ObjectivePatients with panic disorder (PD) are approximately four times more likely to experience suicidal thoughts and attempts compared to healthy controls (HCs). Despite the elevated risk compared to HCs, the relationship between cortical thickness (CT) in PD and suicidality remains underexplored.MethodsWe recruited 161 right-handed participants, including 82 PD patients and 79 HCs, and assessed them using a comprehensive battery of psychological scales, including the Scale for Suicidal Ideation (SSI), Early Trauma Inventory Self Report-Short Form, Neuroticism-Extraversion-Openness Personality Inventory-Neuroticism (NEO-N), State-Trait Anxiety Inventory-Trait Anxiety (STAI-T), Panic Disorder Severity Scale (PDSS), and Beck Depression Inventory.ResultsIn whole-brain vertex-wise group comparison, patients with PD demonstrated significantly lower CT values in the insula, lateral occipital sulcus, and precentral gyrus compared to HCs. Notably, paradoxical significant positive correlations were observed between SSI total scores and CT in the above-mentioned regions within the PD cohort. Pearson’s correlation analyses further indicated that CT in these regions may be linked to high levels of early trauma, trait anxiety (e.g., NEO-N, STAI-T), panic symptom severity (e.g., PDSS), and treatment response in patients with PD.ConclusionThis study suggest that suicidality in PD may be associated with CT in specific EFN regions related to suicidal brain and that CT in these regions could play a critical role in anxiety symptomatology in PD.

ObjectiveRewarding properties of androgens have been suggested. This research aimed to assess the effect of androgen system during the extinction period on morphine induced conditioned place preference (CPP). Androgen and μ-opioid receptor (μ-OR) gene expression were also evaluated in prefrontal cortex (PFC) and nucleus accumbens (NAc) in the male rats.MethodsCPP was induced by morphine injection (3, 5 and 7 mg/kg, s.c.) for three consecutive days. Testosterone (androgen receptor [AR] agonist, 2.5 mg/kg; i.m.) or flutamide (AR antagonist 10 mg/kg, i.m.) were administered in subsequent extinction period. In two castration groups, one group was considered as control and the other one received testosterone during extinction phase. The mRNA expression levels of μ-OR and ARs in PFC and NAc were evaluated using quantitative real-time PCR following CPP reinstatement.ResultsTestosterone prolonged while flutamide shortened extinction period. Castration facilitated morphine-extinction and testosterone could not reverse this effect. The expression of μ-OR and ARs were increased in PFC and NAc of castrated animals compared to control group which were reversed by testosterone. This effect was not reversed by testosterone for μ-OR in PFC.ConclusionOur data indicated that decreased level of testosterone facilitates extinction period in morphine CPP model in male rats. This result could be due to the changes in the expression of opioid and androgenic receptors in PFC and NAc. This study confirms the crucial role of androgen system in modulating drug reward.

Ju-Wan Kim, Yeongmin Kim, Inyong Jeong, Taewon Jung, Geesoo Hong, Dae-Kwang Kim, Hee-Ju Kang, Seunghyong Ryu, Il-Seon Shin, Sung-Wan Kim, Min Jhon, Hwamin Lee, Jae-Min Kim. Clin Psychopharmacol Neurosci -0001;0:. https://doi.org/10.9758/cpn.25.1354

ObjectiveSpontaneous remission may influence the outcome of clinical trials and evaluation of antidepressant efficacy, as it is associated with placebo effects and false remission rates. However, the characteristics of spontaneous remission and its biological mechanisms remain poorly understood. This study aimed to explore the metabolic signatures and underlying biological mechanisms of spontaneous remission using metabolomics.MethodsThis study conducted untargeted and targeted metabolomic analyses in a discovery cohort (n = 16) comprising patients with major depressive disorder (MDD) and those who were spontaneously remitted without medication. Findings were validated in an independent cohort (n = 185), comprising drug-treated patients and healthy controls.ResultsAcetylcarnitine levels were significantly increased in spontaneous remission compared to depression, whereas glycerophosphocholine levels were decreased in spontaneous remission. Both metabolites showed the highest concentration in the control group, followed by the remission group, and the lowest concentration in the depression group, regardless of medication status. These changes suggest alterations in mitochondrial and membrane lipid metabolism.ConclusionAltered levels in acetylcarnitine and glycerophosphocholine may reflect key pathogenic mechanisms of MDD. These findings offer new insight into spontaneous remission as a distinct clinical subtype of depression and may highlight the potential of these metabolites as biomarkers for treatment monitoring in MDD.