December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Adenosine Modulates Glutamate-Induced Calcium Influx in Retinal Neurons
Author Affiliations & Notes
  • AT E Hartwick
    Retina and Optic Nerve Research Laboratory Depts Anatomy & Neurobiology and Ophthalmology Dalhousie University Halifax NS Canada
  • WH Baldridge
    Retina and Optic Nerve Research Laboratory Depts Anatomy & Neurobiology and Ophthalmology Dalhousie University Halifax NS Canada
  • Footnotes
    Commercial Relationships   A.T.E. Hartwick, None; W.H. Baldridge, None. Grant Identification: Support: CIHR Grant MT-15683, NSERC, COETF, and a TLC-AOF Ezell Fellowship
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4752. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      AT E Hartwick, WH Baldridge; Adenosine Modulates Glutamate-Induced Calcium Influx in Retinal Neurons . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4752.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: There is considerable evidence that adenosine acts as a neuromodulator in the central nervous system. Although adenosine receptors (A1 and A2) have been identified in the retina, adenosine's role here is not fully understood. The purpose of this work is to investigate the action of adenosine on the glutamate-induced calcium influx in isolated rat retinal neurons. Methods: Retinae were obtained from neonatal rats and dissociated enzymatically into a suspension of single cells. The retinal cells were cultured in serum-free medium containing neurotrophic factors and forskolin. After four to nine days in culture, the cells were loaded with the ratiometric calcium-indicator dye Fura-2 and exposed to a short application (30 s) of 10 micromolar glutamate, both with and without the presence of 100 micromolar adenosine or 1 micromolar CHA (an A1 agonist). Changes in fluorescence at 340 and 380 nm were monitored, and the resulting ratio was used to determine changes in intracellular calcium levels. Results: In the majority of retinal neurons (84% of the total number of neurons imaged), adenosine did not modulate the glutamate-induced calcium influx. However, in one subpopulation of neurons (9% of the total number), the glutamate-induced calcium influx was repeatedly increased when adenosine was present, while in another group (7% of the total) the influx was repeatedly decreased by adenosine. In the former group, the mean increase in the peak Fura-2 ratio was 15.7 +/- 3.1%, and in the latter group, the mean decrease was 16.3 +/- 1.8%. In presence of CHA, only the subset of neurons with a decreased response to glutamate were evident, suggesting that the inhibitory effect of adenosine is mediated through the A1 receptor. Conclusion: This work shows that adenosine can affect the glutamate-induced calcium influx in certain populations of retinal neurons, and provides evidence that adenosine can function as a neuromodulator in the retina. Adenosine can either increase or decrease the calcium influx, an effect that may be due to the presence of different adenosine receptor sub-types (A1 or A2) in each of these two sub-groups. The identity of the adenosine-sensitive retinal neurons is currently being investigated.

Keywords: 306 adenosine • 490 neurotransmitters/neurotransmitter systems • 334 calcium 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×