Activation of the β-Adrenoceptor–Protein Kinase A Signaling Pathway within the Ventral Bed Nucleus of the Stria Terminalis Mediates the Negative Affective Component of Pain in Rats

Deyama, Satoshi; Katayama, Takahiro; Ohno, Atsushi; Nakagawa, Takayuki; Kaneko, Shuji; Yamaguchi, Taku; Yoshioka, Mitsuhiro; Minami, Masabumi

doi:10.1523/jneurosci.1480-08.2008

Cited by 67 publications

(65 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such neural connectivity provides a route by which contextual information encoded by the HPF could bypass the BLA and activate the vPAG to generate freezing. Conversely, the BST is capable of receiving noxious information (i.e., footshock) both directly and indirectly (37,38). Consistent with this hypothesis, lesions or inactivations of the BST result in a wide range of fear-and anxiety-related deficits (39)(40)(41)(42).…”

mentioning

confidence: 67%

Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis

Poulos

Ponnusamy²,

Dong³

et al. 2010

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

View full text Add to dashboard Cite

The basolateral amygdala (BLA) is thought to be essential for fear learning. However, extensive training can overcome the loss of conditional fear evident following lesions and inactivation of the BLA. Such results suggest the existence of a primary BLA-dependent and a compensatory BLA-independent neural circuit. We tested the hypothesis that the bed nuclei of the stria terminalis (BST) provides this compensatory plasticity. Using extensive context-fear conditioning, we demonstrate that combined BLA and BST lesions prevented fear acquisition and expression. Additionally, protein synthesis in the BST was critical only for consolidation of BLA-independent but not BLA-dependent fear. Moreover, fear acquired after BLA lesions resulted in greater activation of BST regions that receive hippocampal efferents. These results suggest that the BST is capable of functioning as a compensatory site in the acquisition and consolidation of context-fear memories. Unlocking such neural compensation holds promise for understanding situations when brain damage impairs normal function or failure to regulate compensatory sites leads to anxiety disorders. amygdala | basolateral amygdala | context | plasticity | bed nucleus of the stria terminalis A largely supported view in the neuroscience of associative memory is the existence of essential neural circuits that have the capacity to learn, retain, and retrieve specific classes of experience 1-7). For example, in reflexive motor learning or Pavlovian eyeblink-conditioning, the integration of sensory stimuli within the cerebellar interpositus nuclei are required for the acquisition, retention, and retrieval conditional responses (8). Similarly, the striatum is considered critical for habit learning (9, 10) and the hippocampus essential for spatial learning (11). In fearconditioning, a circuit centered around the basolateral amygdala complex (BLA; consisting of the lateral amygdala, basomedial, basolateral, and posterior nuclei) is viewed essential for the acquisition and expression of fear memories (12-16). The importance of the BLA for fear memory has been supported by numerous studies showing that disruption of protein synthesis, NMDA receptor function, neuronal activity, synaptic transmission, and plasticity all prevent the establishment of fear memories (14-18).Context fear learning normally occurs when hippocampal context information, which exits the subiculum, converges with aversive information in the BLA (15). In turn, when the contextual information activates the BLA, this information is relayed to the central nucleus of the amygdala (CEA), whose efferents to the ventral periaqueductal gray (vPAG) trigger the expression of fear as indexed by conditional freezing (conditional response) (19). Lesions or inactivations of the CEA can disrupt contextual fear (20, 21; but see 22). Of particular relevance in this study is that pretraining lesions or inactivations of the BLA have been shown to strongly impair the acquisition of fear (23-25). However, with extensive overtraining (∼75 tr...

show abstract

mentioning

confidence: 67%

Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis

Poulos

Ponnusamy²,

Dong³

et al. 2010

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

View full text Add to dashboard Cite

show abstract

“…β-Adrenergic receptors are closely related to opioids (12), and the β 1 -adrenergic receptor is reported to be especially involved in the negative affective component of pain (14). The A145G SNP (rs1801252) causes an amino acid substitution.…”

Section: A145g Snpmentioning

confidence: 99%

“…The BNST also reportedly plays an important role in the generation of the negative affective component of pain and is densely innervated by noradrenergic fibers (13). A report that examined the role of noradrenergic transmission within the BNST found that an intra-ventral BNST injection of the β-adrenergic antagonist timolol dose-dependently attenuated intraplantar formalin-induced conditioned place aversion without reducing nociceptive behaviors (14). Thus, β-adrenergic receptors, whose involvement in the negative affective component of pain has been demonstrated, are also considered likely to affect pain sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Association Between Genetic Polymorphisms of the ^|^beta;1-Adrenergic Receptor and Sensitivity to Pain and Fentanyl in Patients Undergoing Painful Cosmetic Surgery

et al. 2013

View full text Add to dashboard Cite

Abstract. Individual differences in the sensitivity to fentanyl, a widely used opioid analgesic, can hamper effective pain treatment. The adrenergic system is reportedly involved in the mechanisms of pain and analgesia. Here, we focused on one of the adrenergic receptor genes, ADRB1, and analyzed the influence of single-nucleotide polymorphisms (SNPs) in the ADRB1 gene on individual differences in pain and analgesic sensitivity. We examined associations between pain and fentanyl sensitivity and the two SNPs, A145G and G1165C, in the human ADRB1 gene in 216 Japanese patients who underwent painful orofacial cosmetic surgery, including bone dissection. The patients who carried the A-allele of the A145G SNP were more sensitive to cold pressorinduced pain than those who did not carry this allele, especially in male patients. The analgesic effect was significantly less in females who carried the G-allele of the G1165C SNP than the females who did not carry the G-allele. The haplotype analysis revealed a significant decrease in 24-h postoperative fentanyl use in female 145A/1165C haplotype carriers. These results suggest that SNPs in the ADRB1 gene are associated with individual differences in pain and analgesic sensitivity, and analyzing these SNPs may promote personalized pain treatment in the future.

show abstract

“…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). …”

mentioning

confidence: 99%

What is the bed nucleus of the stria terminalis?

Dumont

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

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

show abstract

Activation of the β-Adrenoceptor–Protein Kinase A Signaling Pathway within the Ventral Bed Nucleus of the Stria Terminalis Mediates the Negative Affective Component of Pain in Rats

Cited by 67 publications

References 21 publications

Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis

Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis

Association Between Genetic Polymorphisms of the ^|^beta;1-Adrenergic Receptor and Sensitivity to Pain and Fentanyl in Patients Undergoing Painful Cosmetic Surgery

What is the bed nucleus of the stria terminalis?

Contact Info

Product

Resources

About