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Bidirectional Shift in the Cornu Ammonis 3 Pyramidal Dendritic Organization Following Brief Stress
The negative impact of chronic stress at the structure of apical dendrite branches of cornu ammonis 3 (CA3) pyramidal neurons is well established. However, there is no information available on the CA3 dendritic organization related to short-lasting stress, which suffices to produce long-term habituation or sensitization of anxiety behaviors and neuroendocrine responses. Here, we tested the effects evoked by brief stress on the arrangements of CA3 pyramidal neuron dendrites, and the activity-dependent properties of the commissural-associational (C/A) excitatory postsynaptic potentials (EPSPs). Adult male rats were socially defeated followed by 3 weeks without further treatment or as comparison exposed to a regimen of a social defeat every second day for the same time period. We assessed CA3 pyramidal neurons with somatic whole-cell recording and neurobiotin application in acute hippocampal slices. The results from morphometric analysis of post hoc reconstructions demonstrated that CA3 dendrites from repeatedly stressed rats were reduced in surface area and length selectively at the apical cone (70% of control, approximately 280 µm from the soma). Brief stress, however, produced a similar decrease in apical dendritic length (77% of control, approximately 400 µm from the soma), accompanied by an increased length (167% of control) and branch complexity at the basal cone. The structural changes of the dendrites significantly influenced signal propagation by shortening the onset latency of EPSPs and increasing input resistance (r=0.45, P<0.01), of which the first was significantly changed in repeatedly stressed animals. Both brief and repeated stress long-lastingly impaired long-term potentiation of C/A synapses to a similar degree (P<0.05). These data indicate that the geometric plasticity of CA3 dendrites is dissociated from repetition of aversive experiences. A double social conflict suffices to drive a dynamic reorganization, by site-selective elimination and de novo growth of dendrite branches over the course of weeks after the actual experience.
Effects of sleep deprivation on cardiac autonomic and pituitary-adrenocortical stress reactivity in rats
A demanding life style, often associated with restricted time for sleep, is a growing problem in our society and may become a major health issue in the near future. Since the physiological stress system plays a critical role in coping with a challenge, it is important to know whether this system is affected by sleep loss. Although some information is available concerning the effect of sleep loss on the basal activity of the two main limbs of the stress system, the sympathetic-adrenomedullary (SAM) and the hypothalamic-pituitary-adrenocortical (HPA) axes, little is known about the effect of sleep loss on the subsequent response to a stressor. This study investigated the effects of sleep deprivation on cardiac autonomic and HPA axis (re)activity, under baseline conditions and in response to an acute emotional stressor (15-min of restraint). Rats were subjected to 48 h of sleep deprivation by placing them in slowly rotating wheels. Electrocardiographic recordings were performed via radiotelemetry and autonomic balance was quantified via time-domain indexes of heart rate variability. HPA axis activity was examined by collecting blood samples which were analyzed for plasma ACTH and corticosterone concentrations. The results show that sleep deprivation produced a tonic increase of heart rate and HPA axis activity. When the animals in a state of sleep debt were exposed to an acute restraint stress, a blunted parasympathetic antagonism was observed following sympathetic activation, together with an increased susceptibility to cardiac arrhythmias. The HPA axis response to restraint stress was also altered, but while pituitary ACTH response was attenuated, adrenal corticosterone release was unchanged, indicating an increased adrenocortical sensitivity to ACTH. The data show that sleep deprivation not only affects the baseline activity of the stress system, but it also alters its response to a subsequent stressor
Brainstem alpha2-adrenoreceptor density and behaviour in mice lacking the NPY Y1 receptor.
Chronic psychosocial stress persistently alters autonomic function and physical activity in mice
We investigated heart rate (HR), temperature (T), and physical activity (Act) (by means of radiotelemetry) in male mice subjected to chronic psychosocial stress. Resident/intruder dyads lived in sensory contact for 15 days with the possibility to physically interact daily during the light phase for a maximum of 15 min. Intruders becoming dominants (InD) or subordinates (InS) were investigated here. The aims were to investigate; if a daily aggressive interaction would result in adaptation of autonomic responses; the effects of the social stress on daily rhythmicity and the way these effects change over time; whether acute and long-term autonomic changes do correlate; to compare dominants and subordinates. InD and InS showed a strong autonomic activation during the interactions, with moderate (InS) or no (InD) habituation over time. On the long term, InD showed tachycardia and marked hyperthermia but normal physical activity, while InS showed tachycardia, slight hyperthermia, and depressed physical activity. No correlation emerged between the acute and the long-term autonomic responses. These results highlight the existence of a sustained autonomic activation under chronic stress, which was also affected by mice social status
P16 Brainstem Α2-Adrenoreceptor Density and Behaviour in Mice Lacking the Npy Y1 Receptor
Social Stress, ventricular arrhytmogenesis and strctural damage in senescent hypertrnsive rats
Cardiac structural remodeling and ventricular arrhythmias in spontaneously hypertensive rats
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