March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Effects of Nicotine on Processing in the Visual Pathways
Author Affiliations & Notes
  • Naser T. Naser
    Vision Science,
    University of Alabama at Birmingham, Birmingham, Alabama
  • Vance M. Zemon
    Ferkauf Grad School of Psychology, Yeshiva University, Bronx, New York
  • Stefanie B. Varghese
    Vision Science,
    University of Alabama at Birmingham, Birmingham, Alabama
  • Kent T. Keyser
    Vision Science,
    University of Alabama at Birmingham, Birmingham, Alabama
  • E. Eugenie Hartmann
    Department of Optometry,
    University of Alabama at Birmingham, Birmingham, Alabama
  • Footnotes
    Commercial Relationships  Naser T. Naser, None; Vance M. Zemon, VeriSci Corp (C, P); Stefanie B. Varghese, None; Kent T. Keyser, None; E. Eugenie Hartmann, None
  • Footnotes
    Support  Clinical Research Advisory Committee Research Award, School of Optometry, UAB, Birmingham, AL; NIH Grant EY015015-02
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5735. doi:
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      Naser T. Naser, Vance M. Zemon, Stefanie B. Varghese, Kent T. Keyser, E. Eugenie Hartmann; Effects of Nicotine on Processing in the Visual Pathways. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5735.

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

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Purpose: : To examine the effects of nicotine on cortical visual processing using visual evoked potentials (VEPs) in adults who are not smokers.

Methods: : Twelve healthy, non-smokers (22-33 years old) received a comprehensive eye exam including visual field and color assessment to determine eligibility. Subjects were tested in two separate sessions using 2- and 4-mg nicotine gum with random assignment to level of nicotine for the first session. VEPs (Neucodia, VeriSci Corp.) were recorded twice during each testing session: pre-gum and 30 minutes post-gum chewing. Tests included contrast-reversing checkerboards yielding transient VEPs, as well as isolated-check patterns (bright or dark) to elicit steady-state VEPs that reveal underlying contributions from the parvo- (P) and magno-cellular (M) pathways (high or low contrasts) and windmill-dartboard (WD)/partial-windmill (PW) patterns to elicit ssVEPs that reflect lateral interactions in visual cortex. Amplitude, phase, signal-to-noise ratio (SNR), and magnitude-squared coherence (MSC) measures were used to evaluate the effects of nicotine on the ssVEPs.

Results: : High quality recordings with good SNRs were obtained from the majority of subjects. No changes were observed pre- vs post-nicotine for the transient responses. Under the isolated-check M-bright condition for both dose levels, amplitudes were increased (p < 0.001) and SNRs were higher (p < 0.033). No significant changes were seen under other M/P conditions. A shunting-inhibition model applied to the data revealed specific interactions associated with nicotine. Under the WD condition, changes in amplitude (p < 0.037) were seen in the fundamental frequency component (F1). Changes in phase were observed in both F1 and the second harmonic (F2) of the WD (F1: p < 0.012; F2: p < 0.001) and PW responses (F1: p < 0.011; F2: p < 0.01). MSC values increased in both even and odd frequency components for the WD responses, but only in the even ones of the PW.

Conclusions: : Nicotinic receptors have been shown to exist in the retina, LGN, and visual cortex. Previous studies have examined effects of nicotine on animals or smoking on adults’ VEPs. The results from "smokers" and/or "cigarettes" are not strictly attributable to nicotine alone, or may only occur after chronic nicotine exposure. Studies from our laboratory have found changes in ERG waveforms and in color-vision, in response to nicotine. This project extends this work to investigations of the visual system at the cortical level. These preliminary data implicate nicotine as the key agent for the observed changes in VEP measures that reflect specific cortical mechanisms.

Keywords: electrophysiology: non-clinical • acetylcholine • visual cortex 

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