PubMed · 7059135
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I Darian-Smith. 1982. Touch in primates.. https://doi.org/10.1146/annurev.ps.33.020182.001103
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Topographic projections of the nervous system are essential to numerous brain functions. They arise during development as a result of encounters between projecting growth cones and particular target cells. Cellular localization of guidance cues can indicate the sequential processes involved in establishment of such topography. The map formed by retinal ganglion cells on their target nuclei has served widely as a model system to investigate mechanisms underlying the highly precise and stereotypic connectivity of the nervous system. To investigate cellular localization of guidance cues in the developing retinotectal system, a three-compartment chamber was created to delimit areas where cultured embryonic chick retinal ganglion axons and tectal cells encounter one another and guidance behavior could be readily assessed. Whereas explants from nasal retinae extended fibers across their natural target population, fibers from temporal regions of retinae failed to invade areas of growing posterior tectal cells. This preservation of relevant guidance information on living cell populations enabled an evaluation of retinal ganglion cell growth cone behavior after encounter with individual tectal cells. Posterior tectal neurons appeared selectively repulsive for temporal retinal ganglion cell growth cones, causing growth cone collapse and retraction. On the contrary, neuroepithelial cells from all regions of the tectum attenuated retinal ganglion axon extension, without inducing sudden retraction. Nasal growth cones traversed or tracked more often along neuroepithelial cells from their natural target area, potentially indicating a second set of guidance cues possibly localized to posterior glia. Together, these differential interactions suggest that development of retinotectal topography critically depends on cell-specific cues, which are distributed selectively on particular populations of target cells.
The entorhinal cortex is a major relay between the hippocampus and other cortical and subcortical regions. Glutamatergic axons from layer II neurons form the entorhinal cortical projection to the hippocampus via the perforant pathway. We have demonstrated previously that lesion of the perforant pathway causes the death of approximately 30% of entorhinal layer II (ECL2) neurons. To elucidate mechanisms contributing to neuronal death and to investigate strategies preventing it, we identified the phenotype of the vulnerable neuronal population. Sections were immunolabeled with antibodies to the neuronal markers NeuN, glutamate, and calbindin-D28k, and to receptors for fibroblast growth factor-2 (FGFR1) and NMDA (NMDAR1) and were examined using confocal microscopy. Calbindin immunoreactivity was strikingly lamina-specific to ECL2, where one-third of all ECL2 neurons were calbindin-positive. Localization of glutamate revealed that half of the glutamatergic ECL2 neurons coexpressed calbindin. Quantification using unbiased stereology at 9 weeks after lesion of the perforant pathway revealed that the only ECL2 neuronal population that experienced a significant (70%) loss (20% of the total) was the population of glutamatergic ECL2 neurons that did not coexpress calbindin. All ECL2 neurons expressed FGFR1; therefore, we tested the role of FGF-2 in the survival of glutamatergic ECL2 neurons. We grafted fibroblasts genetically engineered to express nerve growth factor or FGF-2 and found that only FGF-2 grafts prevented loss of the vulnerable glutamatergic/calbindin-negative neurons. We present a hypothesis for the selective vulnerability of these glutamatergic/calbindin-negative ECL2 neurons and address the role of FGF-2 in neuronal rescue.
In the cat, stimulation of group II afferents from hindlimb muscles evokes different crossed reflex actions depending on the integrity of the spinal cord: with the cord intact, extensor motoneurons are inhibited by activation of contralateral group II afferents; after spinal transection, the same stimuli excite these neurons (crossed extension reflex). We have investigated the mechanisms underlying this descending control. To delimit the descending pathway, the effects of funicular lesions of the thoracic cord on the crossed actions on motoneurons were examined. Bilateral lesions of the dorsolateral funiculi abolished the crossed IPSPs as effectively as complete spinal section. If either dorsolateral funiculus was spared, the IPSPs remained. To examine whether serotonergic fibers were involved, the effects of agents selective for 5-hydroxytryptamine (5-HT)1A receptors were examined. After abolishing the crossed IPSPs by spinal transection, systemic administration of the 5-HT1A receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT; 0.1-1.3 mg/kg, i.v.) restored the crossed inhibition. This effect was antagonized by the selective 5-HT1A receptor antagonist WAY-100135 (0.7-3.7 mg/kg, i.v.). The simplest explanation of these findings is that a serotonergic pathway, descending via the dorsolateral funiculi and acting via 5-HT1A receptors, is involved: with the spinal cord intact, the pathway would be tonically active and thus enable the crossed inhibition. This raises the possibility that a serotonergic pathway is involved in the selection of specific spinal reflex patterns via 5-HT1A receptors.