Cartoon of AFM force indentation measurements.

<p><b>A</b>. A neuron cultured with astrocytes is depicted approximately to scale against a 20 µm sphere whose maximum downward displacement during an indent excursion is shown shaded; force is measured during “down”. Cortical neuron excitotoxicity was mimicked using agonists for glutamate and Nav channels; NMDA opens NMDA-glutamate channels, dissipating the [Ca²⁺] and [Na⁺] gradients, whereas veratridine opens Nav channels, dissipating the [Na⁺] gradient. Neurons enlarge on exposure to hypotonic medium and to excitotoxic agonists. <b>B</b>. Our expectations for the state of an enlarged neuron in the presence of excitotoxic levels of agonist is depicted at early and later stages: at left, once the initial channel-mediated Na⁺ influx and osmotically-obligated H₂O has hydrostatically inflated the neuron (countered to some extent by Ca²⁺-mediated actomyosin contractility), and at right, after Ca²⁺-toxicity has damaged the previously adherent (and contractile) neuronal membrane skeleton, allowing the plasma membrane to bleb pathologically.