ArticleThe Journal of pharmacology and experimental therapeutics2012
β1-adrenoceptor activation is required for ethanol enhancement of lateral paracapsular GABAergic synapses in the rat basolateral amygdala.
Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Chronic Intermittent Ethanol and Withdrawal Suppress Evoked and Spontaneous GABA Release Onto Distinct Populations of Basolateral Amygdala Principal Neurons.Addiction biology · 2025Article
- Noradrenergic Mechanisms and Circuitry of Hyperkatifeia in Alcohol Use Disorder.Biological psychiatry · 2025Review
- Acute Ethanol Modulates Synaptic Inhibition in the Basolateral Amygdala via Rapid NLRP3 Inflammasome Activation and Regulates Anxiety-Like Behavior in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Chronic ethanol alters adrenergic receptor gene expression and produces cognitive deficits in male mice.Neurobiology of stress · 2023Article
- Opioid-Induced Reductions in Amygdala Lateral Paracapsular GABA Neuron Circuit Activity.International journal of molecular sciences · 2023Article
- Neurosteroids (allopregnanolone) and alcohol use disorder: From mechanisms to potential pharmacotherapy.Pharmacology & therapeutics · 2022Review
- The Role of Beta-Adrenergic Receptors in Depression and Resilience.Biomedicines · 2022Review
- The Amygdala Noradrenergic System Is Compromised With Alcohol Use Disorder.Biological psychiatry · 2022Article
- Pindolol Rescues Anxiety-Like Behavior and Neurogenic Maladaptations of Long-Term Binge Alcohol Intake in Mice.Frontiers in behavioral neuroscience · 2019Article
- Noradrenergic targets for the treatment of alcohol use disorder.Psychopharmacology · 2018Review
- Role of GABAMolecular brain · 2017Review
- Chronic alcohol exposure disrupts CBAddiction biology · 2017Article
- Strain-Dependent Effects of Acute Alcohol on Synaptic Vesicle Recycling and Post-Tetanic Potentiation in Medial Glutamate Inputs to the Mouse Basolateral Amygdala.Alcoholism, clinical and experimental research · 2017Article
- Fear conditioning selectively disrupts noradrenergic facilitation of GABAergic inhibition in the basolateral amygdala.Neuropharmacology · 2017Article
- Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala.Neuropharmacology · 2016Article
- The basolateral amygdala γ-aminobutyric acidergic system in health and disease.Journal of neuroscience research · 2016Review
- Phosphodiesterase regulation of alcohol drinking in rodents.Alcohol (Fayetteville, N.Y.) · 2015Review
- Identifying the role of pre-and postsynaptic GABA(B) receptors in behavior.Neuroscience and biobehavioral reviews · 2015Review
- Chronic social isolation during adolescence augments catecholamine response to acute ethanol in the basolateral amygdala.Synapse (New York, N.Y.) · 2015Article
- Animal models of post-traumatic stress disorder and recent neurobiological insights.Behavioural pharmacology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
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 Sprague-Dawley rats. Exogenous norepinephrine (NE) enhanced LPCS-evoked inhibitory postsynaptic currents (eIPSCs) via the activation of β-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 β1-, but not β2- or β3-, 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 β1-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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Registered trials
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