Posttraining Intraamygdala Infusions of Oxotremorine and Propranolol Modulate Storage of Memory for Reductions in Reward Magnitude

Salinas, Juan A.; Introini-Collison, Ines B.; Dalmaz, Carla; McGaugh, James L.

doi:10.1006/nlme.1997.3776

Cited by 68 publications

(53 citation statements)

References 20 publications

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“…Studies using in vivo microdialysis have shown that footshock stimulation of the kind typically used in inhibitory avoidance training (i.e., a single footshock of low intensity and short duration) induces the release of norepinephrine in the amygdala and the magnitude of the release is modulated by drugs and hormones known to affect memory consolidation (14, 44-46). Posttraining activation of amygdala adrenoceptors (both ␣ 1 and ␤) enhances memory for several kinds of training, including (the hippocampus-dependent) Morris water-maze spatial task (12,19,20,(47)(48)(49). Furthermore, the memory enhancement induced by pharmacological stimulation of the amygdala is blocked by inactivation of the ipsilateral hippocampus with lidocaine immediately after training or shortly before the retention test (refs.…”

Section: Discussionmentioning

confidence: 99%

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Roozendaal

Nguyen²,

Power³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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263

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Previously, we reported that bilateral excitotoxic lesions of the basolateral nucleus of the amygdala ( There is considerable evidence that the basolateral nucleus of the amygdala (BLA) is critically involved in regulating the consolidation of different forms of memory, including explicit͞ declarative memory. Many findings indicate that this amygdala nucleus mediates the memory-modulatory effects of adrenal stress hormones released by emotional arousal (1, 2). Findings of several recent studies from our laboratory indicate that posttraining infusions of the specific glucocorticoid receptor (GR or type II) agonist RU 28362 administered into the BLA induce dose-dependent enhancement of inhibitory avoidance retention (3) and that excitotoxic lesions of the BLA induced before training block the memory-enhancing effects of systemically administered glucocorticoids (4) as well as the memory-impairing effects induced by adrenalectomy (5, 6). BLA lesions also block the memory-enhancing effects of the GR agonist administered directly into the hippocampus (7). These findings suggest that BLA neuronal activity modulates stress-induced memory consolidation processes in, or involving, the hippocampus and are consistent with the view that the BLA is not a locus of memory storage but regulates consolidation processes in other brain regions (2).Extensive evidence indicates that noradrenergic and cholinergic systems in the amygdala participate in modulating memory consolidation (8-13). Although the activation of these two neurotransmitter systems in the BLA may occur under different experimental conditions (14, 15) and induce slightly differential electrophysiological responses in BLA neurons (16-18), they have highly comparable effects on memory consolidation. Posttraining infusion of either a ␤-adrenoceptor or muscarinic cholinergic agonist into the amygdala enhances inhibitory avoidance retention (11,12,19,20), and inactivation of either receptor type in the BLA blocks the memoryenhancing effects of systemic glucocorticoids (ref. 13; and A.E.P., B.R. and J.L.M, unpublished observation). Moreover, previous findings indicate that the BLA is a critical locus of interaction between glucocorticoids and the noradrenergic system in memory consolidation modulation (13, 21).The present experiments examined whether ␤-adrenoceptor or muscarinic cholinergic receptor activation in the BLA is critically involved in enabling facilitation of memory consolidation induced by activation of GRs in the hippocampus. In the first experiment, rats received unilateral microinfusions into the BLA of either the ␤-adrenoceptor antagonist atenolol or the muscarinic cholinergic antagonist atropine 10 min prior to training in an inhibitory avoidance task. The GR agonist RU 28362 was administered ipsilaterally into the dorsal hippocampus immediately after training, and retention was tested 48 h later. In a second experiment, we examined whether BLAhippocampus interactions in memory consolidation involve unilateral projections between these brain reg...

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Section: Discussionmentioning

confidence: 99%

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Roozendaal

Nguyen²,

Power³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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263

157

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“…Cholinergic agonists and cholinesterase antagonists can facilitate memory (Introini-Collison & McGaugh, 1988;Stratton & Petrinovich, 1963), promote recovery of memory from brain damage (Russell, Escobar, Booth, & Bermudez-Rattoni, 1994) and achieve rescue from memory deficits in transgenic mice (Fisher, Brandeis, Chapman, Pittel, & Michaelson, 1998). In addition, several non-cholinergic treatments that facilitate memory, such as adrenergic agents and stress hormones, exert their effects via the cholinergic system (Salinas, Introini-Collison, Dalmaz, & McGaugh, 1997).…”

Section: Introductionmentioning

confidence: 99%

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

Miasnikov

Chen

Weinberger

2008

Neurobiology of Learning and Memory

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Although the cholinergic system has long been implicated in the formation of memory, there had been no direct demonstration that activation of this system can actually induce specific behavioral memory. We have evaluated the "cholinergic-memory" hypothesis by pairing a tone with stimulation of the nucleus basalis (NB), which provides acetylcholine to the cerebral cortex. We found that such pairing induces behaviorally-validated auditory memory. NB-induced memory has the key features of natural memory: it is associative, highly-specific and rapidly induced. Moreover, the level of NB stimulation controls the amount of detail in memory about the tonal conditioned stimulus. While consistent with the hypothesis that properly-timed release of acetylcholine (ACh) during natural learning is sufficient to induce memory, pharmacological evidence has been lacking. This study asked whether scopolamine, a muscarinic antagonist, impairs or prevents the formation of NB-induced memory. Adult male rats were first tested for responses (disruption of ongoing respiration) to tones (1-15 kHz), constituting a pre-training behavioral frequency generalization gradient (BFGG). Then, they received a single session of 200 trials of a tone (8.00 kHz, 70 dB, 2 s) paired with electrical stimulation of the NB (100 Hz, 0.2 s). Immediately after training, they received either scopolamine (1.0 mg/kg, i.p.) or saline. Twenty-four hours later, they were tested for specific memory by obtaining post-training BFGGs. The saline group developed CS-specific memory, manifested by maximum increase in response specific to the CS frequency band. In contrast, the scopolamine group exhibited no such memory. These findings indicate that NB-induced specific associative behavioral memory requires the action of intrinsic acetylcholine at muscarinic receptors, and supports the hypothesis that natural memory formation engages the nucleus basalis and muscarinic receptors.

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“…In particular, reduced retention was seen with local intra-amygdala injections of GABA agonists (Castellano et al 1989), ␤-adrenergic antagonists (Gallagher et al 1977), and glutamate receptor antagonists (Izquierdo and Medina 1993). Enhanced retention was seen with intra-amygdaloid injections of bicuculline (Dickinson et al 1993), and agonists of ␤-adrenergic (Ferry and McGaugh 1999;Hatfield and McGaugh 1999) and muscarinic (Salinas et al 1997) receptors. Similarly, post-training intra-amygdaloid injections of glucocorticoids were also reported to enhance memory consolidation (for review, see Roozendaal 1999).…”

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confidence: 97%

Lasting increases in basolateral amygdala activity after emotional arousal: Implications for facilitated consolidation of emotional memories

Pelletier¹,

Likhtik²,

Filali³

et al. 2005

Learn. Mem.

125

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Manipulations that reduce or enhance the activity of basolateral amygdala (BLA) neurons in the minutes to hours after training have been shown to respectively impair or facilitate retention on the inhibitory avoidance task. Although this suggests that BLA activity is altered after emotional arousal, such changes have not been directly demonstrated. To test this, we devised a feline analog of the inhibitory avoidance task and recorded BLA unit activity before and after a single inescapable footshock. Single-unit recordings revealed that the firing rate of many BLA neurons gradually increased after the footshock, peaking 30-50 min post-shock and then subsiding to baseline levels 2 h later. During this period of increased activity, the discharges of simultaneously recorded BLA cells were more synchronized than before the shock. Although it was known that pairing innocuous (conditioned stimulus, CS) and noxious stimuli modifies the responsiveness of BLA neurons to the CS, our results constitute the first demonstration that emotional arousal produces lasting increases in the spontaneous firing rates of BLA neurons. We propose that these changes in BLA activity may promote Hebbian interactions between coincident but spatially distributed activity patterns in BLA targets, facilitating the consolidation of emotional memories.Much evidence indicates that emotional arousal generally improves memory consolidation (Christianson 1992) and that the basolateral amygdala (BLA) is responsible for this effect (McGaugh 2004). It was first shown that systemic administration of adrenal stress hormones after learning could facilitate retention in appetitively or aversively motivated tasks (for review, see Cahill and McGaugh 1998). The effects of stress hormones and their pharmacological analogs were timedependent, their impact on retention decreasing as the interval between the training and hormone treatment increased. These results suggested that the extent of memory consolidation depended on the motivational or arousing consequences of an experience, as expressed by the release of stress hormones .Subsequently, it was reported that the memory modulation produced by manipulations of stress hormone levels could be blocked by lesioning or inactivating the BLA or stria terminalis, but not the central amygdaloid nucleus (Liang and McGaugh 1983;Liang et al. 1990;Introini-Collison et al. 1991;. Consistent with these findings, post-training injections of drugs that presumably enhanced or reduced BLA activity facilitated or impaired retention, respectively. In particular, reduced retention was seen with local intra-amygdala injections of GABA agonists (Castellano et al. 1989), ␤-adrenergic antagonists (Gallagher et al. 1977), and glutamate receptor antagonists (Izquierdo and Medina 1993). Enhanced retention was seen with intra-amygdaloid injections of bicuculline (Dickinson et al. 1993), and agonists of ␤-adrenergic (Ferry and McGaugh 1999;Hatfield and McGaugh 1999) and muscarinic (Salinas et al. 1997) receptors. Similarly, post-training i...

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Posttraining Intraamygdala Infusions of Oxotremorine and Propranolol Modulate Storage of Memory for Reductions in Reward Magnitude

Cited by 68 publications

References 20 publications

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

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

Lasting increases in basolateral amygdala activity after emotional arousal: Implications for facilitated consolidation of emotional memories

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