Evidence of increased serotonin-1A receptor binding in type 2 diabetes: a positron emission tomography study

  title={Evidence of increased serotonin-1A receptor binding in type 2 diabetes: a positron emission tomography study},
  author={Julie C. Price and David E. Kelley and Christopher M. Ryan and Carolyn C. Meltzer and Wayne C. Drevets and Chester A. Mathis and Sati Mazumdar and Charles F. Reynolds},
  journal={Brain Research},

Age, Sex, and Reproductive Hormone Effects on Brain Serotonin-1A and Serotonin-2A Receptor Binding in a Healthy Population

Endocrine standardization minimized confounding introduced by endogenous hormonal fluctuations and reproductive stage and permitted us to detect small effects of sex, age, and endogenous sex steroid exposures upon 5HT1A binding.

PET tracers for 5-HT(1A) receptors and uses thereof.

Serotonin 1A receptor reductions in postpartum depression: a PET study

Postsynaptic 5HT1A receptor binding is reduced in PD by a similar magnitude as has been shown in other depression samples, and recognition of this neurobiological deficit in PD may be useful in the development of treatments and prevention strategies for this disabling disorder.

Measurement of serotonin 5-HT1A receptor binding using positron emission tomography and [carbonyl-11C]WAY-100635—considerations on the validity of cerebellum as a reference region

Exceptionally high uptake of [carbonyl-11C]WAY-100635 in the gray matter of cerebellum in one healthy male subject, which was reproducible in repeated PET scanning and most likely represents specific binding to 5-HT1A receptors in cerebellar gray matter.

Measurement of 5‐HT1A receptor binding in depressed adults before and after antidepressant drug treatment using positron emission tomography and [11C]WAY‐100635

Chronic antidepressant drug treatment did not significantly change cerebral 5‐ HT1AR binding, consistent with preclinical evidence that the alterations in serotonergic function associated with antidepressant drug administration are not accompanied by changes in 5‐HT1AR density.

Low central nervous system serotonergic responsivity is associated with the metabolic syndrome and physical inactivity.

The metabolic syndrome, recognized by the co-occurrence of general or abdominal obesity, hypertension, dyslipidemia, insulin resistance, and dysglycemia, appears to involve disturbances in

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

The results suggest that the antidepressant-like effect mediated by 5-HT1A receptors may be attenuated by diabetes.

Hypothesis of the neuroendocrine cortisol pathway gene role in the comorbidity of depression, type 2 diabetes, and metabolic syndrome

  • C. Gragnoli
  • Biology, Medicine
    The application of clinical genetics
  • 2014
Depression, type 2 diabetes (T2D), and metabolic syndrome (MetS) are often comorbid. Depression per se increases the risk for T2D by 60%. This risk is not accounted for by the use of antidepressant



Brain serotonin1A receptor binding measured by positron emission tomography with [11C]WAY-100635: effects of depression and antidepressant treatment.

Binding potential values were reduced across many of the regions examined, including frontal, temporal, and limbic cortex in both unmedicated and medicated depressed patients compared with healthy volunteers.

Validation and Reproducibility of Measurement of 5-HT1A Receptor Parameters with [carbonyl-11C]WAY-100635 in Humans: Comparison of Arterial and Reference Tissue Input Functions

  • R. ParseyM. Slifstein M. Laruelle
  • Biology
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2000
In conclusion, derivation of BP by kinetic analysis using the arterial plasma input function appeared as the method of choice because of its higher test—retest reproducibility, lower vulnerability to experimental noise, and absence of bias.

Cerebral complications of diabetes: clinical findings and pathogenetic mechanisms.

  • G. Biessels
  • Medicine, Psychology
    The Netherlands journal of medicine
  • 1999