Memory modulation

The arousal levels related with an event modulate the likelihood of exact memories being consolidated. The arousal signals to that the brain memory circuits respond are adrenal hormones (both catecholamines and steroids) and various CNS peptide neurotransmitters released in response to stress.

An Evidence for the involvement of catecholamines involves:

- Better recall of emotionally neutral learning tasks through noradrenaline (norepinephrine) or adrenaline (epinephrine) given within a short time of the learning trials.

- No enhanced recall of an emotionally charged version of a story compared with the neutral version after administration of the β-adrenoceptor antagonist propranolol.

Persons with higher levels of sympathetic activity are more likely to suffer from post-traumatic stress disorder after a traumatic experience.

The catecholamine dose–response curve has an inverted U shape moderate concentrations are more effectual enhancers of memory than either low or high levels. As neither of these hormones crosses the blood–brain barrier their actions on the CNS must be exerted peripherally. The catecholamines act at β -adrenoceptors on visceral afferents which run in the vagus (X) nerve to the nucleus of the solitary area. This results in activation of noradrenergic neurons of the locus coeruleus which are categories of a brain arousal system. This system projects to the hippocampus and amygdala to modulate studying or learning. Electrically stimulating the vagus nerve immediately after training improves recall in a reversed U relationship with firing frequency. Through Cutting the vagus nerves or lesioning the nucleus of the solitary tract blocks the effects of systematically administered catecholamines on memory.

Glucocorticoids released through activation of the hypothalamic–pituitary adrenal axis in stress also have effects on memory and learning. These hormones readily cross the blood–brain barrier to act on steroid receptors which are located in high density in the hippocampus and amygdala. Low doses of glucocorticoids enhance although high doses (or chronic exposure in long-term stress) impairs memory. Little concentrations occupy the high-affinity MR (mineralocorticoid receptors) and this facilitates strengthening of synapses by to be crucial for learning. In compare high glucocorticoid concentrations fully saturate the low-affinity glucocorticoid receptors (GR) and this blocks the synaptic strengthening necessary for learning.

The anterior pituitary corticotrophs manufacture, from a single precursor, ACTH (adrenocorticotrophic hormone) and the opioid peptide, β endorphin, both of that impair learning through direct action on the CNS. The Enkephalins also opioid peptides are co-released from the adrenal medulla along with catecholamines and impair memory by a peripheral action. A Naloxone an antagonist of opioid receptors facilitates memory.

Cholinergic enhancement of memory is fine documented. Muscarinic receptor antagonists impair memory, although inhibitors of acetylcholinesterase make it better. Acetylcholine modulation of memory is mediated by the septohippocampal pathway and the cholinergic nuclei of the basal forebrain. The amygdala may enhance consolidation through activating the cholinergic attentional system in the basal forebrain.