Research update for articles published in<scp>EJCI</scp>in 2013

Abbate, Rosanna; Al-Daghri, Nasser M.; Andreozzi, Paolo; Borregaard, Niels; Can, Günay; Caridi, Gianluca; Carstensen‐Kirberg, Maren; Cioni, Gabriele; Conte, Enrico; Cuomo, Rosario; Denis, Marie Armelle; Fakhfouri, Gohar; Fiasse, Renné; Glenthøj, Andreas; Goliasch, Georg; Gremmel, Thomas; Herder, Christian; Iemmolo, Maria; Jing, Zhi‐Cheng; Krause, Robert; Marrone, Oreste; Miazgowski, Bartosz; Miazgowski, Tomasz; Minchiotti, Lorenzo; Mousavizadeh, Kazem; Ndrepepa, Gjin; Niessner, Alexander; Luque, Cristina Ogayar; Onat, Altan; Papassotiriou, Ioannis; Ortiz, Martín Ruiz; Sabico, Shaun; Schooling, CM; Sakka, Sophia; Sołtysiak, Paweł; Visseren, Frank L.J.; Wagner, Jasmin; Wang, Xiaojian; Westerink, Jan

doi:10.1111/eci.12512

Cited by 1 publication

(1 citation statement)

References 94 publications

(119 reference statements)

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“…Adjacent free-floating sections from mice in each group were taken for single-and double-label immunohistochemistry as previously described (Abbate et al, 2015;Chen et al, 2017). EGFP transgene expression was enhanced using an antibody to green fluorescence protein (GFP) (rabbit anti-GFP, 1:5000, CAT#: AB290, AbCam ® , UK Abcam, Cambridge, UK).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Delayed citalopram administration reduces brain inflammation and enhances skilled motor function after ischaemic stroke in ‘MacGreen’ mice

Chen

McGregor

2022

Eur J of Neuroscience

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Recent evidence suggests that treatment with antidepressants may promote functional recovery. However, the timeframe in which these pharmacological agents can influence stroke recovery is not well understood. This research investigated whether delayed administration of citalopram, used clinically in the management of post-stroke depression, could improve long-term functional recovery following experimental stroke. MacGreen mice carrying an enhanced green fluorescent protein reporter gene in monocyte and macrophage populations were subjected to 45 min occlusion of the middle cerebral artery. Animals were administered citalopram (10 mg/kg/day, n = 20) or saline (n = 20) starting 3 days after stroke for 28 days. Neurological deficits and skilled motor performance in the staircase task were recorded for 9 weeks post stroke. Grey and white matter structural lesions were quantified at Week 9, and enhanced green fluorescent protein immunohistochemistry was used to evaluate the effect of citalopram on inflammation. Twenty-five animals were included in the final analysis. Citalopram-treated animals (n = 13) showed a significant increase in impaired forepaw use in the staircase task compared with saline-treated animals (n = 12) 2, 3 and 7 weeks post stroke but no difference in neurological score at any time point examined. Citalopram treatment was associated with decreased monocyte/macrophage cell density and increased white matter tract integrity within the ipsilateral cortex. In conclusion, delayed administration of citalopram decreased brain inflammation and produced functional gains in our mouse model of stroke. Beneficial effects on skilled motor functions were long-lasting.

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Section: Immunohistochemistrymentioning

confidence: 99%