As advances in neuroscience have furthered our understanding of the role of brain circuitry, genetics, stress, and neuromodulators in the regulation of normal behavior and in the pathogenesis of psychopathology, an increasing appreciation of the role of neurobiology in individual differences in personality and their pathology in personality disorders has emerged. Individual differences in the regulation and organization of cognitive processes, affective reactivity, impulse/action patterns, and anxiety may in the extreme provide susceptibilities to personality disorders such as borderline and schizotypal personality disorder. A low threshold for impulsive aggression, as observed in borderline and antisocial personality disorders, may be related to excessive amygdala reactivity, reduced prefrontal inhibition, and diminished serotonergic facilitation of prefrontal controls. Affective instability may be mediated by excessive limbic reactivity in gabaminergic/glutamatergic/cholinergic circuits, resulting in an increased sensitivity or reactivity to environmental emotional stimuli as in borderline personality disorder and other cluster B personality disorders. Disturbances in cognitive organization and information processing may contribute to the detachment, desynchrony with the environment, and cognitive/perceptional distortions of cluster A or schizophrenia spectrum personality disorders. A low threshold for anxiety may contribute to the avoidant, dependent, and compulsive behaviors observed in cluster C personality disorders. These alterations in critical regulatory domains will influence how representations of self and others are internalized. Aspects of neurobiological functioning themselves become cognized through the medium of figurative language into an ongoing narrative of the self, one that can be transformed through the analytic process, allowing for the modulation of genetic/biological thresholds.
"Previous studies indicate that dysfunctional interactions in ligands and receptors, e.g., serotonin, norepinephrine, GABA, glutamate and hormones, are associated with anxiety [62-65]. The reagents strengthening the efficacy of their interactions were applied for the psychotropic medication of anxiety disorders, such as selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors and benzodiazepine . "
[Show abstract][Hide abstract] ABSTRACT: Anxiety is a prevalent psychological disorder, in which the atypical expression of certain genes and the abnormality of amygdala are involved. Intermediate processes between genetic defects and anxiety, pathophysiological characteristics of neural network, remain unclear. Using behavioral task, two-photon cellular imaging and electrophysiology, we studied the characteristics of neural networks in basolateral amygdala and the influences of metabotropic glutamate receptor (mGluR) on their dynamics in DBA/2 mice showing anxiety-related genetic defects. Amygdala neurons in DBA/2 high anxiety mice express asynchronous activity and diverse excitability, and their GABAergic synapses demonstrate weak transmission, compared to those in low anxiety FVB/N mice. mGluR1,5 activation improves the anxiety-like behaviors of DBA/2 mice, synchronizes the activity of amygdala neurons and strengthens the transmission of GABAergic synapses. The activity asynchrony of amygdala neurons and the weakness of GABA synaptic transmission are associated with anxiety-like behavior.
"First, endophenotypes may enhance the understanding of the underlying mechanisms of mental illnesses by reducing the gap between genes and behavior through the study of neural circuits and neurochemistries (Doyle et al., 2005; Goodman et al., 2010; Gould & Gottesman , 2006; Mitterschiffthaler, Ettinger, Mehta, Mataix-Cols, & Williams, 2006; Pearlson & Calhoun, 2007; Savitz & Drevets, 2009). Second, endophenotypes could help increase the effectiveness of therapeutic practices, both psychological and somatic, by setting up tailored therapeutic approaches focusing on the impaired skills (Siever & Weinstein, 2009; Treasure, 2007). "
[Show abstract][Hide abstract] ABSTRACT: The study of endophenotypes, notably with configured self-reports, represents a promising research pathway to overcome the limits of a syndromal approach of psychiatric diseases. The Affective Neuroscience Personality Scales (ANPS) is a self-report questionnaire, based on neuroethological considerations, that could help to assess emotional endophenotypes related to the activity in 6 core cerebral emotional systems (FEAR, ANGER, SADNESS, CARING, PLAYFULNESS, SEEKING). We further investigated its psychometric properties among 830 young adults and showed that they were satisfactory. As participants also completed several other self-reports that shared potential traits with the ANPS, we offer new validity evidence based on relations to other variables. We also provide additional evidence to consider that the ANPS scores can be validly interpreted for the characterization of emotional endophenotypes involved in a variety of psychiatric disorders. On the grounds of present results, of previous clinical studies, as well as some preliminary neuroimaging findings, we discuss new steps in the ANPS validation.
[Show abstract][Hide abstract] ABSTRACT: Borderline Personality Disorder (BPD) patients are characterized by increased levels of aggressivity and reduction of impulse control, which are behavioural dimensions mainly sustained by hippocampus and dorsolateral prefrontal cortex (DLPFC). In this study we aimed at investigating whether hippocampus and DLPFC anatomy may sustain impulsive and aggressive behaviours in BPD.
Fifteen DSM-IV BPD patients (11 females, 4 males) and fifteen 1:1 matched healthy controls (11 females, 4 males) were studied with a 1.5T magnetic resonance imaging (MRI) and underwent a psychopathological assessment in order to measure the severity of aggressive and impulsive traits.
Right hippocampal volumes were significantly reduced in BPD patients compared to healthy subjects (p=0.027), particularly in those with a history of childhood abuse (p=0.01). Moreover, in patients but not in controls, right hippocampal volumes significantly inversely correlated with aggressiveness and DLPFC grey matter volumes significantly inversely associated with impulsiveness (p<0.05).
Our results provide evidence that hippocampus and DLPFC play a separate and unique role in sustaining the control of impulse and aggressive behaviours in BPD patients.
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