of these disorders. In particular, brain-derived neurotrophic factor BDNF and its receptor TrkB have been connected with the pathophysiology in mood disorders, and there is strong evidence that BDNF signaling is critically involved in the recovery from depression with both pharmacological and psychological means. Neurotrophins play a central role in neuronal plasticity and network connectivity in developing adult brain, and recent evidence links plasticity and network rewiring with mood disorders and their treatment. Therefore, neurotrophins should not be seen as happiness factors but as critical tools in the process where brain networks are optimally tuned to environment, and it is against this background that the effects of neurotrophins on neuropsychiatric disorders should be looked at.

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Altered trkB neurotrophin receptor activation does not influence the N-methyl-d-aspartate receptor antagonist-mediated neurotoxicity in mouse posterior cingulate cortex

Cited by 5 publications

References 16 publications

Functional mobility and balance in community-dwelling elderly submitted to multisensory versus strength exercises

Functional mobility and balance in community-dwelling elderly submitted to multisensory versus strength exercises

Brain-derived neurotrophic factor prevents phencyclidine-induced apoptosis in developing brain by parallel activation of both the ERK and PI-3K/Akt pathways

Neurotrophins and Psychiatric Disorders

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