Altered synaptic and electrical properties of lumbar motoneurons in the neurological glial mutant taiep rat

Maturation and differentiation of electrical properties of neurons and synaptic transmission are modulated by neuronal interaction. In vitro experiments have shown that these processes also seem to be regulated by signals from non-neuronal elements such as glial cells. It is not known, however, whether glial alterations in intact neural networks may also affect the maturation of electrical properties and synaptic transmission during development. We used the taiep rat, a neurological mutant with a progressive demyelination and astrogliosis, as an experimental model to study the postnatal development of motoneurons in an altered glial environment. Using the patch-clamp technique, we made intracellular recording from motoneurons of Rexed’s lamina IX in spinal cord slices of neonatal rats (postnatal day P4–P10). The electrical properties of normal motoneurons changed significantly with age, showing decreasing input resistance (Rin) and increasing membrane capacity (Cm). The rheobase increased with age, accompanied by an increase of the amplitude and a decrease of the duration of action potentials (APs). In contrast, mutant neurons showed no age-dependent changes of Rin, Cm, or AP characteristics. After blocking inhibitory transmission, intralaminar bipolar stimulation elicited, in both control and taiep motoneurons, fast glutamatergic excitatory postsynaptic potentials (EPSPs). Two types of taiep motoneurons were identified according to the temporal patterns of synaptic responses; (1) taiep SYN neurons, which showed no significant differences to control motoneurons, and (2) taiep ASYN neurons, in which the initial EPSP was followed by a variable number of delayed, asynchronous EPSP responses (for up to 300 ms). All these electrophysiological findings suggest that the mutation in taiep rats interfered with the development of the electrical properties of neurons and with the maturation of synaptic transmission, probably due to alterations in the neuron-glia interactions.