Dose-dependent effects of high intensity focused ultrasound on compound action potentials in an ex vivo rodent peripheral nerve model: comparison to local anesthetics.

BACKGROUND: In animal models, focused ultrasound can reversibly or permanently inhibit nerve conduction, suggesting a potential role in managing pain. We hypothesized focused ultrasound's effects on action potential parameters may be similar to those of local anesthetics. METHODS: In an ex vivo rat sciatic nerve model, action potential amplitude, area under the curve, latency to 10% peak, latency to 100% peak, rate of rise, and half peak width changes were assessed after separately applying increasing focused ultrasound pressures or concentrations of bupivacaine and ropivacaine. Focused ultrasound's effects on nerve structure were examined histologically. RESULTS: Increasing focused ultrasound pressures decreased action potential amplitude, area under the curve, and rate of rise, increased latency to 10% peak, and did not change latency to 100% peak or half peak width. Increasing local anesthetic concentrations decreased action potential amplitude, area under the curve, and rate of rise and increased latency to 10% peak, latency to 100% peak, and half peak width. At the highest focused ultrasound pressures, nerve architecture was altered compared with controls. DISCUSSION: While some action potential parameters were altered comparably by focused ultrasound and local anesthetics, there were small but notable differences. It is not evident if these differences may lead to differences in clinical pain effects when focused ultrasound is applied in vivo or if focused ultrasound pressures that result in clinically relevant changes damage nerve structures. Given the potential advantages of a non-invasive technique for managing pain conditions, further investigation may be warranted in an in vivo pain model.

In Vivo Whole-Nerve Electrophysiology Setup, Action Potential Recording, and Data Analyses in a Rodent Model.

In vivo rodent, whole peripheral nerve models are useful for studying the electrical conduction of sensory and motor fibers under normal physiological conditions as well as for assessing neurological outcomes after the application of physical alterations or pharmacological agents to the nervous system. Significant literature has focused on single-neuron and central nervous system electrophysiology protocol development. However, creation and development of in vivo whole-nerve electrophysiological recording protocols are sparse in the scientific literature. Here, detailed protocols for designing and building an in vivo whole-nerve electrophysiology system are described, including straightforward techniques to create working stimulation and recording electrodes that may be adapted to numerous study designs. Further, we include details for rodent anesthesia, surgical dissection (for the sciatic nerve), compound action potential signal optimization, data acquisition, data analyses, and troubleshooting tips. © 2021 Wiley Periodicals LLC. Basic Protocol 1: In vivo electrophysiology system wiring, hardware, and software setups Support Protocol 1: Design and 3D printing of electrophysiology base electrodes Support Protocol 2: Building needle electrodes Basic Protocol 2: Rodent anesthesia and surgery for nerve exposure Basic Protocol 3: Compound action potential recording and troubleshooting using WinWCP Basic Protocol 4: Compound action potential data analysis using WinWCP.

Ex Vivo Whole Nerve Electrophysiology Setup, Action Potential Recording, and Data Analyses in a Rodent Model.

Ex vivo rodent whole nerves provide a model for assessing the effects of interventions on nerve impulse transmission and consequent sensory and/or motor function. Nerve impulse transmission can be measured through sciatic nerve compound action potential (CAP) recordings. However, de novo development and implementation of an ex vivo whole nerve resection protocol and an electrophysiology setup that retains nerve viability, that produces low noise CAP signals, and that allows for data analysis is challenging. Additionally, some of the existing literature lacks detail and accuracy and may be out of date. This article describes detailed protocols for rodent ex vivo sciatic nerve dissection and handling; importance of an optimal physiologic solution; computer-aided designs for 3D printing of readily adaptable ex vivo rodent whole nerve electrophysiology chambers; construction of low-cost, effective suction electrodes; setup and use of nerve stimulators and amplifiers; acquisition of low noise, small voltage CAP data and digital conversion; use of software for data analyses of CAP components; and tips for troubleshooting. © 2020 Wiley Periodicals LLC. Basic Protocol 1: Electrophysiology wiring and hardware setup Support Protocol 1: 3D printing an electrophysiology chamber Support Protocol 2: Building suction electrodes Basic Protocol 2: Sciatic nerve dissection and compound action potential recording Basic Protocol 3: Data export and analysis Support Protocol 3: Preparation of HEPES-buffered physiologic solution.

Concordant Patterns of Brain Structure in Mothers with Recurrent Depression and Their Never-Depressed Daughters.

BACKGROUND: A growing body of research has demonstrated that having a mother with a history of major depressive disorder (MDD) is one of the strongest predictors of depression in adolescent offspring. Few studies, however, have assessed neural markers of this increased risk for depression, or examined whether risk-related anomalies in adolescents at maternal risk for depression are related to neural abnormalities in their depressed mothers. We addressed these questions by examining concordance in brain structure in two groups of participants: mothers with a history of depression and their never-depressed daughters, and never-depressed mothers and their never-depressed daughters. METHOD: We scanned mothers with (remitted; RMD) and without (control; CTL) a history of recurrent episodes of depression and their never-depressed daughters, computed cortical gray matter thickness, and tested whether mothers' thickness predicted daughters' thickness. RESULTS: Both RMD mothers and their high-risk daughters exhibited focal areas of thinner cortical gray matter compared with their CTL/low-risk counterparts. Importantly, the extent of thickness anomalies in RMD mothers predicted analogous abnormalities in their daughters; this pattern was not present in CTL/low-risk dyads. CONCLUSIONS: We identified neuroanatomical risk factors that may underlie the intergenerational transmission of risk for MDD. Our findings suggest that there is concordance in brain structure in dyads that is affected by maternal depression, and that the location, direction, and extent of neural anomalies in high-risk offspring mirror those of their recurrent depressed mothers.