Hippocampal disinhibition reduces contextual and elemental fear conditioning while sparing the acquisition of latent inhibition

Hippocampal neural disinhibition, i.e. reduced GABAergic inhibition, is a key feature of schizophrenia pathophysiology. The hippocampus is an important part of the neural circuitry that controls fear conditioning and can also modulate prefrontal and striatal mechanisms, including dopamine signalling, which play a role in salience modulation. Therefore, hippocampal neural disinhibition may contribute to impairments in fear conditioning and salience modulation reported in schizophrenia. To test this hypothesis, we examined the effect of ventral hippocampus (VH) disinhibition in male rats on fear conditioning and salience modulation, as reflected by latent inhibition (LI), in a conditioned emotional response procedure (CER). A flashing light was used as the conditioned stimulus (CS) and conditioned suppression was used to index conditioned fear. In Experiment 1, VH disinhibition via infusion of the GABA-A receptor antagonist picrotoxin prior to CS pre-exposure and conditioning markedly reduced fear conditioning to both the CS and context; LI was evident in saline-infused controls, but could not be detected in picrotoxin-infused rats due to the low level of fear conditioning to the CS. In Experiment 2, VH picrotoxin infusions prior to CS pre-exposure only did not affect the acquisition of fear conditioning or LI. Together, these findings indicate that VH neural disinhibition disrupts contextual and elemental fear conditioning, without affecting the acquisition of LI. The disruption of fear conditioning resembles aversive conditioning deficits reported in schizophrenia and may reflect disruption of neural processing within the hippocampus and its projection sites.

Differential modulation of the contextual conditioned emotional response by CB1 and TRPV1 receptors in the ventromedial prefrontal cortex: Possible involvement of NMDA/nitric oxide-related mechanisms

Background: Blockade of cannabinoid CB1 or vanilloid TRPV1 receptors in the ventromedial prefrontal cortex of rats respectively increases or decreases the conditioned emotional response during re-exposure to a context previously paired with footshocks. Although these mechanisms are unknown, they may involve local modulation of glutamatergic and nitrergic signaling. Aim: We investigated whether these mechanisms are involved in the reported effects of CB1 and TRPV1 modulation in the ventromedial prefrontal cortex. Methods: Freezing behavior and autonomic parameters were recorded during the conditioned response expression. Results: The CB1 receptors antagonist NIDA, or the TRPV1 agonist capsaicin (CPS) in the ventromedial prefrontal cortex increased the conditioned emotional response expression, and these effects were prevented by TRPV1 and CB1 antagonism, respectively. The increased conditioned emotional response evoked by NIDA and CPS were prevented by an NMDA antagonist or a neuronal nitric oxide synthase inhibitor. A nitric oxide scavenger or a soluble guanylate cyclase inhibitor prevented only the NIDA effects and the CPS effect was prevented by a non-selective antioxidant drug, as nitric oxide can also induce reactive oxygen species production. Conclusion: Our results suggest that CB1 and TRPV1 receptors in the ventromedial prefrontal cortex differently modulate the expression of conditioned emotional response through glutamatergic and nitrergic mechanisms, although different pathways may be involved.

一例大学生失眠问题的元认知干预报告

文章介绍了对一例大学生失眠问题进行元认知技术干预的过程。女大学生C因对睡眠存在条件性焦虑情绪，进而产生不利于睡眠的思维和行为反应，最终形成潜意识状态下自动运行的失眠程序。咨询师运用元认知干预技术，高效干预来访者潜意识心理活动过程，解决失眠问题。一年后的回访结果表明心理干预效果明显、持久。 The article introduces the process of using Meta-cognitive intervention method to solve the college student's insomnia. The female college student had an anxiety about sleep, a kind of conditioned emotional response, and then her thinking and behavior responses are not conducive to sleep, eventually forming the subconscious state insomnia programs to run automatically. Consultant intervened the visitor's subconscious mental activity process and solved her insomnia by using Meta-cognitive intervention method. A year later, the return results showed that the effect of psychological intervention was obvious and persistent.

Treating the Initial Physical Reflex of Misophonia With the Neural Repatterning Technique: A Counterconditioning Procedure

Misophonia is a condition in which a person has an acute emotional response of anger or disgust to a commonly occurring innocuous auditory or visual stimulus referred to as a trigger. This case details the effective treatment of misophonia in a young woman that included a counterconditioning treatment called the Neural Repatterning Technique (NRT), which combines a continuous positive stimulus and a reduced intensity, intermittent trigger. The treatment was delivered via the Misophonia Trigger Tamer smartphone app and all treatments were conducted independently by the patient. In this patient, the trigger elicited a physical reflex of contraction of the flexor digitorum profundus, which caused her to clench her fist. To enhance the effect of the NRT treatment, Progressive Muscle Relaxation was incorporated to increase her ability to deliberately relax the affected muscle during treatment. During NRT treatment sessions, the patient experienced a weak physical reflex to the reduced trigger stimulus but no emotional response. Her emotional response of misophonia was not treated, but when the physical reflex extinguished, the emotional response also extinguished. This case indicates that the misophonic response includes a Pavlovian-conditioned physical reflex. It is proposed that the trigger elicited the physical reflex and the physical reflex then elicited the conditioned emotional response that is characteristic of misophonia. Because of the conditioned reflex nature of misophonia, it is proposed that a more appropriate name for this disorder would be Conditioned Aversive Reflex Disorder.