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Related Experiment Video

Updated: May 16, 2026

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
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Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons

Published on: June 24, 2015

Imaging changes in synaptic acetylcholine availability in living human subjects.

Irina Esterlis1, Jonas O Hannestad, Frederic Bois

  • 1Department of Psychiatry, Yale University, New Haven, Connecticut, USA. irina.esterlis@yale.edu

Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine
|November 20, 2012
PubMed
Summary

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Physostigmine increased acetylcholine levels, reducing the binding of (123)I-5-IA to beta(2)-nicotinic acetylcholine receptors in humans. This neuroimaging method may help study acetylcholine changes.

Area of Science:

  • Neuroscience
  • Molecular Imaging
  • Pharmacology

Background:

  • Estimating beta(2)-nicotinic acetylcholine receptor availability using molecular neuroimaging is challenging due to competition between acetylcholine and radioligands.
  • The radioligand (123)I-3-[2(S)-2-azetidinylmethoxy]pyridine ((123)I-5-IA) is used for in vivo estimation.
  • Previous studies in nonhuman primates suggested sensitivity to acetylcholine levels.

Purpose of the Study:

  • To investigate if (123)I-5-IA binding is affected by increased extracellular acetylcholine levels in humans.
  • To validate the use of (123)I-5-IA for assessing changes in extracellular acetylcholine.

Main Methods:

  • A SPECT study was conducted on six healthy subjects.
  • Baseline scans were performed before intravenous administration of physostigmine (1-1.5 mg) over 60 minutes.

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Last Updated: May 16, 2026

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
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Published on: June 24, 2015

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  • Nine additional scans were acquired after physostigmine administration.

    • Main Results:

    • Physostigmine administration significantly reduced the total volume of distribution for (123)I-5-IA across brain regions (cortex, thalamus, striatum, cerebellum).
    • Reductions ranged from 19% in the thalamus and striatum to 36% in the cerebellum.
    • This decrease was attributed to reduced tracer concentration in tissues and increased plasma parent concentration.

    Conclusions:

    • Increased acetylcholine levels compete with (123)I-5-IA for binding to beta(2)-nicotinic acetylcholine receptors.
    • The findings support the potential of this neuroimaging paradigm to interrogate extracellular acetylcholine changes.
    • Further validation is recommended for clinical application.