Memory-enhancing corticosterone treatment increases amygdala norepinephrine and Arc protein expression in hippocampal synaptic fractions

Abstract

Considerable evidence indicates that glucocorticoid hormones enhance the consolidation of memory for emotionally arousing events through interactions with the noradrenergic system of the basolateral complex of the amygdala (BLA). We previously reported that intra-BLA administration of a β-adrenoceptor agonist immediately after inhibitory avoidance training enhanced memory consolidation and increased hippocampal expression of the protein product of the immediate early gene activity-regulated cytoskeletal-associated protein (Arc). In the present experiments corticosterone (3 mg/kg i.p.) was administered to male Sprague-Dawley rats immediately after inhibitory avoidance training to examine effects on long-term memory, amygdala norepinephrine levels, and hippocampal Arc expression. Corticosterone increased amygdala norepinephrine levels 15 min after inhibitory avoidance training, as assessed by in vivo microdialysis, and enhanced memory tested at 48 h. Corticosterone treatment also increased expression of Arc protein in hippocampal synaptic tissue. The elevation in BLA norepinephrine appears to participate in corticosterone-influenced modulation of hippocampal Arc expression as intra-BLA blockade of β-adrenoceptors with propranolol (0.5 μg/ 0.2 μL) attenuated the corticosterone-induced synaptic Arc expression in the hippocampus. These finding indicate that noradrenergic activity at BLA β-adrenoceptors is involved in corticosterone-induced enhancement of memory consolidation and expression of the synaptic-plasticity-related protein Arc in the hippocampus.

Object recognition testing: Methodological considerations on exploration and discrimination measures

“…Indeed, all discrimination measures of the 3 rd familiarization session were higher compared to any of other individual sessions except the 4 th . Many studies have shown that stress can have varying effects on memory functioning [50][51][52][53][54][55]. Memory can be facilitated when stress is experienced in the same context and around the time of learning [56].…”

Glucocorticoids interact with the hippocampal endocannabinoid system in impairing retrieval of contextual fear memory

“…However, it is not understood how GCs interact with the noradrenergic system in influencing memory retrieval, because these effects seem to be too rapid to act through the classical genomic mode of action of GCs (6,10,11,[20][21][22][23]. Findings of recent studies investigating the cellular mechanism underlying the rapid effects of GCs suggest a possible involvement of the endocannabinoid system (24-27).…”

Role of Norepinephrine in Modulating Inhibitory Avoidance Memory Storage: Critical Involvement of the Basolateral Amygdala

“…Other findings in our laboratory have shown that training conditions that evoke emotional arousal (e.g. footshock stimulation) or direct injection of epinephrine or corticosterone in doses that facilitate memory significantly increases NE release in the amygdala and this effect is directly related to the stimulus intensity [92][93][94][95][96].…”

“…Interestingly, it has been shown that the relative severity of the stressor and its physiologic impact can vary between individuals [93]. Thus, the severity of stress produced by a stimulus, whether physiologic or psychogenic, has typically been defined in terms of the magnitude of the physiological response it elicits, e.g., by measuring activation of the hormonal hypothalamic-pituitary-adrenal (HPA) stress axis or of the peripheral sympathoadrenal autonomic response system.…”