Effects of repetitive scanning ultrasound on the intraneuronal dendritic signalling of CA1 pyramidal neurons.

Introduction: Neural development is regulated by several spatiotemporally changing factors, which are essential for enabling neurons to develop functional networks, during early developmental stages. Additionally, external physical stimuli, like scanning prenatal ultrasound (US) examination, may influence neural development. Aim of our study is to examine potential consequences of diagnostic level ultrasound exposure during the early phase of hippocampal CA1 neural network development by using computational models. Methods: Using Results: Our computer models predict that diagnostic level US treatment does not induce changes in specific membrane resistance and capacitance of neuronal membrane. Correlative analyses of simulated dendritic impulse propagation in US treated (UT) and non-treated control neurons (NT) revealed minor differences in attenuations and delays of somatopetally propagating PSPs in the passive model, and these alterations became even less pronounced when hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels and A-type potassium (K Discussion: We conclude that subthreshold somatopetal signalling properties of US-treated CA1 neuronal membranes remain predominantly at the level of non-treated cells. This conservation is due primarily to HCN channels, contributing to net membrane conductance at rest in an inhomogeneous manner over the somato-dendritic surface. The HCN channels balance the effects of US-induced morphological alterations on dendritic signalling. Conservation of signalling properties align with our independent prediction on the conservation of synaptic integration and input pattern recognition in UT neurons.