Neuro biologia da memoria

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Neuro biologia da memoria
2010-04-20 03:25:23

Notes from Memory a Century of Consolidation James L. McGaugh VOL 287 SCIENCE
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  1. Endogenous Modulation of Consolidation
    Adrenal stress hormones, epinephrine and cortisol (corticoste-rone in the rat), released by emotional arousal appear to play an important role in enabling the significance of an experience to regulate the strength of memory of the experience

    Epinephrine and corticosterone , as well as drugs that activate adren-ergic receptors and glucocorticoid (type II)receptors , enhance memory formany kinds of training experiences.
  2. Critical Involvement of the Amygdala in Memory Consolidation

    Epinephrine does not freely pass the blood-brain barrier and appears to modulate memory consolidation by activating b-adrenergic receptors located peripherally on vagal afferents projecting to the nucleus of the solitarytract in the brainstem
    Noradrenergic projections from this region influence neuronal ac-tivity in other brain regions, including the amygdala

    Glucocorticoids released from the adrenal cortex readily enter the brainand activate intracellular glucocorticoid rereptors

    Activation of the amygdala,a brain region important for emotional arous-al, is critical for mediating the influences ofepinephrine and glucocorticoids, becauseamygdala lesions block the effects of thesemodulators on consolidation

    • Most important,activation of b-adrenergic receptors in theamygdala is essential
    • infusions of b-adrenergic receptoragonists enhance memory
  3. Critical Involvement of the Amygdalain Memory Consolidation

    Lesions of the amygdala and infusions of b-adrenergic receptor antagonists into the amygdala also block the memory-modulating effects of drugs
    affecting systems containing g-amino-butyric acid (GABA) and opioid peptides

    basolateral nucleus of the amygdala(BLA) mediates the influences of drugs andhormones on memory consolidation. b-Ad-renergic receptor agonists infused selectivelyinto the BLA after training enhance memory

    Modulatory influences on consolidation include releaseof norepinephrine (NE) within the amygdala

    administration of epinephrine or drugs that enhance consolidation (such as GABA and opioid receptor an-tagonists) increases NE release in the amygdala; and the use of drugs that impair memory(such as GABA and opioid receptor agonists)decreases NE release
  4. Locus of Modulation: Brain Systems and Forms of Memory

    hippocampus and striatum process different forms of memory
    the amygdala modulates consolidation by regulating processing in these brain regions
    • Amphetamine infused into the dorsal hippocampus enhances memory ofthe spatial localization
    • striatum selectivelyenhances memory of a prominent visual cue

    amygdala is clearly not the locus of the enhanced memory ,because inactivation of the amygdala (withlidocaine infusions) before the retention testdoes not block expression of the enhancedmemory for either type of training
  5. Locus of Modulation: Brain Systems and Forms of Memory

    glucocorticoid receptors are densely located in the hippocampus
    infusions of a glucocorti-coid agonist into the dorsal hippocampus after training enhance memory

    lesions of the BLA or infusions of a b-adrenergic receptor antagonist into BLA block the induction of LTP inthe dentate gyrus of the hippocampus
  6. Emotional Arousal and Memory Consolidation in Humans
    Amphetamine administered to human subjects either before or after learningof word lists enhances memory of the words

    b-adrenergic receptor antagonists blockthe memory-enhancing effects of emotionalarousal
  7. As Time Goes By: The Orchestration of Consolidation
    shifts in activity among different brain regions occurring over a period of several hours after the learning of a motorskill, suggesting that consolidation involves time-dependent reorganization of the brain representation underlying the motor skill
    Lesions of the hippocampus (or adjacent cortical areas) and sustained drug infusions into the hippocampus impair memory for training given days,or even weeks, earlier

    • hippocampus and anatomically relatedstructures are no doubt involved in consoli-dation, and may well be a locus of temporaryneural changes that influence the establish-ment of long-term memory,
    • (not unique loci of long-termmemory) -> patient H.M

    interaction ofthe hippocampus and related cortex with the neocortex as well as other brain regions => link the sites and enable regions to strengthen or reorganize connections with the others => organize and reorganizethe information being consolidated
  8. Cellular Machinery of Consolidation´╗┐
    cellular and molecular changes occur mostly within hours after LTP induction or training
    Different processes occurring in other brain regions are likely involved in memory consolidation occurring over days, months, or years
    CaMKII(calcium-calmodulin–dependent protein kinaseII) in both consolidation and LTP´╗┐ <= CaMKII is known to phosphorylate the amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid(AMPA) receptor subunit GluR1

    Inhibitors of the signal-transducing enzyme protein kinase C (PKC) are also knownto block the maintenance of hippocampal LTP and to induce retrograde amnesia
  9. Cellular Machinery of Consolidation´╗┐
    PKA activity and CREB (cAMP response element–binding protein) immunoreactivity increase in the hippocampus after training:

    late-phase LTPand memory consolidation involve cAMP-mediated activation, by PKA phosphoryl-ation, of the CREB transcription factor
    • (A) Declarative memoryincludes consciously accessible memories of
    • fact-based information (i.e., knowing ‘‘what’’), and contains several
    • subcategories, including episodicmemory (memory for events in one’s
    • past) and semantic memory (memory for general knowledge) [110]. In
    • contrast, non-declarative memoryincludes all non-conscious memories, and
    • includes subcategories such as conditioning, implicit memory and
    • procedural memory (i.e., knowing‘‘how’’).
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