Association between untreated low back pain and injury proneness and confounding role of behavioral-health difficulties among younger adolescents: a population-based study

Chau, Kénora; Chau, Nearkasèn

doi:10.1007/s00586-023-07679-4

Cited by 1 publication

(1 citation statement)

References 24 publications

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“…Notably, frequent acute pain and pain interference are associated with an elevated risk of being diagnosed with an alcohol use disorder (AUD) (Barry et al, 2013;Edlund et al, 2013;McDermott et al, 2018). This dynamic extends to adolescents where untreated pain correlates with earlier initiation of alcohol use (Chau & Chau, 2023), and alcohol consumption is associated with heightened ongoing and future pain (Hestbaek et al, 2006;Horn-Hofmann et al, 2018;Pascale et al, 2022). Recent preclinical studies in rodents further indicate that adolescent intermittent ethanol (AIE) exposure induces persistent hyperalgesia spanning into adulthood (Bertagna et al, 2024;Kelley et al, 2023;Khan et al, 2023;Secci et al, 2024).…”

Section: Introductionmentioning

confidence: 99%

Adolescent alcohol exposure promotes mechanical allodynia and alters synaptic function at inputs from the basolateral amygdala to the prelimbic cortex

Obray,

Wilkes,

Scofield

et al. 2024

Preprint

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Binge drinking is common among adolescents despite mounting evidence linking it to various adverse health outcomes that includes heightened pain perception. The prelimbic (PrL) cortex is vulnerable to insults from adolescent alcohol exposure and receives input from the basolateral amygdala (BLA) while sending projections to the ventrolateral periaqueductal gray (vlPAG) - two brain regions implicated in nociception. In this study, adolescent intermittent ethanol (AIE) exposure was carried out in male and female rats using a vapor inhalation procedure. Mechanical and thermal sensitivity, assessed throughout adolescence and into adulthood, revealed that AIE exposure induced protracted mechanical allodynia in both male and female rats. However, a carrageenan inflammatory paw pain challenge in adult rats revealed that AIE did not further augment carrageenan-induced hyperalgesia. To investigate synaptic function at BLA inputs onto defined populations of PrL neurons, retrobeads and viral labelling were combined with optogenetics and slice electrophysiology. Recordings from retrobead labelled cells in the PrL revealed AIE reduced BLA driven feedforward inhibition of neurons projecting from the PrL to the vlPAG (PrLPAGneurons), resulting in augmented excitation/inhibition (E/I) balance and increased intrinsic excitability. Consistent with this finding, recordings from virally tagged PrL parvalbumin interneurons (PVINs) demonstrated that AIE exposure reduced both E/I balance at BLA inputs onto PVINs and PVIN intrinsic excitability when assessed in adulthood. These findings provide compelling evidence that AIE and acute pain alter synaptic function and intrinsic excitability within a prefrontal nociceptive circuit.

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