Abstract
Purpose: :
To evaluate the effects of nicotine on cone pathways in humans by use of the electroretinogram (ERG).
Methods: :
ERG responses were obtained from five healthy non-smokers. All individuals were evaluated as visually normal by means of a comprehensive eye exam and visual field test. Individuals presenting with ≥-3D of refraction were excluded. Testing contained two doses of nicotine gum (2mg and 4mg) and a placebo gum. Order of test session (placebo vs. nicotine) was randomized and masked. ERG responses were collected and analyzed using the Espion ERG system under standard ISCEV conditions. Responses were recorded from one eye of each subject using a Burian-Allen lens. Intensity response curves were obtained under photopic (0.283-35.84 cd/m2) testing. The Naka-Rushton equation was used to fit the photopic response series. Student's t-test along with two-factor ANOVA (Excel) and Repeated Measures ANOVA (SPSS) were used for statistical analyses. All research reported was conducted in accordance with the Declaration of Helsinki.
Results: :
The average subject age was 26.2 years (range=24-30). Means of Vmax and K values, derived from the Naka-Rushton equation, for each condition are shown in the table below.
Student t-test, two-factor and repeated measures ANOVA analyses showed statistically significant changes (p≤0.00) between nicotine and placebo conditions for the b-wave amplitude, oscillatory potential (OP) amplitudes and OP latencies. No changes were seen in the a-wave amplitude and a- and b-wave latencies.
Conclusions: :
The peak b-wave amplitude responses show increases with 4mg nicotine and decreases with 2mg nicotine. OP amplitudes and latencies for both 2 and 4mg nicotine show significant increases. These data are consistent with findings of 7 nicotinic acetylcholine receptors expression in rabbit and primate retina. Our previously reported data suggested that nicotine had a greater impact on retinal responses under scotopic than photopic conditions. However, the present data clarify that the time course of exposure to nicotine and its elimination from the system played a role in our initial findings. Nicotine does affect retinal information processing in both the rod and cone pathways.
Keywords: electroretinography: non-clinical • retina: proximal (bipolar, amacrine, and ganglion cells) • neurotransmitters/neurotransmitter systems