We wanted to determine the characteristics associated with electrophysiological and neurochemical changes secondary to ischemic insult as well as correlate these electrophysiological and neurochemical changes. A Ganzfeld source was used to elicit electroretinograms in anesthetized adult Sprague-Dawley rats. Following baseline recordings, one eye was removed for control quantitative
amino acid immunocytochemistry, and ischemic insult was induced by cervical dislocation. Following the induction of
ischemia, a single electroretinogram signal was collected at 1, 2, 4, 6, 8, 16, 32 or 64 min, after which the eye was removed for immunocytochemistry. The post-receptoral b-wave was undetectable after 1 min post-
ischemia, whereas phototransduction declined more gradually and persisted for up to 16 min post-mortem. Both phototransduction saturated amplitude and sensitivity decayed with a similar time course (tc=3.06 (2.73, 3.48) versus 3.29 (2.61, 4.62)min). Significant elevation of
amino acid neurotransmitter levels was not observed until 6 min post-mortem. Between 8 and 16 min post-
ischemia,
glutamate and
GABA were significantly accumulated in neurons and Müller cells (p<0.05). Beyond 16 min, the
neurotransmitter elevation in neurons and Müller cells was relatively attenuated.
Aspartate immunoreactivity was significantly elevated at 4 and 6 min post-
ischemia in neurons, prior to a change in any other
amino acid. Moreover, of the
amino acids assessed the post-ischemic change in
aspartate immunoreactivity showed the best correlation with phototransduction decay (r2=0.68). Our findings show that complete impairment of phototransduction coincides with the accumulation of
amino acid neurotransmitter. The correlation of
aspartate immunoreactivity and phototransduction provides evidence of heightened
glutamate oxidation during ischemic insult.