The appearance and development of neurotransmitter sensitivity in Xenopus embryonic spinal neurones in vitro.

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Abstract
The time of onset and some of the properties of neurotransmitter sensitivity were determined in Xenopus spinal neurons developing in dissociated cell culture. These cells are initially insensitive, but acquire responses to several agonists over a period of 6 h. Nearly 1/3 of the neurons were depolarized by GABA or by both GABA and Gly; these cells were not affected by glutamate. The reversal potential of the ionophoretic GABA response is -35 mV. These neurons are likely to be Rohon-Beard neurons. Roughly 2/3 of the neurons were depolarized by glutamate and hyperpolarized by GABA and by Gly. The reversal potential of the ionophoretic GABA response in -58 mV. These neurons are likely to include motoneurons. A quantitative measure of the sensitivity to a given GABA dose was obtained at early and intermediate stages of development. The mean ''sensitivity index'' (ionophoretic sensitivity/input resistance) for both classes of neurons in vitro was initially the same as that seen in Rohon-Beard neurons in vivo. This sensitivity index did not increase with time in culture to attain the value at intermediate stages in vivo. The development of chemosensitivity in Rohon-Beard-like neurons in these cultures resembles that of Rohon-Beard neurons in the spinal cord with respect to the time of onset of responses to GABA, the reversal potential, pharmacology and desensitization of these responses, and the spectrum of agonists to which they are sensitive. It differs in the absence of a developmental increase in sensitivity to GABA. The development of chemosensitivity in motoneuron-like neurons in these cultures parallels that of Rohon-Beard-like neurons, with respect to the time of onset and level of sensitivity, as well as susceptibility to pharmacological blockers. Several features of normal neurotransmitter sensitivity, like features of the action potential, differentiate in culture in the absence of normal cellular interactions.