IR thermography-based monitoring of respiration phase without image segmentation.

BACKGROUND: Respiratory rate is an essential parameter in biomedical research and clinical applications. Most respiration measurement techniques in preclinical animal models require surgical implantation of sensors. Current clinical measurement modalities typically involve attachment of sensors to the patient, causing discomfort. We have previously developed a non-contact approach to measuring respiration phase in head-restrained rodents using infrared (IR) thermography. While the non-invasive nature of IR thermography offers many advantages, it also bears the complexity of extracting respiration signals from videos. Previously reported algorithms involve image segmentation to identify the nose in IR videos and extract breathing-relevant pixels which is particularly challenging if the videos have low contrast or suffer from suboptimal focusing. NEW METHOD: To address this challenge, we developed a novel algorithm, which extracts respiration signals based on pixel time series, removing the need for nose-tracking and image segmentation. RESULTS & COMPARISON WITH EXISTING METHODS: We validated the algorithm by performing respiration measurements in head-restrained mice and in humans with IR thermography in parallel with established standard techniques. We find the algorithm reliably detects inhalation onsets with high temporal precision. CONCLUSIONS: The new algorithm facilitates the application of IR thermography for measuring respiration in biomedical research and in clinical settings.

Generalized expansion of nociceptive reflex receptive fields in chronic pain patients.

Widespread central hypersensitivity is present in chronic pain and contributes to pain and disability. According to animal studies, expansion of receptive fields of spinal cord neurons is involved in central hypersensitivity. We recently developed a method to quantify nociceptive receptive fields in humans using spinal withdrawal reflexes. Here we hypothesized that patients with chronic pelvic pain display enlarged reflex receptive fields. Secondary endpoints were subjective pain thresholds and nociceptive withdrawal reflex thresholds after single and repeated (temporal summation) electrical stimulation. 20 patients and 25 pain-free subjects were tested. Electrical stimuli were applied to 10 sites on the foot sole for evoking reflexes in the tibialis anterior muscle. The reflex receptive field was defined as the area of the foot (fraction of the foot sole) from which a muscle contraction was evoked. For the secondary endpoints, the stimuli were applied to the cutaneous innervation area of the sural nerve. Medians (25-75 percentiles) of fraction of the foot sole in patients and controls were 0.48 (0.38-0.54) and 0.33 (0.27-0.39), respectively (P=0.008). Pain and reflex thresholds after sural nerve stimulation were significantly lower in patients than in controls (P<0.001 for all measurements). This study provides for the first time evidence for widespread expansion of reflex receptive fields in chronic pain patients. It thereby identifies a mechanism involved in central hypersensitivity in human chronic pain. Reverting the expansion of nociceptive receptive fields and exploring the prognostic meaning of this phenomenon may become future targets of clinical research.

Knockdown of FoxP2 alters spine density in Area X of the zebra finch.

Mutations in the gene encoding the transcription factor FoxP2 impair human speech and language. We have previously shown that deficits in vocal learning occur in zebra finches after reduction of FoxP2 in Area X, a striatal nucleus involved in song acquisition. We recently showed that FoxP2 is expressed in newly generated spiny neurons (SN) in adult Area X as well as in the ventricular zone (VZ) from which the SN originates. Moreover, their recruitment to Area X increases transiently during the song learning phase. The present report therefore investigated whether FoxP2 is involved in the structural plasticity of Area X. We assessed the proliferation, differentiation and morphology of SN after lentivirally mediated knockdown of FoxP2 in Area X or in the VZ during the song learning phase. Proliferation rate was not significantly affected by knockdown of FoxP2 in the VZ. In addition, FoxP2 reduction both in the VZ and in Area X did not affect the number of new neurons in Area X. However, at the fine-structural level, SN in Area X bore fewer spines after FoxP2 knockdown. This effect was even more pronounced when neurons received the knockdown before differentiation, i.e. as neuroblasts in the VZ. These results suggest that FoxP2 might directly or indirectly regulate spine dynamics in Area X and thereby influence song plasticity. Together, these data present the first evidence for a role of FoxP2 in the structural plasticity of dendritic spines and complement the emerging evidence of physiological synaptic plasticity in FoxP2 mouse models.