Lurcher is an autosomal semidominant murine mutation. Lurcher heterozygotes, (+/Lc) lose all their cerebellar Purkinje cells by adulthood. Explants from 2 days postnatal (P2) wild‐type (+/+) and +/Lc cerebellar cortex were grown in vitro to investigate the role of local neuronal environment and afferent input on the degenerating +/Lc Purkinje cell. In Lurcher explants, Purkinje cells were maintained for up to 25 days in vitro. No significant difference was observed between +/+ and +/Lc Purkinje cell numbers from 10 to 20 days in vitro, as revealed by calbindin‐D immunoreactivity. Growing +/Lc explants in association with + / + explants resulted in no significant difference in Purkinje cell survival (10–20 days in vitro). Image analysis of the gross morphology of calbindin‐D‐immunostained Purkinje cells from +/+ and +/Lc explants grown in vitro revealed a significant decrease in the total area and dendritic lengths of +/Lc Purkinje cells (15 and 20 days in vitro). The fine structure of +/Lc and +/+ Purkinje cells was examined under the electron microscope (10–25 days in vitro). No difference in ultrastructure was observed between +/Lc and +/+ Purkinje cells grown in vitro, and many features similar to normal Purkinje cell development in vivo were present. These included monosynaptic parallel fibre synapses with Purkinje cell dendritic spines, other interneuron synapses with Purkinje cell dendrites and soma, astroglial investment, and minimal extracellular space in the neuropil. Unusual features observed included a persistence of the perisomatic spines in some Purkinje cells, an absence of Nissl bodies in the Purkinje cell perikaryon, naked Purkinje cell dendritic spines, and occasional heterol, ogous synapses. The results are discussed in the light of previous chimeric analysis of the Lurcher mutation, and a hypothesis is put forward to explain the survival of + /Lc Purkinje cells in vitro. © 1995 Wiley‐Liss, Inc.

The response characteristics of interpositus neurones (IP) to sciatic nerve stimulation were studied in normal and Lurcher mutant mice under pentobarbitone anaesthesia. The response of IP neurones in the normal mouse was a short latency bimodal excitation (E1-I1-E2) followed by a depression of the firing rate (I2) and ending with a longer latency excitation (E3) which was completed within 225 msec. The response of the majority of IP neurones in the Lurcher mouse was a short latency unimodal excitation (LE1) which corresponded in time to the E1-I1-E2 phase in the normal. This was followed by a pause in the excitation. The response ended with a longer latency excitation (LE2) corresponding in time to the E3 phase in the normal mouse but which persisted for a considerably greater period of time. The response of IP neurones in normal and Lurcher mice appear to be similar to those observed in the normal and experimentally cerebellar decorticate cat, respectively.

Pulse labelling with tritiated thymidine was used to determine the time of the final division of the neuroblasts which subsequently form rat lumbar dorsal root ganglion neurones. The final division occurred during a 4 day period, the maximum frequency being on day 12 of gestation. Separation of the ganglion cells into large light neurones and small dark neurones showed that the large light neurones were formed earlier than the small dark neurones. In both cases the final divisions occurred over a period of 3–4 days, but the peak rate of formation of large neurones was on day 12, and that of the small neurones was on day 13.

The pause in firing of hypoglossal motoneurons following a stimulus to the hypoglossal nerve in the rat could be explained by an afterhyperpolarization or by an inhibition via recurrent collaterals or afferent fibers. Extracellular and intracellular recordings from glass microelectrodes have established the all-or-none nature of both the pause in electrophoretically induced firing and a hyperpolarization which followed antidromic invasion. Only stimulation of the hypoglossal nerve branch which evoked antidromic invasion resulted in the hyperpolarization. The threshold for these two events was identical. Stimulating the hypoglossal nerve branches over a whole range of stimulus strengths produced no other potential changes, neither were any neurons with Renshaw-cell characteristics found. No evidence for the presence of afferent fibers in the hypoglossal nerve was abtained from recording the compound action potential following distal stimulation, from examination of the appropriate segment by electron microscopy, or from a search for reflex effects in other cranial nerves and on blood pressure following stimulation of the hypoglossal nerve. Peaks of increased probability in firing following the pause seen in poststimulus histograms were attributed to synchronization between the computer sweep and the time course of the afterpotential following antidromic invasion.