The molecular dynamics of pain control

By S. Hunt, P. Mantyh. Nature Reviews Neuroscience, 2001

623 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/db28fbb243bd81f42b4701e562d7fd9c1cc5b0f7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Clifford J. Woolf
2. Linda R. Watkins
3. E. Milligan
4. Zhi-qi Zhao
5. Apkar Vania Apkarian
6. J. Scholz
7. Dante R. Chialvo
8. Marwan N. Baliki

In Molecular Biology

1. Linda R. Watkins
2. Clifford J. Woolf
3. E. Milligan
4. J. Scholz
5. Dante R. Chialvo
6. Zhi-qi Zhao
7. Jon-Kar Zubieta
8. Manolo Martínez

In Physiology

1. Marwan N. Baliki
2. Clifford J. Woolf
3. Apkar Vania Apkarian
4. Paul Geha
5. Linda R. Watkins
6. J. Scholz
7. E. Milligan
8. Zhi-qi Zhao

Citations in the corpus

• Neural mechanism underlying acupuncture analgesia. (2008, background): “It is well-documented that SP is one of the most important signal molecules mediating peripheral (Zhang et al., 2007b) and spinal nociception (Hunt and Mantyh, 2001).”
• Sensory neuron-specific GPCR Mrgprs are itch receptors mediating chloroquine-induced pruritus. (2009, neutral): “Small-diameter unmyelinated sensory neurons can be broadly divided into two classes: peptidergic and nonpeptidergic (Hunt and Mantyh, 2001).”
• Imperative content and the painfulness of pain (2011, background): “(Hunt and Mantyh 2001, p. 84) The sensory or discriminative dimension may be thought of as a somatic perception of noxious stimuli; its affective dimension, which I am concerning myself with in this paper, is its characteristic unpleasantness.”
• Common oral complications of head and neck cancer radiation therapy: mucositis, infections, saliva change, fibrosis, sensory dysfunctions, dental caries, periodontal disease, and osteoradionecrosis (2017, background): “Pain prevention and management will improve with further understanding of the molecular and neurophysiologic mechanisms underlying the painful condition (Tables 2 and 3) [43, 44].”
• Pathological and protective roles of glia in chronic pain (2009, background): “For example, presynaptic afferent neurons release substance P (also known as tachykinin, precursor 1), which binds to the neurokinin 1 receptor (also known as tachykinin receptor 1) located on postsynaptic pain-projection neuron”
• Can we conquer pain? (2002, background): “The resultant action potentials are conducted to the dorsal horn of the spinal cord, and the input is conveyed, after synaptic processing, via the spinothalamic and spinoparabrachial pathways to higher center”
• Chronic Pain and the Emotional Brain: Specific Brain Activity Associated with Spontaneous Fluctuations of Intensity of Chronic Back Pain (2006, background): “…outside the spinothalamic tract, such as spinoparabrachial, spinostriatal, and spinoreticular pathways (Willis and Westlund, 1997; Gauriau and Bernard, 2002; Braz et al., 2005), as predicted in animal models of neuropathic pain (Hunt and Mantyh, 2001); (3) the interaction between mPFC and DLPFCa.”
• Human brain mechanisms of pain perception and regulation in health and disease (2005, background): “A similar conclusion was arrived at by Hunt and Mantyh (2001) based on studying peripheral and spinal cord changes that accompany neuropathic pain-like behavior in ro- dents.”