NGF Eye Administration Recovers the TrkB and Glutamate/GABA Marker Deficit in the Adult Visual Cortex Following Optic Nerve Crush

被引:11
作者
Rosso, Pamela [1 ]
Fico, Elena [1 ]
Mesentier-Louro, Louise A. [2 ]
Triaca, Viviana [1 ]
Lambiase, Alessandro [3 ]
Rama, Paolo [4 ]
Tirassa, Paola [1 ]
机构
[1] Natl Res Council CNR Italy, Unit Translat & Biomol Med Rita Levi Montalcini, Viale Univ 33, I-00185 Rome, Italy
[2] Stanford Univ, Sch Med, Dept Ophthalmol, Stanford, CA 94305 USA
[3] Univ Sapienza Rome, Dept Sense Organs, Viale Policlin 155, I-00161 Rome, Italy
[4] Hosp San Raffaele, Cornea & Ocular Surface Unit, Eye Repair Lab, Via Olgettina 60, I-20132 Milan, Italy
关键词
BDNF; neurotrophins; optic nerve crush (ONC); synaptic transmission; rat visual cortex (VCx); GABA; glutamate; GROWTH-FACTOR; CORTICAL MAPS; AREA; 17; C-FOS; PLASTICITY; BRAIN; RAT; REORGANIZATION; LESIONS; ACTIVATION;
D O I
10.3390/ijms221810014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Eye-drop recombinant human nerve growth factor (ed-rhNGF) has proved to recover the retina and optic nerve damage in animal models, including the unilateral optic nerve crush (ONC), and to improve visual acuity in humans. These data, associated with evidence that ed-rhNGF stimulates the brain derived neurotrophic factor (BDNF) in retina and cortex, suggests that NGF might exert retino-fugal effects by affecting BDNF and its receptor TrkB. To address these questions, their expression and relationship with the GABAergic and glutamatergic transmission markers, GAD65 and GAD67, vesicular inhibitory amino acid transporter (VGAT), and vesicular glutamate transporters 1 and 2 (VGLUT-1 and VGLUT-2) were investigated in adult ONC rats contralateral and ipsilateral visual cortex (VCx). Ed-rhNGF recovers the ONC-induced alteration of GABAergic and glutamatergic markers in contralateral VCx, induces an upregulation of TrkB, which is positively correlated with BDNF precursor (proBDNF) decrease in both VCx sides, and strongly enhances TrkB+ cell soma and neuronal endings surrounded by GAD65 immuno-reactive afferents. These findings contribute to enlarging the knowledge on the mechanism of actions and cellular targets of exogenously administrated NGF, and suggest that ed-rhNGF might act by potentiating the activity-dependent TrkB expression in GAD+ cells in VCx following retina damage and/or ONC.
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页数:15
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