Origin of some enkephalin-containing afferents to the ventro-medial region of the globus pallidus in the rat

Arluison, Michel; Vankova, Myriana; François, Clément; Leviel, Vincent

doi:10.1016/0361-9230(90)90249-y

Cited by 19 publications

(9 citation statements)

References 47 publications

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“…If OT also excites CRF neurons of the BNST, presynaptic CRFR2 on OT terminals may act in a feedback fashion to modulate OT release in the BNST ALG . Furthermore, small-caliber CRFR2-ir axonal terminals observed in EM study, which presumably are glutamatergic and make asymmetric axo-spinous synapses, might preferentially target local circuit GABAergic interneurons, or neurons containing peptide neurotransmitters other than CRF, such as enkephalin, somatostatin, or neuropeptide Y (Arluison et al, 1990; Walter et al, 1991). Activation of this cell population may then inhibit the CRF cell population.…”

Section: Discussionmentioning

confidence: 93%

Neuroanatomical evidence for reciprocal regulation of the corticotrophin-releasing factor and oxytocin systems in the hypothalamus and the bed nucleus of the stria terminalis of the rat: Implications for balancing stress and affect

Dabrowska¹,

Hazra²,

Ahern

et al. 2011

Psychoneuroendocrinology

231

207

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Summary Activation of corticotrophin releasing factor (CRF) neurons in the paraventricular nucleus of the hypothalamus (PVN) is necessary for establishing the classic endocrine response to stress, while activation of forebrain CRF neurons mediates affective components of the stress response. Previous studies have reported that mRNA for CRF2 receptor (CRFR2) is expressed in the bed nucleus of the stria terminalis (BNST) as well as hypothalamic nuclei, but little is known about the localization and cellular distribution of CRFR2 in these regions. Using immunofluorescence with confocal microscopy, as well as electron microscopy, we demonstrate that in the BNST CRFR2-immunoreactive fibers represent moderate to strong labeling on axons terminals. Dual-immunofluorescence demonstrated that CRFR2-fibers co-localize oxytocin (OT), but not arginine-vasopressin (AVP), and make perisomatic contacts with CRF neurons. Dual-immunofluorescence and single cell RT-PCR demonstrate that in the hypothalamus, CRFR2 immunoreactivity and mRNA are found in OT, but not in CRF or AVP-neurons. Furthermore, CRF neurons of the PVN and BNST express mRNA for the oxytocin receptor, while the majority of OT/CRFR2 neurons in the hypothalamus do not. Finally, using adenoviral-based anterograde tracing of PVN neurons, we show that OT/CRFR2-immunoreactive fibers observed in the BNST originate in the PVN. Our results strongly suggest that CRFR2 located on oxytocinergic neurons and axon terminals might regulate the release of this neuropeptide and hence might be a crucial part of potential feedback loop between the hypothalamic oxytocin system and the forebrain CRF system that could significantly impact affective and social behaviors, in particular during times of stress.

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Section: Discussionmentioning

confidence: 93%

Neuroanatomical evidence for reciprocal regulation of the corticotrophin-releasing factor and oxytocin systems in the hypothalamus and the bed nucleus of the stria terminalis of the rat: Implications for balancing stress and affect

Dabrowska¹,

Hazra²,

Ahern

et al. 2011

Psychoneuroendocrinology

231

207

View full text Add to dashboard Cite

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“…These results show that the neurochemical identity of BNST neurons is reflected in important functional differences. It is noteworthy that various neuropeptides, such as enkephalin (Arluison et al, 1990), neuropeptide Y and substance P (Walter et al, 1991) are richly expressed in this structure. Future studies are needed to identify the role of these neurotransmitters in anxiety.…”

Section: Beyond the Amygdala: The Extended Amygdalamentioning

confidence: 99%

Distributed circuits underlying anxiety

Adhikari

2014

Front. Behav. Neurosci.

177

154

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Anxiety is of paramount importance for animals, as it allows assessment of the environment while minimizing exposure to potential threats. Furthermore, anxiety disorders are highly prevalent. Consequently, the neural circuitry underlying anxiety has been a topic of great interest. In this mini review, we will discuss current views on anxiety circuits. We will focus on rodent anxiety paradigms, but we will also consider results from human neuroimaging and clinical studies. We briefly review studies demonstrating the central role that the amygdala and the bed nucleus of the stria terminals (BNST) play in modulating anxiety and present evidence showing how the bed nucleus uses different output pathways to influence specific features of anxiolysis. Lastly, we propose that several brain regions, such as the medial prefrontal cortex (mPFC) and the ventral hippocampus (vHPC), act in a coordinated fashion with the amygdala and BNST, forming a distributed network of interconnected structures that control anxiety both in rodents and humans.

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“…In addition, they express a variety of neuropeptides including CRF, enkephalin, NPY and substance P (Malsbury and McKay, 1987; Arluison et al, 1990; Walter et al, 1991; Champagne et al, 1998). While the majority of neurons appear somewhat similar in morphology to medium spiny neurons, Golgi-impregnation studies reveal an impressive array of cellular morphologies (McDonald, 1983; Larriva-Sahd, 2006).…”

Section: Properties Of Bnst Neuronsmentioning

confidence: 99%

Modulation of glutamatergic synaptic transmission in the bed nucleus of the stria terminalis

McElligott

Winder

2009

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Glutamate, catecholamine and neuropeptide signaling within the bed nucleus of the stria terminalis (BNST) have all been identified as key participants in anxiety-like behaviors and behaviors related to withdrawal from exposure to substances of abuse. The BNST is thought to serve as a key relay between limbic cognitive centers and reward, stress and anxiety nuclei. Human studies and animal models have demonstrated that stressors and drugs of abuse can result in long term behavioral modifications that can culminate in psychological diseases such as addiction and post-traumatic stress disorder. The ability of catecholamines and neuropeptides to influence synaptic glutamatergic transmission (stemming from cognitive centers) within the BNST may have profound consequences over these behaviors. In this review we highlight studies examining synaptic plasticity and modulation of excitatory transmission within the BNST, emphasizing how such modulation may result in alterations in anxiety and reward related behavior.

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Origin of some enkephalin-containing afferents to the ventro-medial region of the globus pallidus in the rat

Cited by 19 publications

References 47 publications

Neuroanatomical evidence for reciprocal regulation of the corticotrophin-releasing factor and oxytocin systems in the hypothalamus and the bed nucleus of the stria terminalis of the rat: Implications for balancing stress and affect

Neuroanatomical evidence for reciprocal regulation of the corticotrophin-releasing factor and oxytocin systems in the hypothalamus and the bed nucleus of the stria terminalis of the rat: Implications for balancing stress and affect

Distributed circuits underlying anxiety

Modulation of glutamatergic synaptic transmission in the bed nucleus of the stria terminalis

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