Age-related changes in peripheral nociceptor function

Jennings, Elaine M.; Sullivan, Laura C.; Jamshidi, Raehannah J.; LoCoco, Peter M.; Smith, Hudson R.; Chavera, Teresa A.; Berg, Kelly A.; Clarke, William P.

doi:10.1016/j.neuropharm.2022.109187

Cited by 7 publications

(3 citation statements)

References 110 publications

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“…Although the thresholds for normal tactile sensations such as gentle touch and vibration are greater in the elderly, − their thresholds for noxious mechanical stimuli are easier to reach . For example, inflammatory injury causes more severe thermal and mechanical hyperalgesia in aged rats compared to normal adult rats . As a result, older adults are more likely to suffer from neuropathic pain due to increased pain sensitivity.…”

Section: Introductionmentioning

confidence: 99%

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Molecular and Cellular Mechanisms of Neuropathic Pain in Aging

Huang

Chang

et al. 2023

ACS Chem. Neurosci.

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Neuropathic pain is a chronic condition that tends to worsen over time, leading to a significant decline in patients' quality of life. The elderly population is disproportionately affected by this burden, as evidenced by the high prevalence of this condition in such a demographic. While previous studies have demonstrated the involvement of various signaling pathways critical to neuropathic pain, the relationship between aging and the onset or persistence of this condition has been overlooked. Greater focus was placed on the efficacy and tolerability of medications, as well as new protocols for assessing pain in patients with cognitive impairment, with less regard for reasons underlying the increased susceptibility of elderly individuals to pain. This Review thus aims to summarize the contributions of aging to neuropathic pain, covering weakened repair function, increased intracellular calcium signaling, enhanced oxidative stress, dysfunctional brain function, impaired descending inhibition, alterations in the innate immune cell population, and the effects of comorbidity caused by aging. A better understanding of these aspects could drive new treatment options thereby yielding better outcomes for elderly patients in pain.

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Section: Introductionmentioning

confidence: 99%

“…5 For example, inflammatory injury causes more severe thermal and mechanical hyperalgesia in aged rats compared to normal adult rats. 6 As a result, older adults are more likely to suffer from neuropathic pain due to increased pain sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Molecular and Cellular Mechanisms of Neuropathic Pain in Aging

Huang

Chang

et al. 2023

ACS Chem. Neurosci.

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“…Pain sensing is a complicated phenomenon that typically requires the stimulation of local nociceptive neurons (nociceptors) that transmit pain-signaling messages to the spinal cord and brain ( Jennings et al, 2022 ). As an immunological potentiator, CFA enhances cell-mediated immunity and boosts the synthesis of immunoglobulins.…”

Section: Introductionmentioning

confidence: 99%

Catalpol ameliorates CFA-induced inflammatory pain by targeting spinal cord and peripheral inflammation

Zhao

Fu²,

Ni³

et al. 2022

Front. Pharmacol.

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Chronic, inflammatory pain is an international health concern that severely diminishes individuals’ quality of life. Catalpol is an iridoid glycoside derived from the roots of Rehmannia glutinosa that possesses anti-inflammatory, antioxidant, and neuroprotective properties for the treating multiple kinds of disorders. Nevertheless, catalpol’s impacts on inflammatory pain and its potential methods of action are still unclear. The purpose of this investigation is to determine the mechanism of catalpol to reduce the inflammatory pain behaviors in a rat model with complete Freund’s adjuvant (CFA). Catwalk, Von-Frey, and open field testing were performed for behavioral assessment. Western blot analysis and real-time quantitative PCR (RT-PCR) were employed to identify variations in molecular expression, while immunofluorescence was utilized to identify cellular localization. Catalpol effectively reduced CFA-induced mechanical allodynia and thermal hyperalgesia when injected intrathecally. Moreover, catalpol can regulate the HDAC4/PPAR-γ-signaling pathway in CFA rat spinal cord neurons. Meanwhile catalpol significantly decreased the expression of the NF-κB/NLRP3 inflammatory axis in the spinal cord of CFA rats. In addition, both in vivo and in vitro research revealed that catalpol treatment inhibited astrocyte activation and increase inflammatory factor expression. Interestingly, we also found that catalpol could alleviate peripheral pain by inhibiting tissue inflammation. Taken together, the findings declared that catalpol may inhibit inflammatory pain in CFA rats by targeting spinal cord and peripheral inflammation.

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