β1- and β2-adrenoceptor induced synaptic facilitation in rat basolateral amygdala

Abraham, Preetha; Xing, Guoqiang; Zhang, Lei; Yu, E.; Post, Robert M.; Gamble, Eleanore H.; Li, He

doi:10.1016/j.brainres.2008.02.082

Cited by 35 publications

(28 citation statements)

References 36 publications

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“…We were surprised to find that ␤1-ARs play the predominant role in mediating EtOH enhancement of LPCS synapses, whereas blockade of ␤3-ARs had no discernible effect on EtOH enhancement of these responses. Although the density of ␤-AR subtypes in the BLA has yet to be determined, ␤2-and ␤3-ARs probably are expressed at lower levels than ␤1-ARs in this brain region (Rainbow et al, 1984;Abraham et al, 2008). In addition, ␤1-ARs are thought to have a higher affinity for NE than ␤2-or ␤3-ARs (Molinoff, 1984;Wallukat, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Research has shown that functional ␤1-, ␤2-, and ␤3-ARs may be present in the BLA (Abraham et al, 2008;Silberman et al, 2010). Because propranolol is a nonselective ␤-AR antagonist that can potentially block all three ␤-AR subtypes at the concentration used in this study (Hoffmann et al, 2004) we next sought to determine which ␤-AR subtypes might be responsible for the potentiating effects of EtOH on LPCS eIPSCs.…”

Section: ␤1-ar Activation Is Required For Etoh Potentiation Of Lpcs Ementioning

confidence: 99%

“…Because BLA activation plays an integral role in the regulation of anxiety behaviors, and NE is thought to increase central nervous system excitation in response to anxious stimuli, it has been generally accepted that NE increases BLA excitability. Indeed, activation of ␤1-␤2 ARs can increase excitatory synaptic transmission in the BLA (Abraham et al, 2008;Silberman et al, 2010). Such an effect could serve as a cellular mechanism for enhanced anxiety-like behaviors in the face of external stressors.…”

Section: ␤1-ars Mediate Etoh Enhancement Of Lpcs Gabaergic Synapses 457mentioning

confidence: 99%

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β1-Adrenoceptor Activation Is Required for Ethanol Enhancement of Lateral Paracapsular GABAergic Synapses in the Rat Basolateral Amygdala

Silberman

Ariwodola

Weiner

2012

J Pharmacol Exp Ther

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Ethanol (EtOH) potentiation of GABAergic neurotransmission in the basolateral amygdala (BLA) may contribute to the acute anxiolytic effects of this drug. Previous studies have shown that BLA pyramidal neurons receive GABAergic input from two distinct sources: local interneurons and a cluster of GABAergic cells termed lateral paracapsular (LPCS) interneurons. It is noteworthy that whereas EtOH enhances local GABAergic synapses via a presynaptic increase in GABA release, EtOH potentiation of LPCS inhibition is mediated via a distinct mechanism that requires adrenoceptor (AR) activation. Here, we sought to further characterize the interaction between the AR system and EtOH enhancement of LPCS GABAergic synapses by using in vitro electrophysiology techniques in male SpragueDawley rats. Exogenous norepinephrine (NE) enhanced LPCSevoked inhibitory postsynaptic currents (eIPSCs) via the activation of ␤-ARs, because this effect was blocked by propranolol. EtOH potentiation of LPCS eIPSCs was also blocked by propranolol and significantly reduced by NE pretreatment, suggesting that NE and EtOH may enhance LPCS inhibition via a common mechanism. EtOH enhancement of LPCS eIPSCs was significantly reduced by a selective ␤1-, but not ␤2-or ␤3-, AR antagonist, and both EtOH and NE potentiation of LPCS IPSCs was blocked by postsynaptic disruption of cAMP signaling. These data suggest that EtOH enhances LPCS synapses via a postsynaptic ␤1-AR, cAMP-dependent cascade. Because enhancement of LPCS inhibition can reduce anxiety-like behaviors, these findings shed light on a novel mechanism that may play a role in some of the anxiolytic effects of EtOH that are thought to contribute to the development and progression of alcoholism.

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Section: Discussionmentioning

confidence: 99%

Section: ␤1-ar Activation Is Required For Etoh Potentiation Of Lpcs Ementioning

confidence: 99%

Section: ␤1-ars Mediate Etoh Enhancement Of Lpcs Gabaergic Synapses 457mentioning

confidence: 99%

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β1-Adrenoceptor Activation Is Required for Ethanol Enhancement of Lateral Paracapsular GABAergic Synapses in the Rat Basolateral Amygdala

Silberman

Ariwodola

Weiner

2012

J Pharmacol Exp Ther

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“…Receptor Activation b-Adrenergic receptor activation contributes to postsynaptic changes that underlie NE modulation of long-term memory formation (Sullivan et al, 2000;Abraham et al, 2008;Pu et al, 2009). Further, b-receptor antagonists, such as propranolol, block the beneficial memory effects typically seen with NE activation (Cahill et al, 1994;Berlau and McGaugh, 2006).…”

Section: Reduced Spontaneous Recovery Following Compound Stimulus Extmentioning

confidence: 99%

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

Janak

Bowers²,

Corbit

2011

Neuropsychopharmacol

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Drug abstinence is frequently compromised when addicted individuals are re-exposed to environmental stimuli previously associated with drug use. Research with human addicts and in animal models has demonstrated that extinction learning (non-reinforced cue-exposure) can reduce the capacity of such stimuli to induce relapse, yet extinction therapies have limited long-term success under real-world conditions (Bouton, 2002;O'Brien, 2008). We hypothesized that enhancing extinction would reduce the later ability of drugpredictive cues to precipitate drug-seeking behavior. We, therefore, tested whether compound stimulus presentation and pharmacological treatments that augment noradrenergic activity (atomoxetine; norepinephrine reuptake inhibitor) during extinction training would facilitate the extinction of drug-seeking behaviors, thus reducing relapse. Rats were trained that the presentation of a discrete cue signaled that a lever press response would result in cocaine reinforcement. Rats were subsequently extinguished and spontaneous recovery of drug-seeking behavior following presentation of previously drug-predictive cues was tested 4 weeks later. We find that compound stimulus presentations or pharmacologically increasing noradrenergic activity during extinction training results in less future recovery of responding, whereas propranolol treatment reduced the benefit seen with compound stimulus presentation. These data may have important implications for understanding the biological basis of extinction learning, as well as for improving the outcome of extinction-based therapies.

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“…b-Receptor activation has been shown to modulate many of the postsynaptic mechanisms involved in establishing long-term memories. For example, b-receptor agonists have been shown to facilitate synaptic transmission (Abraham et al 2008;Pu et al 2009) and stimulation of the locus coeruleus or local administration of the b-agonist isoproterenol paired with exposure to a novel odor were sufficient to condition a preference for that odor (Sullivan et al 2000). Further, b-receptor antagonists such as propranolol block the beneficial effects that are typically seen with NE activation, for example, in response to emotional arousal (Cahill et al 1994;De Martino et al 2008), or exposure to a novel context (King and Williams 2009).…”

Section: Experiments 3b: Learning Vs Consolidationmentioning

confidence: 99%

Deepened extinction following compound stimulus presentation: Noradrenergic modulation

Janak¹,

Corbit²

2010

Learn. Mem.

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Behavioral extinction is an active form of new learning involving the prediction of nonreward where reward has previously been present. The expression of extinction learning can be disrupted by the presentation of reward itself or reward-predictive stimuli (reinstatement) as well as the passage of time (spontaneous recovery) or contextual changes (renewal). The following experiments replicated the demonstration that presenting multiple previously rewarded stimuli in compound during extinction enhances extinction learning. To explore the pharmacological basis for this we next examined the effects of pharmacological treatments that either facilitated or blocked noradrenergic activity to test the hypothesis that increased noradrenergic activity at the time of extinction training would improve, whereas blockade of noradrenergic activity would impair the extinction of appetitive stimulus -reward memories. Different groups of rats were trained in a discriminative stimulus paradigm to lever-press for food reward. Once stable responding was achieved, responding was extinguished for 2 d. Prior to a third extinction session, rats received systemic administration of either saline, yohimbine (a2 antagonist), atomoxetine (norepinephrine reuptake inhibitor), or propranolol (b-receptor antagonist). Spontaneous recovery of responding to the stimuli was tested 4 wk later. Our results indicate that increasing noradrenergic activity during extinction augments extinction learning resulting in less recovery of responding at test. These results have important implications for models of relapse to drug seeking and the development of extinction-based therapies.Current theories of associative learning suggest that extinction is not the forgetting or "unlearning" of the original association, but rather involves active new learning involving the prediction of nonreward

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β1- and β2-adrenoceptor induced synaptic facilitation in rat basolateral amygdala

Cited by 35 publications

References 36 publications

β1-Adrenoceptor Activation Is Required for Ethanol Enhancement of Lateral Paracapsular GABAergic Synapses in the Rat Basolateral Amygdala

β1-Adrenoceptor Activation Is Required for Ethanol Enhancement of Lateral Paracapsular GABAergic Synapses in the Rat Basolateral Amygdala

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

Deepened extinction following compound stimulus presentation: Noradrenergic modulation

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