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Screening and Pharmacological Management of Neuropathic Pain
Published in Suvardhan Kanchi, Rajasekhar Chokkareddy, Mashallah Rezakazemi, Smart Nanodevices for Point-of-Care Applications, 2022
Manu Sharma, Ranju Soni, Kakarla Raghava Reddy, Veera Sadhu, Raghavendra V. Kulkarni
Voltage-gated sodium channels (VGSC) are a necessary component of nerve impulse conduction. The utilization of VGSC blockers can augment pain relief during neuropathic pain conditions. Since α subunits of VGSC encode genes potentially relevant for neuropathic pain are namely NaV1.3, NaV1.7, NaV1.8, and NaV1.9. NaV1.3. However, researchers have considered NaV1.3 as a suitable target for pain therapeutics due to its upregulated overexpression in dorsal horn sensory neurons after injury in the nervous system. NaV1.7 is present at excessive levels in growth cones of small-diameter neurons whereas the NaV1.8 channel is particularly expressed in primary sensory neurons to conduct most of the inward current during an action potential. The knockdown of NaV1.8 channel expression in rats reversed injury-induced hyperalgesia in a neuropathic pain model and decreased bladder hyperactivity in a visceral pain model. The peripheral sodium channel NaV1.9 exclusively resides in the dorsal root ganglia and emphasizes neurotrophin (BDNF)-evoked depolarization and excitation. Thus, the development of specific VGSC blockers can be an alternative treatment for pain relief.
Spinal Cord and Reflexes
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Monoamines exercise their effects through G protein second-messenger systems (Section 6.3). Generally speaking, these effects vary progressively from predominantly excitatory in the ventral horn to predominantly inhibitory in the dorsal horn, depending on the receptors involved. The excitatory effects involve Gαq protein subunits and 5-HT2 and NEα1 receptors, whereas the inhibitory effects involve Gi/o protein and 5-HT1 and NEa2 receptors and is mostly extrasynaptic (Section 6.2.3), affecting both interneurons and astrocytes. On the sensory side, the inhibition in the dorsal horn is mostly presynaptic inhibition of high-threshold afferents and is linked to the suppression of pain pathways, as may be required during exposure to a high-stress environment or stimulus. On the motor side, the monoamines strongly suppress the flexion reflex (Section 11.3.2). In the intermediate regions of the spinal cord, there is moderate facilitation of interneurons receiving inputs from Ia, II, and Ib afferents.
Control of Postoperative Pain by Self-Administered Opioids
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
A very interesting aspect of the ascending pain systems is that their “gains” are under neural feedback control from the central nervous system (CNS). This is one reason why individual reactions to pain can vary tremendously. The pain control system consists of efferent nerve fibers originating in the raphe magnus nucleus in the lower pons-upper medulla area. These fibers travel down the spinal cord’s dorsolateral columns to the appropriate segments’ pain inhibitory complex in the dorsal horns, where they synapse with the dorsal horn pain neurons. The neurotransmitter stimulating the descending fibers originating in the raphe magnus nucleus is mostly enkephalin. The descending fibers secrete the neurotransmitter serotonin (5HT) to activate ventral horn pain control interneurons. These interneurons secrete the neurotransmitter enkephalin, which causes presynaptic inhibition of the primary A8 and C pain neurons. This inhibition can last for many minutes or even hours,59blocking primary pain signals at their entry point to the spinal cord and some local pain reflexes. Figures 9.1 A and B show schematically the neural “wiring” associated with pain transmission to the CNS and endogenous, efferent pain control. The pain control system no doubt also acts in the CNS at the various relay points for pain information; however, few details are known of these actions.
Developing an optimized strategy with transcranial direct current stimulation to enhance the endogenous pain control system in fibromyalgia
Published in Expert Review of Medical Devices, 2018
Dante Duarte, Luis Eduardo Coutinho Castelo-Branco, Elif Uygur Kucukseymen, Felipe Fregni
When this endogenous pain control system is dysfunctional, the excessive response can lead to hyperalgesia, allodynia, and ultimately chronic pain. A decreased postsynaptic inhibition in somatosensory neurons of the dorsal horn can lead to central pain sensitization [5] or to a dysfunction in descending pain modulating pathways which include the periaqueductal gray (PAG) and the rostroventromedial medulla [6]. The understanding of chronic pain as a phenomenon resulting from this imbalance has led to the development of interventions aimed at novel targets in the central nervous system [7].