Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During development, the risk of developing mesial temporal lobe epilepsy (MTLE) increases when the developing brain is exposed to more than one insult in early life. Early life insults include abnormalities of cortical development, hypoxic-ischemic injury and prolonged febrile seizures. To study epileptogenesis, we have developed a two-hit model of MTLE characterized by two early-life insults: a freeze lesion-induced cortical malformation at post-natal day 1 (P1), and a prolonged hyperthermic seizure (HS) at P10. As early life stressors lead to sexual dimorphism in both acute response and long-term outcome, we hypothesized that our model could lead to gender-based differences in acute stress response and long-term risk of developing MTLE. Male and female pups underwent a freeze-lesion induced cortical microgyrus at P1 and were exposed to HS at P10. Animals were monitored by video-EEG from P90 to P120. Pre and post-procedure plasma corticosterone levels were used to measure stress response at P1 and P10. To confirm the role of sex steroids, androgenized female pups received daily testosterone injections to the mother pre-natally and post-natally for nine days while undergoing both insults. We demonstrated that after both insults females did not develop MTLE while all males did. This correlated with a rise in corticosterone levels at P1 following the lesion in males only. Interestingly, all androgenized females showed a similar rise in corticosterone at P1, and also developed MTLE. Moreover, we found that the cortical lesion significantly decreased the latency to generalized convulsion during hyperthermia at P10 in both genders. The cortical dysplasia volumes at adulthood were also similar between male and female individuals. Our data demonstrate sexual dimorphism in long-term vulnerability to develop epilepsy in the lesion + hyperthermia animal model of MTLE and suggest that the response to early-life stress at P1 contributes significantly to epileptogenesis in a gender-specific manner.
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PMID:Early-life stress is associated with gender-based vulnerability to epileptogenesis in rat pups. 2288 55

Amygdala is a limbic structure involved in the stress response. The immunohistochemical and morphometric methods were used to examine whether the chronic mild psychological stress during the early postnatal period would change activation of amygdaloid nuclei in response to the same stressor in adult. In the study we focused on the role of neurons containing calbindin (CB), calretinin (CR), parvalbumin (PV) and nitric oxide synthase (NOS). The rats were divided into three groups: control non-stressed animals and two experimental: EI consisted of animals that were exposed to acute stress in the high-light, open-field test (HL-OF) at P90 (P - postnatal day) and EII consisted of rats that were exposed to chronic stress in HL-OF, daily during the first 21 postnatal days and then once at P90. The scheme of activation of amygdaloid nuclei under stress in EI and EII group was similar. The highest density of c-Fos-ir cells (c-Fos - a marker of neuronal activation) was demonstrated by the medial nucleus (Me) and bed nucleus of the accessory olfactory tract (BAOT). The amygdaloid nuclei diversity after HL-OF was determined by the high activation of the NOS-ir cells in the Me and NOS- and CR-ir cells in the BAOT. These are probably projection neurons involved in modulation of defensive, reproductive and autonomic behavior in stress response and creation/storage of aversive memory. However, in comparison with EI group, significant decrease in density of c-Fos-ir cells, in almost all amygdaloid nuclei of EII group was revealed. Particularly in BAOT and Me the strong decrease of activity of NOS- and CR-ir neurons was observed. It probably results in attenuation of stress responses what, depending on the circumstances, can be adaptive or maladaptive.
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PMID:The influence of early postnatal chronic mild stress stimulation on the activation of amygdala in adult rat. 3192 96