Stress-dependent enhancement and impairment of retention by naloxone: Evidence for an endogenous opioid-based modulatory system protective of memory

Schneider, Allen M.; Simson, Peter E.; Spiller, Krista; Adelstein, Jonathan S.; Vacharat, Amanda; Short, Kenneth; Kirby, Lynn G.

doi:10.1016/j.bbr.2009.06.007

Cited by 5 publications

(12 citation statements)

References 24 publications

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“…Thus, these findings, taken together with earlier work (Schneider et al, 2009), not only indicate that the ability of β-adrenergic or opioid-receptor blockade to impair retention is critically dependent upon the intensity of stress, but also that the pharmacologically inactivated adrenergic-based and opioid-based memory-modulation systems interact to prevent impairment of retention.…”

Section: Discussionsupporting

confidence: 63%

“…Combined and opposing action of inhibitory-opioid and excitatory-adrenergic modulation systems can also explain the enhancement of retention produced by naloxone under mildly stressful conditions (mild shock from passive-avoidance training in the absence of swim-stress) seen in previous studies (Introini-Collison et al, 1989; McGaugh et al, 1988; Schneider et al, 2009). Specifically, the unblocked, endogenous opioid-based system, activated by mild stress, serves to limit enhancement of retention by opposing the simultaneous activation (as opposed to over-activation) of the excitatory adrenergic-based system.…”

Section: Discussionmentioning

confidence: 81%

“…A similar hypothesis has previously been tested regarding the effect on retention of blockade of another stress-related memory-modulation system, the opioid system (Schneider et al, 2009). The findings indicated that the effectiveness of opioid-receptor blockade in impairing retention depended on intensity of stress.…”

Section: Introductionmentioning

confidence: 85%

“…The dose of propranolol chosen was similar to doses that have previously been shown to be effective in adrenergic studies on memory modulation (Cahill et al, 2000; Przybyslawski et al, 1999). The dose of naloxone has been used in previous passive-avoidance studies including a dose–response study (Schneider et al, 2006) using the procedures employed in the present study to produce both enhancement and impairment of retention under mild and intense stress, respectively (McGaugh et al, 1988; Schneider et al, 2009). …”

Section: Methodsmentioning

confidence: 99%

“…The forced swim procedure (15 min in duration) was administered in a quiet, dimly lit room and consisted of placing rats in a cylindrical tank (46-cm tall × 20-cm diameter) with water (~22 °C) filled to a depth of 30 cm (Porsolt et al, 1978; Schneider et al, 2009). The water depth of 30 cm forced the rats to swim or float without their tails touching the bottom of the tank.…”

Section: Methodsmentioning

confidence: 99%

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Stress-dependent impairment of passive-avoidance memory by propranolol or naloxone

Schneider

Simson

Atapattu

et al. 2011

Pharmacology Biochemistry and Behavior

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Previous work has shown that the effect of opioid-receptor blockade on memory modulation is critically dependent upon the intensity of stress. The current study determined the effect of adrenergic-receptor blockade on memory modulation under varied levels of stress and then compared the effect of adrenergic-receptor blockade under intense stress to that of a) opioid-receptor blockade and b) concurrent opioid- and adrenergic-receptor blockade. In the first experiment, the β-adrenergic-receptor blocker propranolol impaired retention in the passive-avoidance procedure when administered immediately after exposure to intense stress (passive-avoidance training followed by swim stress) but not mild stress (passive-avoidance training alone). In the second experiment, while separate administration of either propranolol or the opioid-receptor blocker naloxone immediately after exposure to intense stress impaired retention, the combined administration of propranolol and naloxone failed to do so. These findings demonstrate that the effect of β-adrenergic-receptor blockade or opioid-receptor blockade on memory modulation in the passive-avoidance procedure is dependent upon the intensity of stress, and suggest that concurrent inactivation of endogenous adrenergic- and opioid-based memory modulation systems under stressful conditions is protective of memory.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 85%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Stress-dependent impairment of passive-avoidance memory by propranolol or naloxone

Schneider

Simson

Atapattu

et al. 2011

Pharmacology Biochemistry and Behavior

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Stress-dependent opioid and adrenergic modulation of newly retrieved fear memory

Schneider

Simson

Daimon

et al. 2014

Neurobiology of Learning and Memory

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Recent studies on the effect of stress on modulation of fear memory in our laboratory have uncovered endogenous opioid and adrenergic based modulation systems, working in concert, that limit the strengthening or weakening of newly acquired fear memory during consolidation under conditions of mild or intense stress, respectively. The present study sought to determine if similar stress-dependent modulation, mediated by endogenous opioid and adrenergic systems, occurs during reconsolidation of newly retrieved fear memory. Rats underwent contextual fear conditioning followed 24 hr later by reactivation of fear memory; a retention test was administered the next day. Stress was manipulated by varying duration of recall of fear memory during reactivation. In the first experiment, vehicle or the opioid-receptor blocker naloxone was administered immediately after varied durations (30 or 120 sec) of reactivation. The results indicate that 1) reactivation, in the absence of drug, has a marked effect on freezing behavior—as duration of reactivation increases from 30 to 120 sec, freezing behavior and presumably fearinduced stress increases and 2) naloxone, administered immediately after 30 sec (mild stress) or 120 sec (intense stress) of reactivation, enhances or impairs retention, respectively, the next day. In the second experiment, naloxone and the ß-adrenergic blocker propranolol were administered either separately or in combination immediately after 120 sec (intense stress) reactivation. The results indicate that separate administration of propranolol and naloxone impairs retention, while the combined administration fails to do so. Taken together the results of the two experiments are consistent with a protective mechanism, mediated by endogenous opioid and adrenergic systems working in concert, that limits enhancement and impairment of newly retrieved fear memory during reactivation in a stress-dependent manner.

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Endogenous opiates and behavior: 2009

Bodnar

2010

Peptides

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Stress-dependent enhancement and impairment of retention by naloxone: Evidence for an endogenous opioid-based modulatory system protective of memory

Cited by 5 publications

References 24 publications

Stress-dependent impairment of passive-avoidance memory by propranolol or naloxone

Stress-dependent impairment of passive-avoidance memory by propranolol or naloxone

Stress-dependent opioid and adrenergic modulation of newly retrieved fear memory

Endogenous opiates and behavior: 2009

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