Stress affects theta activity in limbic networks and impairs novelty-induced exploration and familiarization

Jacinto, Luis; Reis, Joana; Dias, Nuno; Cerqueira, João José; Correia, J. H.; Sousa, Nuno

doi:10.3389/fnbeh.2013.00127

Cited by 66 publications

(57 citation statements)

References 48 publications

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“…Notably, stress exposure shifted LC-mPFC coherence to a distinct frequency range (7-9 Hz) regardless of day or age. As coherence between the mPFC and other brain regions within the theta range has been implicated in fear memory (Jacinto et al, 2013;Lesting et al, 2013), the current study provides evidence that the LC also participates in this anxiogenic neural circuit. At the same time that repeated stress enhanced LC-mPFC theta coherence, it impaired coherence at higher frequencies (eg, gamma) that have been implicated in higher cognitive processing, selectively in adolescent rats (Benchenane et al, 2011).…”

Section: Social Stress and Lc Network Activitymentioning

confidence: 70%

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Zitnik

Curtis

Wood

et al. 2015

Neuropsychopharmacol

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Early life stress is associated with the development of psychiatric disorders. Because the locus coeruleus-norepinephrine (LC-NE) system is a major stress-response system that is implicated in psychopathology, developmental differences in the response of this system to stress may contribute to increased vulnerability. Here LC single unit and network activity were compared between adult and adolescent rats during resident-intruder stress. In some rats, LC and medial prefrontal cortex (mPFC) coherence was quantified. The initial stress tonically activated LC neurons and induced theta oscillations, while simultaneously decreasing LC auditory-evoked responses in both age groups. Stress increased LC-mPFC coherence within the theta range. With repeated exposures, adolescent LC neuronal and network activity remained elevated even in the absence of the stressor and were unresponsive to stressor presentation. In contrast, LC neurons of adult rats exposed to repeated social stress were relatively inhibited in the absence of the stressor and mounted robust responses upon stressor presentation. LC sensory-evoked responses were selectively blunted in adolescent rats exposed to repeated social stress. Finally, repeated stress decreased LC-mPFC coherence in the high frequency range (beta and gamma) while maintaining strong coherence in the theta range, selectively in adolescents. Together, these results suggest that adaptive mechanisms that promote stress recovery and maintain basal activity of the brain norepinephrine system in the absence of stress are not fully developed or are vulnerable stress-induced impairments in adolescence. The resulting sustained activation of the LC-NE system after repeated social stress may adversely impact cognition and future social behavior of adolescents.

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Section: Social Stress and Lc Network Activitymentioning

confidence: 70%

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Zitnik

Curtis

Wood

et al. 2015

Neuropsychopharmacol

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“…Indeed, in rodent models of stress (Jacinto et al, 2013; Oliveira et al, 2013) and schizophrenia (Sigurdsson et al, 2010) coherences between VH and PFC are decreased. Likewise, the majority of studies in children with ASD have demonstrated reduced coherences (Coben et al, 2008; Khan et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Alterations in sociability and functional brain connectivity caused by early-life seizures are prevented by bumetanide

Holmes¹,

Tian²,

Hernan³

et al. 2015

Neurobiology of Disease

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There is a well-described association between infantile epilepsy and pervasive cognitive and behavioral deficits, including a high incidence of autism spectrum disorders. Despite the robustness of the relationship between early-life seizures and the development of autism, the pathophysiological mechanism by which this occurs has not been explored. As a result of increasing evidence that autism is a disorder of brain connectivity we hypothesized that early-life seizures would interrupt normal brain connectivity during brain maturation and result in an autistic phenotype. Normal rat pups underwent recurrent flurothyl-induced seizures from postnatal (P) day 5-14 and then tested, along with controls, for developmental alterations of development brain oscillatory activity from P18-25. Specifically we wished to understand how normal changes in rhythmicity in and between brain regions change as a function of age and if this rhythmicity is altered or interrupted by early life seizures. In rat pups with early-life seizures, field recordings from dorsal and ventral hippocampus and prefrontal cortex demonstrated marked increase in coherence as well as a decrease in voltage correlation at all bandwidths compared to controls while there were minimal differences in total power and relative power spectral densities. Rats with early-life seizures had resulting impairment in the sociability and social novelty tests but demonstrated no evidence of increased activity or generalized anxiety as measured in the open field. In addition, rats with early-life seizures had lower seizure thresholds than controls, indicating long-standing alterations in the excitatory/inhibition balance. Bumetanide, a pharmacological agent that blocks the activity of NKCC1 and induces a significant shift of ECl toward more hyperpolarized values, administration at the time of the seizures precluded the subsequent abnormalities in coherence and voltage correlation and resulted in normal sociability and seizure threshold. Taken together these findings indicate that early-life seizures alter the development of oscillations and result in autistic-like behaviors. The altered communication between these brain regions could reflect the physiological underpinnings underlying social cognitive deficits seen in autism spectrum disorders.

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“…The hippocampus is a structure that plays a pivotal role in anxiety and emotional-motivated behaviors (Jacinto et al, 2013). In fact, exposure to new environments elicits anxiety-driven defensive behaviors in rats (Gray and McNaughton, 1996).…”

Section: Discussionmentioning

confidence: 99%

Chronic ethanol exposure during adolescence through early adulthood in female rats induces emotional and memory deficits associated with morphological and molecular alterations in hippocampus

et al. 2015

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There is increasing evidence that heavy ethanol exposure in early life may produce long-lasting neurobehavioral consequences, since brain structural maturation continues until adolescence. It is well established that females are more susceptible to alcohol-induced neurotoxicity and that ethanol consumption is increasing among women, especially during adolescence. In the present study, we investigated whether chronic ethanol exposure during adolescence through early adulthood in female rats may induce hippocampal histological damage and neurobehavioral impairments. Female rats were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) by gavage from the 35(th)-90(th) day of life. Ethanol-exposed animals displayed reduced exploration of the central area and increased number of fecal boluses in the open field test indicative of anxiogenic responses. Moreover, chronic high ethanol exposure during adolescence induced marked impairments on short-term memory of female rats addressed on social recognition and step-down inhibitory avoidance tasks. These neurobehavioral deficits induced by ethanol exposure during adolescence through early adulthood were accompanied by the reduction of hippocampal formation volume as well as the loss of neurons, astrocytes and microglia cells in the hippocampus. These results indicate that chronic high ethanol exposure during adolescence through early adulthood in female rats induces long-lasting emotional and memory deficits associated with morphological and molecular alterations in the hippocampus.

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Stress affects theta activity in limbic networks and impairs novelty-induced exploration and familiarization

Cited by 66 publications

References 48 publications

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Adolescent Social Stress Produces an Enduring Activation of the Rat Locus Coeruleus and Alters its Coherence with the Prefrontal Cortex

Alterations in sociability and functional brain connectivity caused by early-life seizures are prevented by bumetanide

Chronic ethanol exposure during adolescence through early adulthood in female rats induces emotional and memory deficits associated with morphological and molecular alterations in hippocampus

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