Anxiety-like behaviour and associated neurochemical and endocrinological alterations in male pups exposed to prenatal stress

Laloux, Charlotte; Mairesse, Jérôme; Camp, Gilles Van; Giovine, Angela; Branchi, Igor; Bouret, Sébastien G.; Morley‐Fletcher, Sara; Bergonzelli, Gabriela; Malagodi, Marithe; Gradini, Roberto; Nicoletti, Ferdinando; Darnaudéry, Muriel; Maccari, Stefania

doi:10.1016/j.psyneuen.2012.02.010

Cited by 108 publications

(67 citation statements)

References 92 publications

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“…Rat offspring of “stressed” mothers, through restraint or external corticosterone administration, have fewer post-synaptic benzodiazepine binding sites and GABA A receptor subunits in the hippocampus 47, 48 and amygdala. 49, 50 The cause of these post-synaptic modifications is unclear—it may be a direct consequence of prenatal stress on receptors or a compensation due to changes in ligand activity. Decreased inhibitory functioning after prenatal stress is seen in presynaptic GABAergic neurons themselves as well as on the post-synaptic side.…”

Section: Prenatal Stress and Inhibition In The Adult Brainmentioning

confidence: 99%

Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders

2014

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Prenatal stress is a risk factor for several psychiatric disorders in which inhibitory neuron pathology is implicated. A growing body of research demonstrates that inhibitory circuitry in the brain is directly and persistently affected by prenatal stress. This review synthesizes research that elucidates how this early, developmental risk factor impacts inhibitory neurons and how these findings intersect with research on risk factors and inhibitory neuron pathophysiology in schizophrenia, anxiety, autism and Tourette syndrome. The specific impact of prenatal stress on inhibitory neurons, particularly developmental mechanisms, may elucidate further the pathophysiology of these disorders.

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Section: Prenatal Stress and Inhibition In The Adult Brainmentioning

confidence: 99%

Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders

2014

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“…A wealth of evidence has correlated prenatal stress effects in the BLA with elevated anxiety-like behavior (Buss et al, 2012; Cratty et al, 1995; Kraszpulski et al, 2006; Sadler et al, 2011). Furthermore, prenatal stress alters amygdala neuron excitability (Ehrlich et al, 2015) and gene expression related to GABA (Laloux et al, 2012; Sarro et al, 2014), an inhibitory neurotransmitter that tightly regulates amygdala function and affective state (Ehrlich et al, 2009; Quirk and Gehlert, 2003; Rainnie et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

Prenatal stress, regardless of concurrent escitalopram treatment, alters behavior and amygdala gene expression of adolescent female rats

Ehrlich¹,

Neigh

Bourke³

et al. 2015

Neuropharmacology

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Depression during pregnancy has been linked to in utero stress and is associated with long-lasting symptoms in offspring, including anxiety, helplessness, attentional deficits, and social withdrawal. Depression is diagnosed in 10-20% of expectant mothers, but the impact of antidepressant treatment on offspring development is not well documented, particularly for females. Here, we used a prenatal stress model of maternal depression to test the hypothesis that in utero antidepressant treatment could mitigate the effects of prenatal stress. We also investigated the effects of prenatal stress and antidepressant treatment on gene expression related to GABAergic and serotonergic neurotransmission in the amygdala, which may underlie behavioral effects of prenatal stress. Nulliparous female rats were implanted with osmotic minipumps delivering clinically-relevant concentrations of escitalopram and mated. Pregnant dams were exposed to 12 days of mixed-modality stressors, and offspring were behaviorally assessed in adolescence (postnatal day 28) and adulthood (beyond day 90) to determine the extent of behavioral change. We found that in utero stress exposure, regardless of escitalopram treatment, increased anxiety-like behavior in adolescent females and profoundly influenced amygdala expression of the chloride transporters KCC2 and NKCC1, which regulate GABAergic function. In contrast, prenatal escitalopram exposure alone elevated amygdala expression of 5-HT1A receptors. In adulthood, anxiety-like behavior returned to baseline and gene expression effects in the amygdala abated, whereas deficits emerged in novel object recognition for rats exposed to stress during gestation. These findings suggest prenatal stress causes age-dependent deficits in anxiety-like behavior and amygdala function in female offspring, regardless of antidepressant exposure.

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“…Adult amygdala function and emotional behavior are altered by PS (Weinstock, 2008;Sadler et al, 2011), and several studies have identified effects of PS on the developing amygdala (Kraszpulski et al, 2006;Laloux et al, 2012). However, no study to date has described how PS influences the developmental trajectory of amygdala function or characterized the effects of PS on amygdala neurophysiology, regardless of age.…”

Section: Introductionmentioning

confidence: 99%

“…Given that amygdala gene expression and socioemotional behavior are influenced by late-term PS (Laloux et al, 2012) and chronic unpredictable shock stress (Hazra et al, 2012), we exposed pregnant rats to unpredictable shocks from gestational days (G) 17-20. We measured the effects of PS on male offspring at P10, 14, 17, 21, and 28, as well as young adults at P60.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Stress Alters the Development of Socioemotional Behavior and Amygdala Neuron Excitability in Rats

Ehrlich

Rainnie

2015

Neuropsychopharmacol

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Prenatal stress (PS) is a risk factor for neurodevelopmental disorders with diverse ages of onset and socioemotional symptoms. Some PS-linked disorders involve characteristic social deficits, such as autism spectrum disorders and schizophrenia, but PS also promotes anxiety disorders. We propose the diversity of symptoms following PS arises from perturbations to early brain development. To this end, we characterized the effects of PS on the developmental trajectory of physiology of the amygdala, a late-developing center for socioemotional control. We found that PS dampened socioemotional behavior and reduced amygdala neuron excitability in offspring during infancy (at postnatal days (P)10, 14, 17 and 21), preadolescence (day 28), and adulthood (day 60). PS offspring in infancy produced fewer isolation-induced vocalizations and in adulthood exhibited less anxiety-like behavior and deficits in social interaction. PS neurons had a more hyperpolarized resting membrane potential from infancy to adulthood and produced fewer action potentials. Moreover, adult amygdala neurons from PS animals expressed larger action potential afterhyperpolarizations and H-current relative to controls, further limiting excitability. Our results suggest that PS can suppress socioemotional behavior throughout development and produce age-specific alterations to amygdala physiology.

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Anxiety-like behaviour and associated neurochemical and endocrinological alterations in male pups exposed to prenatal stress

Cited by 108 publications

References 92 publications

Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders

Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders

Prenatal stress, regardless of concurrent escitalopram treatment, alters behavior and amygdala gene expression of adolescent female rats

Prenatal Stress Alters the Development of Socioemotional Behavior and Amygdala Neuron Excitability in Rats

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