Abstract
BackgroundGlucocorticoid hormones, in interaction with noradrenaline, enable the consolidation of emotionally arousing and stressful experiences in rodents and humans. Such interaction is thought to occur at least partly in the basolateral nucleus of the amygdala (BLA) which is crucially involved in emotional memory formation. Extensive evidence points to long-term synaptic potentiation (LTP) as a mechanism contributing to memory formation. Here we determined in adolescent C57/Bl6 mice the effects of stress on LTP in the LA-BLA pathway and the specific roles of corticosteroid and β-adrenergic receptor activation in this process.Principal FindingsExposure to 20 min of restraint stress (compared to control treatment) prior to slice preparation enhanced subsequent LTP induction in vitro, without affecting baseline fEPSP responses. The role of glucocorticoid receptors, mineralocorticoid receptors and β2-adrenoceptors in the effects of stress was studied by treating mice with the antagonists mifepristone, spironolactone or propranolol respectively (or the corresponding vehicles) prior to stress or control treatment. In undisturbed controls, mifepristone and propranolol administration in vivo did not influence LTP induced in vitro. By contrast, spironolactone caused a gradually attenuating form of LTP, both in unstressed and stressed mice. Mifepristone treatment prior to stress strongly reduced the ability to induce LTP in vitro. Propranolol normalized the stress-induced enhancement of LTP to control levels during the first 10 min after high frequency stimulation, after which synaptic responses further declined.ConclusionsAcute stress changes BLA electrical properties such that subsequent LTP induction is facilitated. Both β-adrenergic and glucocorticoid receptors are involved in the development of these changes. Mineralocorticoid receptors are important for the maintenance of LTP in the BLA, irrespective of stress-induced changes in the circuit. The prolonged changes in BLA network function after stress may contribute to effective memory formation of emotional and stressful events.
Highlights
Arousing and stressful experiences are generally well remembered [1]
Mineralocorticoid receptors are important for the maintenance of long-term synaptic potentiation (LTP) in the basolateral nucleus of the amygdala (BLA), irrespective of stress-induced changes in the circuit
Effect of stress on baseline synaptic transmission We first examined whether basal synaptic field responses in the BLA were altered by stress exposure, by comparing stimulusresponse relationships for evoked field excitatory postsynaptic potentials (fEPSP) amplitudes obtained in brain slices from control and stressed mice
Summary
Arousing and stressful experiences are generally well remembered [1]. Such effective memory for stress-related information is considered to be adaptive [2,3]. Glucocorticoid hormones readily enter the brain and exert rapid nongenomic and slow genomic actions via membrane-bound and nuclear variants respectively of the mineralocorticoid and glucocorticoid receptor (MR and GR) [6,7,8]. Both receptor types are abundantly expressed in structures essential for learning, memory formation and emotional behaviour. Glucocorticoid hormones, in interaction with noradrenaline, enable the consolidation of emotionally arousing and stressful experiences in rodents and humans Such interaction is thought to occur at least partly in the basolateral nucleus of the amygdala (BLA) which is crucially involved in emotional memory formation. We determined in adolescent C57/Bl6 mice the effects of stress on LTP in the LA-BLA pathway and the specific roles of corticosteroid and badrenergic receptor activation in this process
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