Two‐way active avoidance training‐specific increases in phosphorylated cAMP response element‐binding protein in the dorsal hippocampus, amygdala, and hypothalamus

Saha, Sujan; Datta, Subimal

doi:10.1111/j.1460-9568.2005.04166.x

Cited by 39 publications

(27 citation statements)

References 81 publications

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“…Taken together, these data indicate that CREB activation in this subfield is required for spatial LTM formation. However, an induction of CREB phosphorylation in the CA3 region has been also reported after nonspatial learning (Saha and Datta 2005). In accord with the role of CREB signaling in CA3 region in LTM formation, a selective induction of c-fos in this CA3 region during the consolidation processes has previously been demonstrated (Bertaina-Anglade et al 2000; He et al 2002).…”

Section: Discussionsupporting

confidence: 48%

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice

Florian¹,

Mons²,

Roullet³

2006

Learn. Mem.

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The transcription factor cAMP response-element binding protein (CREB) has a pivotal role in hippocampal synaptic plasticity and hippocampus-dependent long-term memory. We recently demonstrated that the dorsal hippocampal CA3 region is involved in memory consolidation of spatial information tested on a Morris water maze in mice. To test whether activation of CREB in the CA3 region is required for memory consolidation of spatial information, bilaterally cannulated mice were infused 18 h before the beginning of the behavioral training with antisense or control sense CREB oligodeoxynucleotides (ODNs) or buffer. Mice were then subjected to massed training in a spatial version of the water maze and tested for retention 0 or 24 h after the last training session. We showed that CREB antisense ODN-infusion in the CA3 region impaired long-term memory when tested 24 h later but had no effect on spatial acquisition or short-term memory tested immediately after behavioral training. These findings provide evidence that the regionally restricted activation of CREB in the dorsal hippocampal CA3 region is critical for the long-term memory consolidation phase of spatial learning but not for short-term memory.Many investigators have demonstrated the involvement of the CA3 region in spatial working memory (Frederickson et al. 1990;Lee andKesner 2002, 2003), in the initial acquisition phase of spatial learning (Handelmann and Olton 1981;Lassalle et al. 2000), and during consolidation of memory for nonassociative (Stupien et al. 2003) and associative spatial learning tasks (Zhao et al. 2000). Previously, we showed that CA3 integrity is important for spatial encoding and particularly for memory consolidation of spatial information in the Morris water maze (MWM) task (Florian and Roullet 2004). Thus, it has been proposed that the CA3 region plays an important role in the formation of longterm memory (LTM) and the regulation of hippocampal synaptic activity during learning and memory. It has become widely accepted that LTM formation requires activation of gene transcription (Alberini et al. 1994;Bailey et al. 1996;Guzowski et al. 2001;Bozon et al. 2002) and de novo protein synthesis (Davis and Squire 1984;Bourtchouladze et al. 1998;Quevedo et al. 1999). A principal candidate, the transcription factor cAMP responseelement binding protein (CREB), plays a prominent role in plasticity processes underlying learning and LTM (Frank and Greenberg 1994;Carew 1996;Silva et al. 1998). Indeed, phosphorylation of CREB (pCREB) in the nucleus plays an essential role in downstream transcriptional regulation of proteins required for LTM in a variety of species. It has been shown that disruption of CREB function in invertebrates selectively blocks long-term synaptic changes and LTM (Dash et al. 1990;Yin et al. 1994;Bartsch et al. 1995) whereas injection of CRE-containing promoter induced CREB activation and long-term facilitation (Kaang et al. 1993). Further, in rodents, suppression of CREB signaling by local administration of CREB antisense oligodeoxynu...

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Section: Discussionsupporting

confidence: 48%

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice

Florian¹,

Mons²,

Roullet³

2006

Learn. Mem.

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“…We are aware of no studies examining IEG activation with Sidman AA, but several have examined signaled AA (Nikolaev et al 1992;Duncan et al 1996;Savonenko et al 1999;Radwanska et al 2002;Saha and Datta 2005). Unfortunately, the results fail to paint a clear picture of the AA neurocircuit.…”

Section: Discussionmentioning

confidence: 99%

“…One study also found elevated c-Fos in mPFC following AA training (Duncan et al 1996). However, most of these studies identified additional brain regions of presumably equal importance, such as the cingulate cortex, lateral septum, and various hypothalamic nuclei (Duncan et al 1996;Saha and Datta 2005), with little overlap between studies.…”

Section: Discussionmentioning

confidence: 99%

Active vs. reactive threat responding is associated with differential c-Fos expression in specific regions of amygdala and prefrontal cortex

et al. 2013

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Active avoidance (AA) is an important paradigm for studying mechanisms of aversive instrumental learning, pathological anxiety, and active coping. Unfortunately, AA neurocircuits are poorly understood, partly because behavior is highly variable and reflects a competition between Pavlovian reactions and instrumental actions. Here we exploited the behavioral differences between good and poor avoiders to elucidate the AA neurocircuit. Rats received Sidman AA training and expression of the activity-dependent immediate-early gene c-fos was measured after a shock-free AA test. Six brain regions with known or putative roles in AA were evaluated: amygdala, periaqueductal gray, nucleus accumbens, dorsal striatum, prefrontal cortex (PFC), and hippocampus. Good avoiders showed little Pavlovian freezing and high AA rates at test, the opposite of poor avoiders. Although c-Fos activation was observed throughout the brain, differential activation was found only in subregions of amygdala and PFC. Interestingly, c-Fos correlated with avoidance and freezing in only five of 20 distinct areas evaluated: lateral amygdala, central amygdala, medial amygdala, basal amygdala, and infralimbic PFC. Thus, activity in specific amygdala -PFC circuits likely mediates the competition between instrumental actions and Pavlovian reactions after AA training. Individual differences in AA behavior, long considered a nuisance by researchers, may be the key to elucidating the AA neurocircuit and understanding pathological response profiles.

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“…To assess postsynaptic BLA neuronal activity, we determined immunoreactivity for the phosphorylated form of the transcription factor cAMP response element-binding (pCREB) protein. Noradrenergic stimulation induces pCREB activation (32,33), and several findings have implicated CREB phosphorylation in the amygdala in the modulation of memory consolidation (33)(34)(35). One-way ANOVA for pCREB immunoreactivity in the BLA revealed a significant group effect (F 7,34 ϭ 5.58; P Ͻ 0.0005).…”

Section: Corticosterone Effects On Basolateral Amygdala Neuronal Actimentioning

confidence: 98%

Glucocorticoid enhancement of memory requires arousal-induced noradrenergic activation in the basolateral amygdala

Roozendaal

Okuda

Zee

et al. 2006

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

442

339

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Considerable evidence indicates that glucocorticoid hormones enhance the consolidation of long-term memories for emotionally arousing experiences but not that for less arousing or neutral information. However, previous studies have not determined the basis of such arousal-induced selectivity. Here we report the finding that endogenous noradrenergic activation of the basolateral complex of the amygdala (BLA) induced by emotional arousal is essential in enabling glucocorticoid memory enhancement. Corticosterone administered immediately after object recognition training enhanced 24-h memory of naïve male rats but not that of rats previously habituated to the training context in order to reduce novelty-induced emotional arousal. The ␤-adrenoceptor antagonist propranolol administered either systemically or into the BLA blocked the corticosterone-induced memory enhancement. Further, in habituated rats, corticosterone activated BLA neurons, as assessed by phosphorylated cAMP response element binding (pCREB) immunoreactivity levels, and enhanced memory only when norepinephrine release was stimulated by administration of the ␣2-adrenoceptor antagonist yohimbine. These findings strongly suggest that synergistic actions of glucocorticoids and emotional arousal-induced noradrenergic activation of the BLA constitute a neural mechanism by which glucocorticoids may selectively enhance memory consolidation for emotionally arousing experiences.corticosterone ͉ emotional arousal ͉ norepinephrine ͉ object recognition ͉ memory consolidation E xtensive evidence indicates that emotionally arousing experiences are typically well remembered (1, 2). Investigations of the underlying neurobiological mechanisms suggest that glucocorticoids, released from the adrenal cortex by emotional arousal, play a key role in the strengthening of new memory traces (3-5). Recent findings of both animal and human studies suggest that glucocorticoids may selectively modulate the consolidation of memories of emotionally arousing stimuli (6-9) or those of experiences occurring during states of emotional arousal (10). Such findings imply that glucocorticoids interact with some other component of emotional arousal in influencing memory consolidation. We reported evidence that selective blockade of noradrenergic activity in the basolateral complex of the amygdala (BLA) of rats with infusions of a ␤-adrenoceptor antagonist prevented the memory-enhancing effects of glucocorticoids administered either systemically or into selected brain regions (11-13). Such findings, considered along with the evidence that emotional arousal activates the BLA (14-19) and induces the release of norepinephrine within the BLA (20, 21), suggest that emotional arousal-induced noradrenergic activation within the BLA may be essential in enabling glucocorticoid effects on memory consolidation. However, because prior experiments investigating glucocorticoid-noradrenergic interactions on memory consolidation have used training conditions that induce the release of high levels of norepineph...

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Two‐way active avoidance training‐specific increases in phosphorylated cAMP response element‐binding protein in the dorsal hippocampus, amygdala, and hypothalamus

Cited by 39 publications

References 81 publications

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice

Active vs. reactive threat responding is associated with differential c-Fos expression in specific regions of amygdala and prefrontal cortex

Glucocorticoid enhancement of memory requires arousal-induced noradrenergic activation in the basolateral amygdala

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