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Katherine Herlinger

I am a Clinical Research Fellow in the Division of Psychiatry. My PhD focuses on the neurobiology of reward and emotional processing in opiate and alcohol dependence. My PhD has been funded through the MRC Addiction Research Clinical Training Programme (MARC).

I am currently working on several translational medicine and neuroimaging projects: the NCORE study, a fMRI study of the effect of NK1 receptor antagonism on reward and emotional processing in opiate dependence; the ICCAM study, a multi-centre fMRI study which investigated the effects of opioid, dopamine and NK1 receptor antagonism on brain pathways involved in reward, inhibitory control and stress/emotional processing in addiction; and the GHADD study, a fMRI study investigating the effect of appetitive gut hormones on eating and addictive behaviours.

I graduated from the University of Leeds Medical School in 2014, prior to completing my Foundation training in Central London. I have since worked in Child and Adolescent, Acute Geriatric, General Adult and Addiction Psychiatry. In addition to my research I work clinically in Addiction services in London.


NK1 antagonism attenuates heightened heroin cue reactivity in methadone-maintained opiate-dependent individuals


Background: Neurokinin 1 (NK1) receptors may play an important role in opiate reward and reinforcement. The NCORE (Neural Correlates of Reward and Emotion) study aimed to characterise neural correlates of drug reward in opiate dependence and the effect of NK1 receptor antagonism, a potential novel treatment target.

Methods: Opiate-dependent participants maintained on low-dose methadone (MD, n=33) and healthy controls (HC, n=23) attended two fMRI scanning sessions employing a heroin cue reactivity task, following administration of a single dose of aprepitant (320mg) compared with placebo. Whole brain voxelwise analysis was performed on the cue>neutral contrast (cluster FWE Z>2.3, P<0.05). It was hypothesised that MD individuals would display elevated cue-related fronto-striatal BOLD responses relative to controls, and that NK1 antagonism would ‘normalise’ this response.

Results: Compared with HC, MD displayed heightened BOLD signal to heroin images in the frontal pole, anterior cingulate, posterior cingulate and precuneus cortex on analysis of the placebo visit. In the MD group alone, aprepitant decreased BOLD signal in the lateral occipital cortex, superior parietal lobule and inferior temporal gyrus compared with placebo. Group*drug interaction analysis revealed significant clusters in the anterior cingulate, frontal pole and middle frontal gyrus, where the interaction was driven by aprepitant decreasing regional BOLD signal in the MD group.

Conclusion: Opiate-dependent individuals display heightened BOLD signal to heroin cues compared with controls, even when maintained on methadone. NK1 antagonism with aprepitant attenuates this heightened BOLD response, suggesting it may be able to dampen reactivity to cues within the environment.