March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
The effect of Brimonidine Tartarate on Circulating Retinal Spreading Depression
Author Affiliations & Notes
  • Nassim S. Calixto, Sr.
    Hospital São Geraldo, Federal Univ of Minas Gerais, Belo Horizonte, Brazil
  • Vinicius V. Oliveira
    Institute of Biophysics Carlos Chagas Filho and Department of Ophthalmology,
    Federal Univ of Rio de Janeiro, Rio de Janeiro, Brazil
  • Adalmir M. Dantas
    Ophthalmology,
    Federal Univ of Rio de Janeiro, Rio de Janeiro, Brazil
  • Sebastiao Cronemberger
    Hospital São Geraldo, Federal Univ of Minas Gerais, Belo Horizonte, Brazil
  • Footnotes
    Commercial Relationships  Nassim S. Calixto, Sr., None; Vinicius V. Oliveira, None; Adalmir M. Dantas, None; Sebastiao Cronemberger, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2461. doi:
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      Nassim S. Calixto, Sr., Vinicius V. Oliveira, Adalmir M. Dantas, Sebastiao Cronemberger; The effect of Brimonidine Tartarate on Circulating Retinal Spreading Depression. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2461.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Spread depression (SD) was originally described by Leão (1944) in the rabbit cerebral cortex and first identified on retina by Gouras (1958). SD is widely associated with neuronal damage. SD can also be seen in the retina as a propagating depolarization wave. While it spreads through retina, electrical and intrinsic optical signs can be measured. The circulating spreading depression is a unique model in which once the first stimulus is done, it continuously propagates through the tissue. The main purpose of this paper is to identify if brimonidine tartarate (BT) is able to reduce, or even stop the spreading phenomena.

Methods: : We performed 9 experiments on fragments of retinal preparations of White Leghorn chicks from 3 to 8 days after hatching. Immediately after decapitation the eyeballs were removed and sectioned along the equator. Fragments of retina were transferred to a chamber and infused with modified Ringer solution (RS) driven by a peristaltic pump in order to maintain the RS flowing at a rate from 0.8 to 0.85 ml/min. The temperature in the chamber was set at 30°C by means of a thermostatic bath. RS composition (in mM) was: NaCl 100.0, KCl 6.0, CaCl2 1.0, MgSO4 1.0, NaHPO4 1.0, NaHCO3 30.0 and glucose 20.0. The presence or absence of SD was detected by recording its concomitant slow voltage variations through two pore electrodes connected to a Grass polygraph. All experiments started with a control procedure. Firstly, the retina infused with RS was mechanically stimulated by a sharpened tungsten wire, triggering a SD. After 9 minutes the infusion was changed to RS containing 0.1% brimonidine tartarate (0.1% RS/BT) for 9 minutes. After that, the infusion was once more changed for a RS containing 0.2% brimonidine tartarate (0.2% RS/BT).

Results: : Our data demonstrated that brimonidine tartarate (0.1% RS/BT) reduces the amplitude of the negative potential shift from 25.89±2.66mV to 21.44±2.11mV; and with 0.2% RS/BT the SD is blocked. The time interval between two passages through the same electrode was increased from 59.17±0.95sec to 78.78±2.26sec (0.1% RS/BT). Although the main BT pathway effect is still not well known, it is clear its powerful effect. The recent association of SD to many traumatic disorders of the central nervous tissue leads us to wonder how BT blocks SD. Possibly, BT acts as a neuroprotector drug.

Conclusions: : Brimonidine tartarate (0.1% RS/BT) was able to reduce the negative potential shift from 25.89±2.66mV to 21.44±2.11mV. With 0.2% RS/BT the SD was blocked.

Keywords: ganglion cells • neuroprotection • glia 
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