Glucocorticoid-regulated kinase CAMKIγ\gamma in the central amygdala controls anxiety-like behavior in mice

The expression of the Calcium/Calmodulin-Dependent Protein Kinase I gamma (encoded by the Camk1g gene) depends on the activation of glucocorticoid receptors (GR) and is strongly regulated by stress. Since Camk1g is primarily expressed in neuronal cells of the limbic system in the brain, we hypothesized that it could be involved in signaling mechanisms that underlie the adaptive or maladaptive responses to stress. Here, we find that restraint-induced stress and the GR agonist dexamethasone robustly increase the expression of Camk1g in neurons of the amygdalar nuclei in the mouse brain. To assess the functional role of Camk1g expression, we performed a virally induced knock-down of the transcript. Mice with bilateral amygdala-specific Camk1g knock-down showed increased anxiety-like behaviors in the light-dark box, and an increase in freezing behavior after fear-conditioning, but normal spatial working memory during exploration of a Y-maze. Thus, we confirm that Camk1g is a neuron-specific GR-regulated transcript, and show that it is specifically involved in behaviors related to anxiety, as well as responses conditioned by aversive stimuli

Does radiation from cell phones affect memory?

Ponad 2,7 mld ludzi na świecie obecnie używa smartfonów. Od dawna spekuluje się, jak wpływa na nas pole elektromagnetyczne o częstotliwości radiowej (ang. radiofrequency electromagnetic field, RF-EMF), którego źródłem jest telefon komórkowy. Przeprowadzono wiele badań dotyczących potencjalnych skutków zdrowotnych narażenia na RF-EMF, których wyniki są w dużej mierze niespójne. Wiadomo, że fale radiowe emitowane przez bezprzewodowe urządzenia elektroniczne mogą wnikać w głąb tkanek i są częściowo pochłaniane również przez mózg. Jednym z pytań, które zadają sobie badacze, jest wpływ ekspozycji na RF-EMF na funkcje poznawcze, takie jak pamięć, szczególnie u dzieci i młodzieży

Genotype-dependent consequences of traumatic stress in four inbred mouse strains

Post-traumatic stress disorder (PTSD) is an anxiety disorder that develops in predisposed individuals following a terrifying event. Studies on isogenic animal populations might explain susceptibility to PTSD by revealing associations between the molecular and behavioural consequences of traumatic stress. Our study employed four inbred mouse strains to search for differences in post-stress response to a 1.5-mA electric foot shock. One day to 6 weeks after the foot shock anxiety, depression and addiction-like phenotypes were assessed. In addition, expression levels of selected stress-related genes were analysed in hippocampus and amygdala. C57BL/6J mice exhibited up-regulation in the expression of Tsc22d3, Nfkbia, Plat and Crhr1 genes in both brain regions. These alterations were associated with an increase of sensitized fear and depressive-like behaviour over time. Traumatic stress induced expression of Tsc22d3, Nfkbia, Plat and Fkbp5 genes and developed social withdrawal in DBA/2J mice. In 129P3/J strain, exposure to stress produced the up-regulation of Tsc22d3 and Nfkbia genes and enhanced sensitivity to the rewarding properties of morphine. Whereas, SWR/J mice displayed increase only in Pdyn expression in the amygdala and had the lowest conditioned fear. Our results reveal a complex genetic background of phenotypic variation in response to stress and indicate the SWR/J strain as a valuable model of stress resistance. We found potential links between the alterations in expression of Tsc22d3, Nfkbia and Pdyn, and different aspects of susceptibility to stress

Cognitive emotion regulation strategies mediate the relationships between Dark Triad traits and negative emotional states experienced during the COVID-19 pandemic

COVID-19 has become a major source of stress as it puts individuals at risk of a range of mental health problems. Personality traits may predispose people to use adaptive or maladaptive coping strategies that lead to different health-related outcomes. The goal of the present study was to examine whether the use of distinct coping strategies during this stressful COVID-19 outbreak mediates the relationships between Dark Triad (DT) traits and stress, depression, and anxiety. The study was conducted in Poland (N = 1086) and Spain (N = 582), thus cross-culturally validated measures were used to assess depression, anxiety and stress (DASS-21), cognitive emotion regulation strategies (CERQ) and socially aversive traits covered by DT (Dirty Dozen scale). The study shows that maladaptive CERS mediates the relationships between narcissism/Machiavellianism and stress, anxiety and depression. Additionally, adaptive CERS mediates the relationship between psychopathy and depression. The results provide a better understanding of the mediating role of CERS on the relationships between DT traits and the stress, anxiety and depression experienced during the COVID-19 pandemic

Alpha1-adrenergic receptor blockade in the VTA modulates fear memories and stress responses

Activity of the ventral tegmental area (VTA) and its terminals has been implicated in the Pavlovian associative learning of both stressful and rewarding stimuli. However, the role of the VTA noradrenergic signaling in fear responses remains unclear. We aimed to examine how alpha1-adrenergic receptor (α1-AR) signaling in the VTA affects conditioned fear. The role of α1-AR was assessed using the micro-infusions into the VTA of the selective antagonists (0.1-1 µg/0.5 µl prazosin and 1 µg/0.5 µl terazosin) in acquisition and expression of fear memory. In addition, we performed control experiments with α1-AR blockade in the mammillary bodies (MB) - a brain region with α1-AR expression adjacent to the VTA. Intra-VTA but not intra-MB α1-AR blockade prevented formation and retrieval of fear memories. Importantly, local administration of α1-AR antagonists did not influence footshock sensitivity, locomotion or anxiety-like behaviors. Similarly, α1-AR blockade in the VTA had no effects on negative affect measured as number of 22 kHz ultrasonic vocalizations during fear conditioning training. We propose that noradrenergic signaling in the VTA via α1-AR regulates formation and retrieval of fear memories but not other behavioral responses to stressful environmental stimuli. It enhances the encoding of environmental stimuli by the VTA to form and retrieve conditioned fear memories and to predict future behavioral outcomes. Our results provide novel insight into the role of the VTA α1-AR signaling in the regulation of stress responsiveness and fear memory

Noradrenergic signaling in the VTA modulates cocaine craving

Exposure to drug-associated cues evokes drug-seeking behavior and is regarded as a major cause of relapse. Conditional stimulus upregulates noradrenaline (NA) system activity, but the drug-seeking behavior depends particularly on phasic dopamine signaling downstream from the ventral tegmental area (VTA). The VTA dopamine-ergic activity is regulated via the signaling of alpha1-adrenergic and alpha2-adrenergic receptors (α1-ARs and α2-ARs); thus, the impact of the conditional stimulus on drug-seeking behavior might involve NAergic signaling in the VTA. To date, the role of VTA ARs in regulating cocaine seeking was not studied. We found that cocaine seeking under extinction conditions in male Sprague-Dawley rats was attenuated by intra-VTA prazosin or terazosin-two selective α1-AR antagonists. In contrast, cocaine seeking was facilitated by intra-VTA administration of the selective α -AR agonist phenylephrine as well as α2-AR antagonist RX 821002, whereas the selective β-AR antagonist propranolol had no effects. In addition, blockade of α1-AR in the VTA prevented α2-AR antagonist-induced enhancement of cocaine seeking. Importantly, the potential non-specific effects of the VTA AR blockade on cocaine seeking could be excluded, because none of the AR antagonists influenced sucrose seeking under extinction conditions or locomotor activity in the open field test. These results demonstrate that NAergic signaling potently and selectively regulates cocaine seeking during early cocaine withdrawal via VTA α1-AR and α2-AR but not β-AR. Our findings provide new insight into the NAergic mechanisms that underlie cocaine craving

COVID-19-related social isolation and symptoms of depression and anxiety in young men in Poland: Does insomnia mediate the relationship?

The need for physical distancing due to COVID-19 mitigation efforts forced prolonged social isolation, which may affect sleep and lead to mental health problems. Previous research has shown that young adults are particularly vulnerable to psychological stress caused by social isolation, the negative psychological impact of the pandemic, and greater frequency and severity of sleep problems. Therefore, the main goal of the present study was to examine whether insomnia could constitute a mediation mechanism that explains the relationship between social isolation experienced during the COVID-19 pandemic and mental health outcomes (depression and anxiety) reported up to 1.5 years later. The study was conducted among young (M±SD; 24.08±3.75) men (N = 1025) in Poland. Data were collected by means of self-report questionnaires, including The Social Isolation Index, The Athens Insomnia Scale, The State-Trait Anxiety Inventory (STAI-S) and Beck's Depression Inventory (BDI-II). The results show that insomnia mediates the relationships between social isolation and both anxiety and depression. The current findings emphasize the role of insomnia in the relationships between social isolation experienced during COVID-19 and negative emotional states. From a clinical perspective, the results suggest that implementing therapeutic components that address social isolation in insomnia treatment programs may prevent the development of depression and anxiety symptoms among young men

Glucocorticoid-Regulated Kinase CAMKIγ in the Central Amygdala Controls Anxiety-like Behavior in Mice

The expression of the Calcium/Calmodulin-Dependent Protein Kinase I gamma (encoded by the Camk1g gene) depends on the activation of glucocorticoid receptors (GR) and is strongly regulated by stress. Since Camk1g is primarily expressed in neuronal cells of the limbic system in the brain, we hypothesized that it could be involved in signaling mechanisms that underlie the adaptive or maladaptive responses to stress. Here, we find that restraint-induced stress and the GR agonist dexamethasone robustly increase the expression of Camk1g in neurons of the amygdalar nuclei in the mouse brain. To assess the functional role of Camk1g expression, we performed a virally induced knock-down of the transcript. Mice with bilateral amygdala-specific Camk1g knock-down showed increased anxiety-like behaviors in the light-dark box, and an increase in freezing behavior after fear-conditioning, but normal spatial working memory during exploration of a Y-maze. Thus, we confirm that Camk1g is a neuron-specific GR-regulated transcript, and show that it is specifically involved in behaviors related to anxiety, as well as responses conditioned by aversive stimuli