Modulation of memory by post-training epinephrine: involvement of cholinergic mechanisms

  title={Modulation of memory by post-training epinephrine: involvement of cholinergic mechanisms},
  author={Ines B. Introini-Collison and J. D. McGaugh},
Extensive evidence indicates that memory storage can be modulated by peripheral epinephrine as well as by drugs affecting the muscarinic cholinergic system. Low doses of epinephrine (Epi) facilitate memory while high doses induce amnesia. Retention is enhanced by post-training administration of cholinergic muscarinic agonists and impaired by antagonists. The present experiments examined the interaction of peripheral Epi and cholinergic drugs in memory modulation. Male CFW mice (60 days old… 

Cholinergic and dopaminergic agents which inhibit a passive avoidance response attenuate the paradigm-specific increases in NCAM sialylation state

  • E. DoyleC. Regan
  • Biology, Psychology
    Journal of Neural Transmission / General Section JNT
  • 2005
Observations provide further evidence of a regulatory role for neural cell adhesion molecule sialylation state in information storage processes in hippocampal immunoprecipitates.

Glucocorticoid-cholinergic interactions in the dorsal striatum in memory consolidation of inhibitory avoidance training

There are mutual interactions between glucocorticoids and the striatal cholinergic system in enhancing the consolidation of memory of inhibitory avoidance training, and this research indicates that long-term memory may be formed through interactions within the dorsal striatum of the rat.

Specific auditory memory induced by nucleus basalis stimulation depends on intrinsic acetylcholine

Behavioral memory induced by stimulation of the nucleus basalis: Effects of contingency reversal

Novelty-induced arousal enhances memory for cued classical fear conditioning: interactions between peripheral adrenergic and brainstem glutamatergic systems.

It is demonstrated that novelty-induced arousal or increasing sympathetic activity with epinephrine in pre-exposed animals enhances memory through adrenergic mechanisms initiated in the periphery and transmitted centrally via the vagus/NTS complex.

β1-noradrenergic system of the dorsal hippocampus is involved in scopolamine state-dependent memory in rat.

The results suggest that β1-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamines-induced amnesia and scopolamine statedependent memory.

Memory modulation with peripherally acting cholinergic drugs

Findings suggest that the induction of amnesia of passive avoidance involves central cholinergic systems, whereas the NEO, and possibly PHYSO, reversal of the SCOP induced amnesia is mediated peripherally by both muscarinic and nicotinic receptors.

Lesions of the nucleus basalis magnocellularis induced by 192 IgG-saporin block memory enhancement with posttraining norepinephrine in the basolateral amygdala

It is found that cholinergic NBM-cortex projections are required for BLA-mediated modulation of memory consolidation and are implicated in learning, memory storage, and plasticity.



Naloxone and β-endorphin alter the effects of post-training epinephrine on memory

It is found that a novel experience given 1 h prior to training blocked the memory-impairing effect of post-training Epi otherwise obtained in both tasks, indicating that theMemory-enhancing and memory-Impairing effects of Epi are mediated by different mechanisms.

Cholinergic modulation of memory in rats

Seven cholinergic drugs with diverse modes of action were found to enhance 72-h retention of passive avoidance; however, the effective doses were different for each of the drugs studied.

Possible interaction between central cholinergic muscarinic and opioid peptidergic systems during memory consolidation in mice.

Memory retention: Effect of prolonged cholinergic stimulation in mice

Attenuation of scopolamine-induced amnesia in mice

The results support the value of scopolamine as a model of age-related memory impairments, but suggest further that these memory deficits may be particularly susceptible to attenuation with non-cholinergic treatments.