Chronic stress induces changes in the structure of interneurons and in the expression of molecules related to neuronal structural plasticity and inhibitory neurotransmission in the amygdala of adult mice

Gilabert-Juan, Javier; Castillo-Gómez, Esther; Pérez-Rando, Marta; Moltó, María Dolores; Nácher, Juan

doi:10.1016/j.expneurol.2011.07.009

Cited by 92 publications

(81 citation statements)

References 52 publications

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“…A single stress experience reduces feedback inhibition (Isoardi et al, 2007) and depresses the interaction between GABAergic and glutamatergic input (Rodriguez Manzanares et al, 2005) in the adult BLA. Repeated stress also leads to decreased responsiveness of BLA interneurons, as measured by c-Fos and GABA efflux in response to acute stress (Reznikov et al, 2008;Reznikov et al, 2009), reduces GAD67, and induces dendritic atrophy of BLA interneurons (Gilabert-Juan et al, 2011). Repeated stress applied to juvenile rats can lead to changes of GABA function in adult rats, such as reduced GAD (Tzanoulinou et al, 2014) as well as changes observed as juveniles, such as reduced 5-HT and noradrenergic facilitation of sIPSCs (Braga et al, 2004;Jiang et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…There are tantalizing hints that single stress (Rodriguez Manzanares et al, 2005;Isoardi et al, 2007) and repeated stress may subtly impair GABAergic regulation in the BLA of adult rodents (Reznikov et al, 2008(Reznikov et al, , 2009Gilabert-Juan et al, 2011). However, little is known about the effects of stress on GABAergic function during adolescence.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Zhang

Rosenkranz

2016

Neuropsychopharmacol

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The adolescent age is associated with lability of mood and emotion. The onset of depression and anxiety disorders peaks during adolescence and there are differences in symptomology during adolescence. This points to differences in the adolescent neural circuitry that underlies mood and emotion, such as the amygdala. The human adolescent amygdala is more responsive to evocative stimuli, hinting to less local inhibitory regulation of the amygdala, but this has not been explored in adolescents. The amygdala, including the lateral nucleus (LAT) of the basolateral amygdala complex, is sensitive to stress. The amygdala undergoes maturational processes during adolescence, and therefore may be more vulnerable to harmful effects of stress during this time period. However, little is known about the effects of stress on the LAT during adolescence. GABAergic inhibition is a key regulator of LAT activity. Therefore, the purpose of this study was to test whether there are differences in the local GABAergic regulation of the rat adolescent LAT, and differences in its sensitivity to repeated stress. We found that LAT projection neurons are subjected to weaker GABAergic inhibition during adolescence. Repeated stress reduced in vivo endogenous and exogenous GABAergic inhibition of LAT projection neurons in adolescent rats. Furthermore, repeated stress decreased measures of presynaptic GABA function and interneuron activity in adolescent rats. In contrast, repeated stress enhanced glutamatergic drive of LAT projection neurons in adult rats. These results demonstrate age differences in GABAergic regulation of the LAT, and age differences in the mechanism for the effects of repeated stress on LAT neuron activity. These findings provide a substrate for increased mood lability in adolescents, and provide a substrate by which adolescent repeated stress can induce distinct behavioral outcomes and psychiatric symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Zhang

Rosenkranz

2016

Neuropsychopharmacol

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“…NCAM participates in synapse formation, maturation and plasticity [60,61,62,63,64], and PSA-NCAM has a role in synapse formation and remodeling [65,66,67]. Moreover, PSA-NCAM decrease has been shown to deregulate the NMDA receptor [68] and compromise trophic support [69], leading to dendritic and synaptic alterations [70,71]. Concomitantly with exploratory and social deficits, we interestingly revealed an increased NCAM/PSA-NCAM ratio in the mPFC and hippocampus of juvenile VPA rats.…”

Section: Discussionmentioning

confidence: 99%

Differential Local Connectivity and Neuroinflammation Profiles in the Medial Prefrontal Cortex and Hippocampus in the Valproic Acid Rat Model of Autism

et al. 2015

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Autism spectrum disorders (ASD) are a group of developmental disabilities characterized by impaired social interaction, communication deficit and repetitive and stereotyped behaviors. Neuroinflammation and synaptic alterations in several brain areas have been suggested to contribute to the physiopathology of ASD. Although the limbic system plays an important role in the functions found impaired in ASD, reports on these areas are scarce and results controversial. In the present study we searched in the medial prefrontal cortex (mPFC) and hippocampus of rats exposed to the valproic acid (VPA) model of ASD for early structural and molecular changes, coincident in time with the behavioral alterations. After confirming delayed growth and maturation in VPA rats, we were able to detect decreased exploratory activity and social interaction at an early time point (postnatal day 35). In mPFC, although typical cortical column organization was preserved in VPA animals, we found that interneuronal space was wider than in controls. Hippocampal CA3 (cornu ammonis 3) pyramidal layer and the granular layer of the dentate gyrus both showed a disorganized spatial arrangement in VPA animals. Neuronal alterations were accompanied with increased tomato lectin and glial fibrillary acidic protein (GFAP) immunostainings both in the mPFC and hippocampus. In the latter region, the increased GFAP immunoreactivity was CA3 specific. At the synaptic level, while mPFC from VPA animals showed increased synaptophysin (SYN) immunostaining, a SYN deficit was found in all hippocampal subfields. Additionally, both the mPFC and the hippocampus of VPA rats showed increased neuronal cell adhesion molecule (NCAM) immunostaining together with decreased levels of its polysialylated form (PSA-NCAM). Interestingly, these changes were more robust in the CA3 hippocampal subfield. Our results indicate that exploratory and social deficits correlate with region-dependent neuronal disorganization and reactive gliosis in the mPFC and hippocampus of VPA rats. While microgliosis is spread in these two limbic areas, astrogliosis, although extended in the mPFC, is circumscribed to the CA3 hippocampal subfield. Our work indicates that neuroinflammation and synaptic alterations do coexist in VPA rats, making this model suitable for studying novel aspects of neuron-glia interactions. Moreover, it suggests that the mPFC and hippocampus might behave differently in the context of the local hyperconnectivity and synaptic hypotheses of autism.

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“…Beyond the type of stressor used and the duration of the stress paradigm, the effects of stress appear to be cell-type specific. In this regard, the studies by Chattarji and colleagues noted above determined that CUS elicited dendritic atrophy of bipolar neurons in the CBL (Vyas et al, 2002), while studies by Nacher and co-workers identified atrophy of interneurons in the CBL and lateral nucleus of the amygdala of mice subjected to 21 days of immobilization stress (Gilabert-Juan et al, 2011). An interesting observation between these studies is that stress-induced morphological changes, irrespective of the direction of the changes, are often observed in radial segments between 60 and 120 lm from the cell body.…”

Section: Stress-induced Morphological Changes In the Rodent Amygdalamentioning

confidence: 97%

“…Interestingly, rodents exposed to stress exhibit structural and functional deficits in the amygdala that are similar to those observed in patients with depressive illness. This includes studies that have demonstrated that repeated stress paradigms may elicit dendritic hypertrophy (Vyas et al, 2002;Johnson et al, 2009) 2002; Gilabert-Juan et al, 2011) in the basolateral nucleus of the amygdala (CBL), morphological changes that appeared to be stressor and cell-type specific. Some studies also suggest that drugs used in the treatment of stress-related mood disorders, such as the antidepressant tianeptine (McEwen and Chattarji, 2004) and the mood-stabilizing drug lithium (Johnson et al, 2009), prevent stress-induced morphological changes in the rat CBL.…”

Section: Introductionmentioning

confidence: 99%

Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine

et al. 2015

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Chronic stress induces changes in the structure of interneurons and in the expression of molecules related to neuronal structural plasticity and inhibitory neurotransmission in the amygdala of adult mice

Cited by 92 publications

References 52 publications

Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Differential Local Connectivity and Neuroinflammation Profiles in the Medial Prefrontal Cortex and Hippocampus in the Valproic Acid Rat Model of Autism

Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine

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