Biology subjects

Boissonade, F. M.

Publications and source records attributed to Boissonade, F. M..

3 recordsLinked to original sources

bioRxiv2026

Identification and quantification of neurological responses in patients with dentine hypersensitivity

Evaluation of the effectiveness of therapeutic interventions for dentine hypersensitivity is limited by a lack of standardisation and objectivity in measuring the associated pain. To address this, we investigated whether electroencephalography (EEG) can provide an objective, quantitative measure of the condition. Participants with and without dentine hypersensitivity underwent evaporative (air puff) and thermal (cooling probe) tooth stimulation during continuous recording of EEG activity. Sensitivity scores (Schiff Sensitivity score for air puff stimuli, and Visual Analogue Scale score (VAS) for thermal stimuli) were recorded, and participants responses to the Dentine Hypersensitivity Experience Questionnaire (DHEQ) collected. There were strong positive correlations between the Schiff and VAS scores, and also between both sensitivity scores and the impact of dentine hypersensitivity on quality of life (DHEQ). Additionally, EEG data analysis revealed significant differences in event-related potentials (ERP) following evaporative stimulation between participants with different Schiff scores, and in cortical activity between traces where participants indicated discomfort and those where participants did not indicate discomfort during thermal stimulation trials. Topographical maps of EEG band power during thermal stimulation showed progressive cortical recruitment and focal activation emerging in the 3 seconds prior to indication of discomfort. Comparison of EEG band power between response and no response trials to thermal stimulation showed significantly higher delta frequency band power in response trials than in no-response trials. Peak-to-peak amplitude of cortical response during thermal stimulation correlated with DHEQ and VAS scores, and the probe temperature at which participants indicated discomfort. These findings suggest that components of EEG responses align with other measures of dentine sensitivity (DHEQ, Schiff and VAS scores) and can serve as objective neurophysiological markers for evaluating the severity of dentine hypersensitivity.

neuroscience↗

bioRxiv2026

Continuous sumatriptan exposure induces persistent trigeminovascular sensitisation and brain perfusion changes in a rat model of medication overuse headache.

BackgroundRepeated exposure to acute antimigraine medication can promote medication overuse headache, but the mechanisms underlying this transition remain incompletely understood. We used a clinically relevant rat model of continuous sumatriptan exposure to investigate whether medication overuse is associated with persistent sensitisation of the trigeminovascular system and longer-lasting changes in brain perfusion. MethodsAdult male Sprague Dawley rats received continuous subcutaneous sumatriptan (0.6 mg/kg/day) or saline infusion for 6 days via osmotic minipumps. Periorbital and hindpaw mechanical thresholds were measured over 20 days. On day 6 and day 20, trigeminal ganglia and trigeminal nucleus caudalis were processed for immunohistochemistry for pERK, pp38, Iba-1, GFAP and NeuN. On day 20, a subgroup received sodium nitroprusside (SNP, 3 mg/kg, i.p.) to unmask latent sensitisation. Cerebral blood flow was assessed by MRI. ResultsSumatriptan induced reversible cephalic and extracephalic allodynia. Previously exposed rats showed evidence of persistent sensitisation, including enhanced biomarker and glial responses after withdrawal and following SNP challenge. pERK and pp38 expression increased in both the trigeminal ganglion and trigeminal nucleus caudalis. In the TNC, marker association shifted over time from predominantly neuronal at day 6 to greater apparent glial association at day 20. Iba-1 and GFAP expression increased after withdrawal of sumatriptan and was further enhanced by SNP challenge. Within the TNC, neuronal marker expression was greatest in the ophthalmic representation. Sumatriptan exposure also produced a persistent reduction in cerebral blood flow that remained evident after behavioural recovery. ConclusionContinuous sumatriptan exposure produces prolonged trigeminovascular neuronal and glial alterations together with persistent changes in brain perfusion. These data support a state of latent sensitisation after repeated triptan exposure and provide mechanistic insight into medication overuse headache. HIGHLIGHTSO_LIRepeated sumatriptan exposure induces reversible cephalic and extracephalic allodynia but leaves persistent trigeminovascular sensitisation after drug withdrawal. C_LIO_LIpERK and pp38 expression increase in the trigeminal ganglion and trigeminal nucleus caudalis, with the strongest regional changes seen in the ophthalmic representation of the TNC. C_LIO_LIDelayed increases in Iba-1 and GFAP in the TNC suggest that glial activation may contribute to maintenance of latent sensitisation, although the colocalisation findings are qualitative and should be interpreted cautiously. C_LIO_LIRepeated sumatriptan exposure is also associated with a persistent reduction in cerebral blood flow, indicating longer-lasting changes in brain perfusion beyond the period of overt allodynia. C_LI

neuroscience↗

bioRxiv2024

Investigation of cellular and molecular changes linked with neuropathic pain in healthy and injured human trigeminal nerves

Injuries to the trigeminal nerve, responsible for sensory innervation to the face, may occur during routine dental procedures, resulting in the formation of a neuroma accompanied by loss of sensation and/or symptoms of pain. In order to gain insight into the molecular mechanisms underpinning the sensory changes, single nuclei RNA sequencing and spatial transcriptomics were employed to profile the transcriptional landscape at single cell resolution of human trigeminal nerves and neuromas. Cellular and transcriptional changes were identified that correlated with the presence of pain, including an expansion of endothelial cells with a pro-inflammatory phenotype and over-expression of HLA-A, CXCL2 and CXCL8. Interactome analysis highlighted signalling changes linked with the presence of pain. HLA-A protein expression was confirmed in neuromas and positively correlated with symptoms of pain. The atlas generated represents a valuable resource for pain research, highlighting the role of inflammation, endothelial cell dysfunction and chemokine signalling in neuropathic pain.

neuroscience↗