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Poster Sessions<br />

2288. Adaptive Changes in Response Inhibition BOLD Responses Following Antidepressant Treatment<br />

Darragh Downey 1 , Karen Elizabeth Davies 1 , Shane McKie 2 , Gabriella Juhasz 2 , Ian Muir Anderson 2 , John<br />

Francis William Deakin 2 , Stephen Ross Williams 1<br />

1 Imaging Science and Biomedical Engineering, University of Manchester, Manchester, Lancashire, United Kingdom; 2 Neuroscience<br />

and Psychiatry Unit, University of Manchester, Manchester, Lancashire, United Kingdom<br />

We investigated adaptive changes in 5-HT signalling following sub-chronic antidepressant treatment in healthy controls performing a response inhibition<br />

paradigm. 24 healthy volunteers were provided with 20mg citalopram or placebo for 11 days and tested with a behavioural inhibition task after 14 days<br />

following a 3 day drug washout. Citalopram pre-treatment compared to placebo was associated with a reduced response bilaterally in the inferior frontal<br />

gyrus and BOLD increases in the right middle frontal gyrus, mid cingulate, precuneus and posterior cingulate when inhibiting responses. These findings<br />

suggest that chronic antidepressant treatment modifies 5-HT pathways involved in cognitive flexibility and inhibitory control.<br />

2289. A Novel FMRI Task to Visualize Frontal Lobe Circuitry Associated with Transient Sadness<br />

Leslie Baxter 1 , Ryan Smith 1 , Richard Fadok 1 , Michael Purcell 1 , Seban Liu 1 , Josef Debbins 1<br />

1 Neuroimaging, Barrow Neurological Institute, Phoenix, AZ, United States<br />

We developed a novel functional magnetic resonance imaging (fMRI) method designed to activate the subgenual anterior cingulate cortex (sACC) and other<br />

frontal regions during transient sadness. We sought to develop a task that would show sufficient and specific activation in individuals to be useful as a<br />

potential target for deep brain stimulation treatment (DBS).<br />

2290. Trait Anxiety and Serotonin Transporter Polymorphism Influence Amygdala Activation as Measured<br />

with FMRI During Fear Extinction at 3 T<br />

Harald Kugel 1 , Christina Sehlmeyer 2,3 , Udo Dannlowski 2,3 , Sonja Schoening 2,3 , Martin Pyka 2,3 , Astrid<br />

Veronika Rauch 2,3 , Katharina Domschke 2 , Bettina Pfleiderer 1 , Pienie Zwitserlood 4 , Walter Heindel 1 , Volker<br />

Arolt 2 , Carsten Konrad 3,5<br />

1 Dept. of Clinical Radiology, University of Muenster, Muenster, NRW, Germany; 2 Dept. of Psychiatry, University of Muenster,<br />

Muenster, NRW, Germany; 3 Research Group 4, Interdisciplinary Center for Clinical Research (IZKF), University of Muenster,<br />

Muenster, NRW, Germany; 4 Dept. of Psychology, University of Muenster, Muenster, NRW, Germany; 5 Dept. of Psychiatry,<br />

University of Marburg, Marburg, HE, Germany<br />

The effect of the serotonin transporter polymorphism 5-HTTLPR and trait anxiety on amygdala activation during fear conditioning and extinction was<br />

investigated with fMRI. 32 volunteers were tested with a fear-conditioning paradigm, presenting neutral faces combined with an acoustic startle. Individual<br />

trait anxiety was determined with the State Trait Anxiety Inventory (STAI). Evaluation showed that trait anxiety and 5-HTTLPR polymorphism did not<br />

affect acquisition, but fear extinction. Trait anxious volunteers and carriers of the short s-allele showed less deactivation of the amygdala during extinction,<br />

demonstrating that they react strongly to fear stimuli, and they can extinct fear reactions less easily.<br />

2291. Functional Differences in Mental Rotation Between Men and Transsexual Patients Before and During<br />

Hormone Therapy Studied with FMRI at 3 T<br />

Harald Kugel 1 , Sonja Schoening 2,3 , Almut Engelien 2,3 , Anette Kersting 2 , Cornelia Roestel 2 , Pienie<br />

Zwitserlood 4 , Wolfgang Lehmann 5 , Walter Heindel 1 , Volker Arolt 2 , Carsten Konrad 6,7<br />

1 Dept. of Clinical Radiology, University of Muenster, Muenster, NRW, Germany; 2 Dept. of Psychiatry, University of Muenster,<br />

Muenster, NRW, Germany; 3 Research Group 4, Interdisciplinary Center for Clinical Research (IZKF), University of Muenster,<br />

Muenster, NRW, Germany; 4 Dept. of Psychology, University of Muenster, Muenster, NRW, Germany; 5 Dept. of Psychology,<br />

University of Magdeburg, Magdeburg, ST, Germany; 6 Research Group 4, Interdisciplinary Center for Clinical Research (IZKF) ,<br />

University of Muenster, Muenster, NRW, Germany; 7 Dept. of Psychiatry, University of Marburg, Marburg, HE, Germany<br />

In order to investigate differences in neurobiological processes in patients with gender identity disorder, 11 male-to-female transsexual patients before, 11<br />

patients during cross-sex hormone therapy, and 11 control males underwent fMRI while performing a sexually dimorph mental rotation paradigm. The<br />

transsexual subjects showed less activation in the left parietal cortex (BA 40). Activation patterns different from controls, i.e. distinct from their biological<br />

sex, did not change during hormonal treatment.<br />

2292. Temporal Modulation in Connectivity Within the Salience Network in Autism Spectrum Disorder<br />

Juha Nikkinen 1 , Jukka Rahko 2 , Tuomo Starck 1 , Jukka Remes 1 , Ahmed Abou Elseoud 1 , Irma Moilanen 2 ,<br />

Osmo Tervonen 1 , Vesa Kiviniemi 1<br />

1 Department of Diagnostic Radiology, Oulu University Hospital, Oulu, Finland; 2 Department of Child Psychiatry, Oulu University<br />

Hospital, Oulu, Finland<br />

Temporal modulation in connectivity within the salience network (SN) has been investigated in autism spectrum disorder (ASD) utilizing group independent<br />

component analysis (ICA). Using the ICA mixing matrix time courses, connectivity between the components including SN structures, anterior insula (AI)<br />

and anterior cingulate cortex (ACC), was investigated. One IC was found to be focused at AI and ACC structure was shown to be detectable in two ICs,<br />

ventral ACC and dorsal ACC. As a result we show that the temporal modulation in connectivity is altered in ASD between the AI and ventral ACC<br />

components.

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