No effect of sustained systemic growth retardation on the distribution of Reelin-expressing interneurons in the neuron-producing hippocampal dentate gyrus in rats.

Reelin signaling plays a role in neuronal migration and positioning during brain development. To clarify the effect of systemic growth retardation on the distribution of Reelin-expressing interneurons in the hilus of the hippocampal dentate gyrus, pregnant rats were fed a synthetic diet with either a normal (20% casein) or low (10% casein) protein concentration from gestational day 10 to postnatal day (PND) 21 at weaning. Male offspring were immunohistochemically examined at PND 21 and on PND 77. Protein-restricted offspring displayed systemic growth retardation through PND 77 and had decreased absolute brain weights and an increased number of external granular cells in the cerebellar cortex, suggestive of retarded brain growth at weaning. However, maternal protein restriction did not change the cellular distribution of immunoreactivity for Reelin, Calbindin-D-28K, or glutamic acid decarboxylase 67 or of NeuN-positive postmitotic neurons in the dentate hilus either at PND 21 or PND 77, which suggests that the population of γ-aminobutyric acid-ergic interneurons involving synthesis of Reelin was not affected. Furthermore, as well as the distribution of hilar neurons expressing neurogenesis-related FoxG1, cell proliferation and apoptosis in the subgranular zone were unaffected through PND 77. These results suggest that systemic growth retardation caused by maternal protein restriction does not affect neuronal migration and postnatal neurogenesis of the dentate gyrus resulting in unaltered distribution of Reelin-synthesizing interneurons.

Disynaptic and polysynaptic statocyst pathways to an identified set of premotor nonspiking interneurons in the crayfish brain.

Nonspiking giant interneurons (NGIs) in the crayfish brain occupy a key position in the neuronal circuit for eyestalk motor control and, hence, play a crucial role in the central compensation process following unilateral deprivation of the statocyst that functions as an equilibrium sensory system. The synaptic organization of their input pathways, however, remains unknown. In the present study we identified 11 local interneurons that were polysynaptically connected to NGIs by making simultaneous intracellular recordings. We also identified three other local interneurons that connected to NGIs monosynaptically. PLNI-2 was a nonspiking interneuron making an excitatory synaptic connection to an NGI that had its cell body on the opposite side. PLSI was a spiking interneuron that made an inhibitory connection to an ipsilateral NGI. These cells were entirely confined to the protocerebrum. Another local spiking interneuron termed UGLI-1 was found to make an excitatory connection with a contralateral NGI, extending dendrites in the anterior and posterior medial protocerebral neuropils and the lateral antenna I neuropil in the deutocerebrum where statocyst afferents project. When a depolarizing current was injected into the UGLI-1, the frequency of discrete excitatory PSPs increased remarkably in the postsynaptic NGI, each PSP following the UGLI-1 spike in one-to-one correspondence. The UGLI was previously reported to be activated monosynaptically by statocyst afferents. The present study thus finally demonstrates the tri-synaptic organization of the statocyst-to-eyestalk motor neuron pathway in its simplest form, suggesting the critical role of the UGLI-1 in the central compensation.

Physiological changes of premotor nonspiking interneurons in the central compensation of eyestalk posture following unilateral sensory ablation in crayfish.

We investigated how the physiological characteristics and synaptic activities of nonspiking giant interneurons (NGIs), which integrate sensory inputs in the brain and send synaptic outputs to oculomotor neurons innervating eyestalk muscles, changed after unilateral ablation of the statocyst in order to clarify neuronal mechanisms underlying the central compensation process in crayfish. The input resistance and membrane time constant in recovered animals that restored the original symmetrical eyestalk posture 2 weeks after operation were significantly greater than those immediately after operation on the operated side whereas in non-recovered animals only the membrane time constant showed a significant increase. On the intact side, both recovered and non-recovered animals showed no difference. The frequency of synaptic activity showed a complex pattern of change on both sides depending on the polarity of the synaptic potential. The synaptic activity returned to the bilaterally symmetrical level in recovered animals while bilateral asymmetry remained in non-recovered ones. These results suggest that the central compensation of eyestalk posture following unilateral impairment of the statocyst is subserved by not only changes in the physiological characteristics of the NGI membrane but also the activity of neuronal circuits presynaptic to NGIs.