PubMed · 6199649
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L W Swanson. 1983. Techniques for tracing peptide-specific pathways.. https://doi.org/10.1016/s0076-6879(83)03047-5
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We have previously shown that not only motoneurons and dorsal root ganglion cells but also small neurons, presumably interneurons in the spinal cord, may undergo apoptotic cell death as a result of neonatal peripheral nerve transection in the rat. With the aid of electron microscopy, we have here demonstrated that apoptosis in the spinal cord is confined to neurons and does not involve glial cells at the survival time studied (24 hours). To define the relative importance of the loss of a potential target (motoneuron) and a potential afferent input (dorsal root ganglion cell) for the induction of apoptosis in interneurons in this situation, we have compared the distributions and time courses for TUNEL labeling, which detects apoptotic cell nuclei, in the L5 segment of the spinal cord and the L5 dorsal root ganglion after sciatic nerve transection in the neonatal (P2) rat. In additional experiments, we studied the effects on TUNEL labeling of interneurons after treatment of the cut sciatic nerve with either ciliary neurotrophic factor (CNTF) to rescue motoneurons or nerve growth factor (NGF) to rescue dorsal root ganglion cells. The time courses of the TUNEL labeling in motoneurons and interneurons induced by the lesion show great similarities (peak at 8-48 hours postoperatively), whereas the labeling in dorsal root ganglion cells occurs later (24-72 hours). Both CNTF and NGF decrease the number of TUNEL-labeled interneurons, but there is a regional difference, in that CNTF preferentially saves interneurons in deep dorsal and ventral parts of the spinal cord, whereas the rescuing effects of NGF are seen mainly in the superficial dorsal horn. The results are interpreted as signs of a trophic dependence on both the target and the afferent input for the survival of interneurons neonatally.
Neuropeptide FF (NPFF) is a morphine modulatory peptide that plays an important role in a wide variety of physiological functions, including those related to nociception and central autonomic regulation. NPFF fibers and cells have been shown to be discretely localized in key autonomic centers within the brain, including the brainstem nucleus of the solitary tract (NTS). Central applications of NPFF evoke a number of important biological effects through activation of central neuronal circuits whose identities remain unknown at present. NPFF administered in this manner may also be capable of up- or down-regulating its own gene expression. In this study, we investigated the effects of intracerebroventricular (i.c.v.) administration of NPFF on the activation and the gene expression of NPFF in NTS neurons. Conscious rats received saline or NPFF (8 or 10 microg i.c.v.), with concomitant monitoring of arterial blood pressure. Brains were prepared for Fos immunohistochemistry to identify neuronal activation and NPFF in situ hybridization to determine cells expressing NPFF mRNA in the NTS. At a dose of 8 microg, i.c.v., NPFF did not evoke alterations in blood pressure, but, at 10 microg, there was an increase in arterial blood pressure of 30-40 mmHg. Image analysis showed a dose-dependent increase in number of NPFF neurons that were activated in rats receiving i.c.v. NPFF compared with saline controls. NPFF gene expression in the NTS showed a similar dose-dependent increase following i.c.v. administration of either 8 or 10 microg of NPFF. Significantly greater numbers of activated neurons expressing the NPFF gene (double labeled) were observed in the NTS at the level of the area postrema in animals receiving i.c.v. NPFF compared with saline controls. These data indicate that centrally administered NPFF is capable of up-regulating its own gene expression in the NTS and that this effect appears in part to be independent of elevations in arterial blood pressure that this peptide can evoke when administered i.c.v. at the higher dose. The up-regulation of NPFF may play a homeostatic role in response to specific cardiovascular challenges, such as hypotension.
Distinctive subsets of glutamatergic neurons in cerebral cortex sequester the transition metal zinc within the synaptic vesicles of their axon terminals. In the present study we used histochemical localization of synaptic zinc to investigate normal postnatal development and experience-dependent plasticity of zinc-containing circuits in somatosensory barrel cortex of rats. First, we found that zinc-containing cortical circuits are dynamically reorganized between postnatal day (P) 0 and P28. Whereas most cortical laminae exhibited idiosyncratic increases in zinc histochemical staining with advancing age, lamina IV barrels were darkly reactive early in life and then lost much of their complement of synaptic zinc during postnatal weeks 2-4. Second, we established that sensory experience plays a major role in sculpting the zinc-containing innervation of cortical barrels. Trimming a particular facial whisker arrested the normal postnatal decline in synaptic zinc in the corresponding, deprived barrel. This resulted in more intense zinc staining in deprived barrels compared with adjacent, nondeprived barrels. Notably, the influence of experience on development of zinc circuits was most robust during a critical period extending from about P14, when an effect of whisker trimming first could be observed, through P28, after which time chronic deprivation no longer resulted in heightened levels of synaptic zinc in lamina IV. These findings indicate that sensory input can have a marked influence on development of cortical circuits, including those within lamina IV, throughout the first postnatal month.