Self-administration enhances excitatory synaptic transmission in the bed nucleus of the stria terminalis

Dumont, Éric C.; Mark, Gregory P.; Mader, Sarah; Williams, John T.

doi:10.1038/nn1414

Cited by 123 publications

(116 citation statements)

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“…In accordance with the idea that glutamatergic inputs to the VTA are crucial for the regulation of DA neuron basal activity, we hypothesized that the hyperactivity of VTA DA neurons was driven by changes in afferent glutamatergic circuitry to the VTA, perhaps from the BNST or the prefrontal cortex (Dumont et al, 2005;Massi et al, 2008;Peters et al, 2008).…”

Section: History Of Voluntary Nicotine Consumption Triggers Potentiatmentioning

confidence: 82%

“…The efficiency of this BNST-VTA excitatory projection is enhanced in rats performing an operant task to obtain food or cocaine. In contrast, no changes were observed in glutamate synaptic transmission in the BNST in rats that received food or cocaine in a passive manner (Dumont et al, 2005). Thus, the difference between active responding versus passive exposure is possibly related to the establishment of reinforcement learning processes, as self-administering animals would be the only ones able to make the action-outcome association.…”

Section: Introductionmentioning

confidence: 86%

“…This excitatory projection has been implicated in cocaine and food self-administration (Dumont et al, 2005;Grueter et al, 2006), drug-seeking (Aston-Jones and Harris, 2004), and stressinduced relapse to cocaine (Erb et al, 2001). The efficiency of this BNST-VTA excitatory projection is enhanced in rats performing an operant task to obtain food or cocaine.…”

Section: Introductionmentioning

confidence: 99%

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Voluntary Nicotine Consumption TriggersIn VivoPotentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Caillé¹,

Guillem

Cador³

et al. 2009

J. Neurosci.

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Active response to either natural or pharmacological reward causes synaptic modifications to excitatory synapses on dopamine (DA) neurons of the ventral tegmental area (VTA). Here, we examine these modifications using nicotine, the main addictive component of tobacco, which is a potent regulator of VTA DA neurons. Using an in vivo electrophysiological technique, we investigated the role of key components of the limbic circuit, the infralimbic cortex (ILCx) and the bed nucleus of the stria terminalis (BNST), in operant behaviors related to nicotine reward. Our results indicated that nicotine self-administration in rats, but not passive delivery, triggers hyperactivity of VTA DA neurons. The data suggest that potentiation of the ILCx-BNST excitatory pathway is involved in these modifications in VTA DA neurons. Thus, recruitment of these specific excitatory inputs to VTA DA neurons may be a neural correlate for the learned association between active responding and the reward experience.

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Section: History Of Voluntary Nicotine Consumption Triggers Potentiatmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

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Voluntary Nicotine Consumption TriggersIn VivoPotentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Caillé¹,

Guillem

Cador³

et al. 2009

J. Neurosci.

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“…Specifically, a population of neurons in the vBNST that projects to the VTA was identified in the rat using a retrograde labeling technique (Dumont and Williams, 2004). Interestingly, these projection neurons have been shown to be differentially modulated by norepinephrine (Dumont and Williams, 2004) as well as altered following cocaine selfadministration (Dumont et al, 2005). In order to more completely understand the ability of ethanol to modulate the important interactions between the vBNST and the VTA, we wanted to specifically determine if vBNST neurons that project to the VTA were similarly sensitive to ethanol.…”

Section: Nr2a Is Not Required For Ethanol Inhibition Of Nmda-epscs Inmentioning

confidence: 99%

Alcohol Inhibits NR2B-Containing NMDA Receptors in the Ventral Bed Nucleus of the Stria Terminalis

Kash

Matthews

Winder

2007

Neuropsychopharmacol

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Components of the mesolimbic dopamine system, in particular dopaminergic cells in the ventral tegmental area (VTA), have been implicated in the acute reinforcing actions of ethanol. The ventral bed nucleus of the stria terminalis (vBNST) potently regulates dopaminergic cell firing in the VTA, and has been implicated in the behavioral actions of ethanol. The N-methyl-D-asparate receptor (NMDAR) is a major molecular target of ethanol, however, current evidence suggests that ethanol regulation of NMDAR function is widely variable and likely depends on a number of factors. Thus, it is critical to investigate ethanol regulation of NMDAR function at synapses relevant to ethanol-regulated behaviors, such as in the vBNST. Here we show, using multiple techniques, that ethanol inhibits NMDAR function in vBNST neurons in a postsynaptic fashion. Further, we demonstrate the functional presence of both NR2A and NR2B-containing NMDARs in the vBNST. While genetic removal of NR2A did not alter the magnitude of ethanol inhibition, pharmacological blockade of NR2B rendered synaptically activated NMDARs insensitive to ethanol inhibition. Finally, we demonstrate that ethanol inhibits NMDARs in cells in the vBNST that project to the VTA, providing a direct means by which ethanol in the vBNST can modulate the dopaminergic system.

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“…To date, lesions (reversible or irreversible) or pharmacological manipulations of the BST suggest roles in the physiology of fear, food intake, social behaviours, pain, and goal-directed behaviours and the associated pathophysiological states such as anxiety, anorexia, and addiction (Ciccocioppo et al, 2003;Colussi-Mas et al, 2005;Crown et al, 2000;Delfs et al, 2000;Deyama et al, 2007Deyama et al, , 2008Deyama et al, , 2009Dumont et al, 2005;Dunn and Williams, 1995;Epping-Jordan et al, 1998;Erb and Stewart,1999;Fendt et al, 2003;Gewirtz et al,1998;Jasnow et al, 2004;Lee and Davis, 1997;Leri et al, 2002;Liu et al, 2009;Nakagawa et al, 2005;Sajdyk et al, 2008;Sullivan et al, 2004;Walker and Davis, 1997;Walker et al, 2000;Wang et al, 2001). …”

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confidence: 99%

What is the bed nucleus of the stria terminalis?

Dumont

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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What exactly is this bed nucleus of the stria terminalis? This is a question that I, and possibly all of my colleague neuroscientists with interest in this region of the brain, get on a regular basis. Unfortunately, the simplest questions are often the most difficult to answer.Firstly, what's in a name? Researchers have failed to reach consensus on whether "BST" or "BNST" is the most effective acronym for their structure of interest. It seems there is little hope for clarification, as there is no scientific or grammatical justification using which we might choose one or the other. To our chagrin, both will probably continue to be commonly used. A description of the BST [sic] should start by reporting that it is a cluster of about 12 nuclei surrounding the caudal part of the anterior commissure, deep in the cerebral hemispheres. The exact number of BST nuclei varies depending on the criteria used, which are, at the moment, mostly anatomical. This may change in the future with more precise and localized permanent or reversible lesion approaches.The BST is so named because it is located at one extremity of the stria terminalis, a bundle of axons that connects it with the amygdaloid nuclei. Although work is still needed to fully understand the function (s) of the BST, extensive anatomical studies of its connectivity suggest that it is a relay center within neurocircuits coordinating the activity of autonomic, neuroendocrine, and somatic motor systems into fully organized physiological functions and behaviours (Dong et al., 2001a,b;Dong and Swanson, 2003, 2004a, b, 2006aHasue and Shammah-Lagnado, 2002;Li and Kirouac, 2008;McDonald et al.,1999;Prewitt and Herman, 1998;Rodaros et al., 2007;Saggu and Lundy, 2007;Shin et al., 2008;Wood and Swann, 2005). Altogether, the BST seems to be a coordinating and relay center where descending cortical information meets ascending interoceptive and exteroceptive information regarding homeostatic states or potential changes in homeostasis. Information likely flows into the BST from exteroceptive (main and accessory olfactory, touch and nociception, gustatory) or interoceptive (energy and fluid levels, tissue damage, sexual hormone levels) sources through all central nervous system levels (from cortical to brain stem and spinal cord). The BST then has widespread descending projections to motor regions of the hindbrain that may trigger or contribute to the elaboration of coordinated physiological and behavioural responses necessary for a well-balanced homeostasis.The BST can be roughly divided into anterior and posterior subdivisions, each containing several nuclei, which can be identified based on their projection pattern and neurochemical identity (Cassell et al., 1986;Day et al

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Self-administration enhances excitatory synaptic transmission in the bed nucleus of the stria terminalis

Cited by 123 publications

References 13 publications

Voluntary Nicotine Consumption TriggersIn VivoPotentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Voluntary Nicotine Consumption TriggersIn VivoPotentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Alcohol Inhibits NR2B-Containing NMDA Receptors in the Ventral Bed Nucleus of the Stria Terminalis

What is the bed nucleus of the stria terminalis?

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