A synaptocentric view of the neuroendocrine response to stress

Wamsteeker, Jaclyn I.; Bains, Jaideep S.

doi:10.1111/j.1460-9568.2010.07513.x

Cited by 33 publications

(33 citation statements)

References 159 publications

(148 reference statements)

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“…This stimulus-defined afferent ‘set’ then mediates a CRH neuronal response to the stressor that is appropriately graded to the nature and strength of the stimulus [Watts, 2005; Watts & Khan, 2011]. It will involve a controlled and coordinated activation of ACTH secretogogue synthesis and release processes, including increased action potential frequency, the accumulation of phospho-(p)CREB, nuclear TORC2, pERK1/2, Fos, CRH hnRNA and mRNA, ACTH secretogogue release, etc [Herman et al, 2003; Khan & Watts, 2004; Liu et al, 2008, 2010, 2012; Wamsteeker & Bains, 2010; Osterlund et al, 2012].…”

Section: Stressors Crh Neurons and The Hypothalamo-pituitary-adrmentioning

confidence: 99%

“…[see Herman et al, 2002, 2003; Levy & Tasker, 2012; Wamsteeker & Bains, 2010; Watts, 2005, for reviews]. So a fundamental part of understanding how CRH neuroendocrine control systems function is resolving how stressors impact CRH neurons using a pre-motor network that is comprised of the neurons that form direct synaptic connections with CRH neurons.…”

Section: A Pre-motor Network That Controls the Neuroendocrine Pvhmentioning

confidence: 99%

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Identifying Links in the Chain

Watts

Khan²

2013

A New Era of Catecholamines in the Laboratory and Clinic

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Compared to conventional neurons that use synaptic mechanisms to communicate with closely apposed targets, peptidergic neuroendocrine neurons release relatively large quantities of peptide into the vasculature to control neuroendocrine function at more distal sites. This means that maintaining adequate amounts of peptide for release through controlled biosynthesis is critical for their function. But the flexible and adaptive responses these neurons generate to many different challenges require synthesis and release must be coordinated in some way. How neuroendocrine—or in fact, any neuropeptide—neurons link appropriate levels of peptide biosynthesis with the patterns of action potentials that drive peptide release is unknown. Here we review possible mechanisms used by CRH neuroendocrine neurons in the paraventricular nucleus of the hypothalamus to achieve this coordination as they are driven by catecholaminergic inputs from the hindbrain. These particular inputs are essential for ACTH responses to glycemic challenges. We then compare this situation to the one seen across the day in the absence of stress when circulating ACTH and corticosterone exhibit predictable variations throughout the day. This activity pattern is driven by a completely different set of inputs. Based on these and other results, we propose that CRH synthesis and release mechanisms are not tightly and invariably linked together as CRH neurons are activated. Instead, complex coupling mechanisms exist both as a property of the pre-motor network that provides direct synaptic inputs to CRH neurons, and in the complex intracellular signal transduction mechanisms engaged by the very diverse set of receptors expressed by CRH neurons. This coupling process provides neuroendocrine CRH neurons with a versatile and dynamic mechanism that links peptide biosynthesis and release in an efficient and highly adaptable manner.

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Section: Stressors Crh Neurons and The Hypothalamo-pituitary-adrmentioning

confidence: 99%

Section: A Pre-motor Network That Controls the Neuroendocrine Pvhmentioning

confidence: 99%

Identifying Links in the Chain

Watts

Khan²

2013

A New Era of Catecholamines in the Laboratory and Clinic

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“…Parvocellular neuroendocrine cells in the paraventricular nucleus of the hypothalamus are at the head of the hypothalamic-pituitaryadrenal axis, both mediating glucocorticoid release and responding to negative feedback (Wamsteeker and Bains, 2010). Sustained stress unmasks presynaptic LTD GABA in which the probability of GABA release onto these neurons is decreased by retrograde opioid release (Wamsteeker Cusulin et al, 2013).…”

Section: Rgs4mentioning

confidence: 99%

Roles for Regulator of G Protein Signaling Proteins in Synaptic Signaling and Plasticity

2015

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The regulator of G protein signaling (RGS) family of proteins serves critical roles in G protein-coupled receptor (GPCR) and heterotrimeric G protein signal transduction. RGS proteins are best understood as negative regulators of GPCR/G protein signaling. They achieve this by acting as GTPase activating proteins (GAPs) for Ga subunits and accelerating the turnoff of G protein signaling. Many RGS proteins also bind additional signaling partners that either regulate their functions or enable them to regulate other important signaling events. At neuronal synapses, GPCRs, G proteins, and RGS proteins work in coordination to regulate key aspects of neurotransmitter release, synaptic transmission, and synaptic plasticity, which are necessary for central nervous system physiology and behavior. Accumulating evidence has revealed key roles for specific RGS proteins in multiple signaling pathways at neuronal synapses, regulating both pre-and postsynaptic signaling events and synaptic plasticity. Here, we review and highlight the current knowledge of specific RGS proteins (RGS2, RGS4, RGS7, RGS9-2, and RGS14) that have been clearly demonstrated to serve critical roles in modulating synaptic signaling and plasticity throughout the brain, and we consider their potential as future therapeutic targets.

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“…Hewitt and colleagues (2009) demonstrated that following acute restraint stress, the parvocellular neuroendocrine cells undergo a depolarizing shift in the reversal potential for chloride ions by activation of α 1 -adrenoceptors thereby inhibiting the activity of transmembrane potassium-chloride-cotransporter 2. This impaired chloride ion extrusion within the parvocellular neuroendocrine cells leads to impaired GABA-A receptor-mediated inhibitory control of the HPA axis following the onset of stress (Wamsteeker and Bains, 2010). Under stressful conditions, the HPA axis is regulated by glucocorticoid-mediated negative feedback to extra-hypothalamic centres, hypothalamus, and anterior pituitary to terminate the stress response and restore homeostasis (Pardridge and Mietus, 1979;De Kloet et al, 1998).…”

Section: The Stress Systemsmentioning

confidence: 99%

“…The autonomic nervous system (ANS) quickly responds to stress exposure through the sympathetic and parasympathetic divisions. The rapidly activated sympathetic catecholamines are responsible for generation of the 'fight or flight' response in addition to potentiating the pituitary gland to subsequent hypothalamic activation (Wamsteeker and Bains, 2010). The hypothalamic-spinal-adrenocortical (HSA) axis modulates adrenal sensitivity to adrenocorticotropic hormone (ACTH) through a nitric oxide-mediated pathway (Jansen et al, 1995;Mohn et al, 2005;Ulrich-Lai et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The effects of short term stress on the central and peripheral nitrergic system

Chen¹

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The mammalian stress response is generated by several integrated neural systems that allow rapid adaptation to homeostatic disturbances. This is principally mediated through the hypothalamicpituitary-adrenal axis which mobilises energy reserves by adrenal glucocorticoids. This in turn accelerates cellular metabolism which consequently increases free radical formation through the mitochondrial electron transport chain. Excess generation of free radicals such as reactive oxygen and nitrogen species (RNS) may potentially cause damage to fatty acids, proteins, and DNA by oxidative and nitrosative stress. Nitric oxide is a ubiquitous signalling molecule belonging to the family of RNS and is endogenously synthesised from ʟ-arginine by nitric oxide synthase (NOS).Three distinct subtypes of NOS have been identified, with the neuronal and endothelial isoforms being constitutively expressed enzymes responsible for synaptic signalling and smooth muscle relaxation. The inducible isoform is primarily present in cells of the inflammatory immune system where its activity is transcriptionally induced by cytokines and other inflammatory agents and thus, is thought to play an important role in immunomodulation. Recently, a number of studies have demonstrated that the nitrergic system have significant implications in neuropsychiatric disorders including anxiety and depression. Specifically, chronic stress-induced hippocampal neuronal NOS upregulation is responsible for glucocorticoid receptor downregulation, a factor linked to the development of depressive disorders. Although stress and nitrergic signalling are intrinsically linked in pathological states, little is known about the acute physiology between these two systems.Therefore, the primary aim of this thesis was to establish the profile of nitrosative changes in peripheral blood and brain regions known to be impacted by stress following an acute psychological challenge. The observed changes were subsequently investigated by employing a pharmacological intervention using a novel stress-alleviating and anti-inflammatory endocannabinoid enhancer. To achieve the aims for this thesis, Male Wistar rats aged 5-7 weeks postnatal were maintained under control conditions or subjected to acute stress. Blood samples were collected at time-points immediately before, during, and following treatment in order to estimate the levels of stress hormones and redox parameters including oxidative/nitrosative status, glutathione and glutathione disulphide ratio, and lipid peroxidation. Post mortem neural tissue was collected and specific brain regions were isolated for the determination of nitrosative status, NOS enzymatic activity, and relative gene expression of stress and nitrergic-related genes. Following the establishment of these measurements, a separate group of animals was used to examine the effects of endocannabinoid modulation on the nitrergic and inflammatory-related indicators following acute stress.ii We found that exposure to a single episode of psychological stress causes e...

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A synaptocentric view of the neuroendocrine response to stress

Cited by 33 publications

References 159 publications

Identifying Links in the Chain

Identifying Links in the Chain

Roles for Regulator of G Protein Signaling Proteins in Synaptic Signaling and Plasticity

The effects of short term stress on the central and peripheral nitrergic system

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