Time filter

Source Type

Chauveau F.,University of Munster | Chauveau F.,Institute Of Recherche Biomedicale Des Armees | Lange M.D.,University of Munster | Lange M.D.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | And 4 more authors.
Neuropsychopharmacology | Year: 2012

Stressful and traumatic events can create aversive memories, which are a predisposing factor for anxiety disorders. The amygdala is critical for transforming such stressful events into anxiety, and the recently discovered neuropeptide S transmitter system represents a promising candidate apt to control these interactions. Here we test the hypothesis that neuropeptide S can regulate stress-induced hyperexcitability in the amygdala, and thereby can interact with stress-induced alterations of fear memory. Mice underwent acute immobilization stress (IS), and neuropeptide S and a receptor antagonist were locally injected into the lateral amygdala (LA) during stress exposure. Ten days later, anxiety-like behavior, fear acquisition, fear memory retrieval, and extinction were tested. Furthermore, patch-clamp recordings were performed in amygdala slices prepared ex vivo to identify synaptic substrates of stress-induced alterations in fear responsiveness. (1) IS increased anxiety-like behavior, and enhanced conditioned fear responses during extinction 10 days after stress, (2) neuropeptide S in the amygdala prevented, while an antagonist aggravated, these stress-induced changes of aversive behaviors, (3) excitatory synaptic activity in LA projection neurons was increased on fear conditioning and returned to pre-conditioning values on fear extinction, and (4) stress resulted in sustained high levels of excitatory synaptic activity during fear extinction, whereas neuropeptide S supported the return of synaptic activity during fear extinction to levels typical of non-stressed animals. Together these results suggest that the neuropeptide S system is capable of interfering with mechanisms in the amygdala that transform stressful events into anxiety and impaired fear extinction. © 2012 American College of Neuropsychopharmacology.

Eden A.S.,University of Munster | Schreiber J.,Max Planck Institute for Human Cognitive and Brain Sciences | Anwander A.,Max Planck Institute for Human Cognitive and Brain Sciences | Keuper K.,University of Munster | And 6 more authors.
Journal of Neuroscience | Year: 2015

Diffusion tensor imaging revealed that trait anxiety predicts the microstructural properties of a prespecified fiber tract between the amygdala and the perigenual anterior cingulate cortex. Besides this particular pathway, it is likely that other pathways are also affected. We investigated white matter differences in persons featuring an anxious or a nonanxious personality, taking into account all potential pathway connections between amygdala and anxiety-related regions of the prefrontal cortex (PFC). Diffusion-weighted images, measures of trait anxiety and of reappraisal use (an effective emotion-regulation style), were collected in 48 females. With probabilistic tractography, pathways between the amygdala and the dorsolateral PFC, dorsomedial PFC, ventromedial PFC, and orbitofrontal cortex (OFC) were delineated. The resulting network showed a direct ventral connection between amygdala and PFC and a second limbic connection following the fornix and the anterior limb of the internal capsule. Reappraisal use predicted the microstructure of pathways to all calculated PFC regions in the left hemisphere, indicating stronger pathways for persons with high reappraisal use. Trait anxiety predicted the microstructure in pathways to the ventromedial PFC and OFC, indexing weaker connections in trait-anxious persons. These effects appeared in the right hemisphere, supporting lateralization and top-down inhibition theories of emotion processing. Whereas a specific microstructure is associated with an anxious personality, a different structure subserves emotion regulation. Both are part of a broad fiber tract network between amygdala and PFC. © 2015 the authors.

Lurzel S.,University of Munster | Lurzel S.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | Kaiser S.,University of Munster | Kaiser S.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | And 3 more authors.
Hormones and Behavior | Year: 2011

The maturation of the hypothalamo-pituitary-adrenal (HPA) axis is a key-component of the changes that occur during adolescence. In guinea pigs, HPA responsiveness during late adolescence depends strongly on the quantity and quality of social interactions: Males that lived in a large mixed-sex colony over the course of adolescence exhibit a lower stress response than males that were kept in pairs (one male/one female). Since colony-housed males have higher testosterone (T) levels than pair-housed males, and inhibiting effects of T on HPA function are well known, we tested the hypothesis that the decrease in stress responsiveness found in colony-housed males is due to their high T concentrations. We manipulated T levels in two experiments: 1) gonadectomy/sham-gonadectomy of colony-housed males (which usually have high T levels), 2) application of T undecanoate/vehicle to pair-housed males (which usually have low T levels). As expected, gonadectomized males showed a significantly increased stress response in comparison with sham-gonadectomized males, and T-injected males had a significantly lower stress response than vehicle-injected males. Both experiments thus confirm an inhibiting effect of T on HPA responsiveness during adolescence, which can mediate the influence of social interactions. The reduction in stress responsiveness is hypothesized to have a biologically adaptive value: A sudden increase in glucocorticoid concentrations can enhance aggressive behavior. Thus, pair-housed males might be adapted to aggressively defend their female ('resource defense strategy'), whereas colony-housed males display little aggressive behavior and are capable of integrating themselves into a colony ('queuing strategy'). © 2011 Elsevier Inc.

Lurzel S.,University of Munster | Lurzel S.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | Kaiser S.,University of Munster | Kaiser S.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | And 2 more authors.
Psychoneuroendocrinology | Year: 2011

Adolescence is the transition from infancy to adulthood and encompasses major changes in the brain, the endocrine systems, and behavior. During late adolescence, male guinea pigs living in mixed-sex colonies exhibit a lower cortisol (C) response to novelty compared with animals in other ages and housing conditions. It was hypothesized that this reduction in stress responsiveness is induced by a high amount of social interactions in the colonies. In a previous study (Lürzel et al., 2010), late adolescent colony-housed males (CM) were compared with similarly aged males that were housed in heterosexual pairs (PM) as well as with males that were also housed in pairs, but regularly received additional social stimulation by allowing them ten times to interact with unfamiliar adult animals of both sexes for 10. min (SM). CM had a significantly lower stress response than PM, with SM being intermediate and not significantly different from either of the other groups. We assumed that the amount of social stimulation in SM was insufficient in order to achieve a significant reduction of stress responsiveness compared with PM. For the present study, we hypothesized that with a higher amount of social stimulation, a significant difference in stress responsiveness between PM and SM becomes apparent during late adolescence. Thus, PM were again compared with SM that, this time, had received twice as much social stimulation as in the previous study. As a result, stress responsiveness was indeed significantly lower in SM than in PM during late adolescence. Thus, a high amount of social interactions during the course of adolescence leads to a decreased stress responsiveness. Furthermore, SM showed an increase in testosterone (T) levels caused by social stimulation. We hypothesize that the reduction in stress responsiveness is brought about by high T levels that organize central neural structures over the course of adolescence. © 2011 Elsevier Ltd.

Lange M.D.,University of Munster | Lange M.D.,Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience | Doengi M.,University of Munster | Lesting J.,University of Munster | And 2 more authors.
Journal of Physiology | Year: 2012

Long-lasting changes of synaptic efficacy are thought to be a prerequisite for memory formation and maintenance. In the basolateral complex of the amygdala (BLA), one of the main regions for fear and extinction learning of the brain, various forms of long-term potentiation (LTP) have been described for excitatory glutamatergic synapses. In contrast, little is known about the mechanisms of LTP at inhibitory GABAergic synapses. Here we provide evidence that (1) LTP at inhibitory GABAergic synapses (LTP i) between inhibitory interneurons and principal neurons (PNs) can be induced by theta-burst stimulation (TBS), (2) this LTP i is prevented by AMPA- or NMDA-receptor antagonists, and (3) this LTP i is abolished by the NO synthase (NOS) inhibitor l-NAME or the NO scavenger PTIO, and thus is critically dependent on nitric oxide (NO) signalling. These findings are corroborated by immunocytochemical stainings for neuronal (n) NOS, which revealed the existence of nNOS-positive neurons and fibres in the BLA. We conclude that LTP of GABAergic synaptic transmission to PNs is induced by activation of AMPA and NMDA receptors at glutamatergic synapses and subsequent retrograde NO signalling to enhance GABAergic transmission. This form of LTP at GABAergic synapses comprises a novel form of heterosynaptic plasticity within the BLA, apt to shape conditioned fear responses. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.

Loading Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience collaborators
Loading Otto Creutzfeldt Center for Cognitive and Behavioural Neuroscience collaborators