The Journal of comparative neurology
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Orexin and melanin-concentrating hormone (MCH) have been implicated in mediating a variety of different behaviors. These include sleep and wakefulness, locomotion, ingestive behaviors, and fight-or-flight response, as well as anxiety- and panic-like behaviors in rodents. Despite such diversity, all these processes require coordinated recruitment of the autonomic and somatomotor efferents. ⋯ Our findings demonstrate that PSPMNs synthesizing either MCH or orexin are present within LH, where they form two separate populations. PSPMNs located around the fornix express orexin, whereas those located around the cerebral peduncle are more likely to express MCH. These two clusters of PSPMNs within LH likely play distinct functional roles in autonomic homeostasis and stress coping mechanisms.
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Inflammatory pain is thought to induce functional plasticity of spinal dorsal horn neurons and may produce changes in glutamate receptor expression. Plasticity of group I metabotropic glutamate receptors (mGluR1 and mGluR5) is important in various neuronal systems, and these receptors are also known to modulate nociceptive neurotransmission in the spinal dorsal horn. The present study aimed at determining whether persistent inflammatory pain produces alterations in intracellular and plasma membrane-associated mGluR1alpha and mGluR5 in spinal cord dorsal horn. ⋯ Compared to untreated rats, CFA-treated rats had a significant increase in the number of plasma membrane-associated mGluR5 immunogold-labeled particles in lamina I-II neurons of the spinal cord. Although no changes to mGluR1alpha expression were found in CFA-treated rats, plasma membrane-associated mGluR1alpha was significantly closer to the synapse. Therefore, in CFA-treated rats there was a specific increase in the ratio of plasma membrane-associated versus intracellular immunogold-labeled particles for mGluR5, and lateral movement of mGluR1alpha toward the synapse, indicating that peripheral inflammation-induced trafficking of group I mGluRs in spinal dorsal horn neurons may be an important factor in the development of plastic changes associated with inflammation-induced chronic pain.
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Genetic and biochemical evidence has established that clathrin assembly protein AP180 is required for the proper assembly of synaptic vesicles via clathrin-mediated endocytosis. The assembly protein CALM, the ubiquitously expressed homolog of AP180, also regulates the formation of clathrin-coated vesicles. In this study we found high expression levels of AP180 and CALM in hippocampal tissues as early as embryonic day 18, before the expression of synaptophysin. ⋯ We found AP180 and CALM in synapses at all developmental stages and in nonsynaptic growing processes. In addition to localization on the plasma membrane and clathrin-coated vesicles that originated from the plasma membrane, we also report the presence of AP180 and CALM on other types of membrane structures. Our observations link AP180 and CALM to multiple vesicular organelles and raise the possibility that these proteins may play additional roles in developing neurons.
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Many Rexed's lamina I neurons are nociceptive and project to the brain. Lamina I projection neurons can be classified as multipolar, fusiform, or pyramidal, based on cell body shape and characteristics of their proximal dendrites in the horizontal plane. There is also evidence that both multipolar and fusiform cells are nociceptive and pyramidal neurons nonnociceptive. ⋯ Most of the SPB neurons expressing NK-1r were either multipolar or fusiform. Pyramidal SPB neurons were seldom immunoreactive for NK-1r, an observation that provides further support to the concept that most lamina I projection neurons of the pyramidal type are nonnociceptive. In addition, our study provides further evidence that these distinct morphological types of neurons differ in their phenotypic properties, but not in their projection patterns.
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Sprouting of peptidergic nociceptive and descending supraspinal projections to the dorsal horn following spinal cord injury (SCI) has been proposed as a mechanism of neuropathic pain. To identify structural changes that could initiate or maintain SCI pain, we used a complete transection model in rats to examine how structural remodeling in the dorsal horn rostral to the lesion relates to distance from injury, laminar region, and duration of injury. The major classes of C-fiber primary afferents differed greatly in their susceptibility to structural and chemical changes and their ability to undergo plasticity. ⋯ This was restricted to the superficial laminae. Our results show that SCI caused a loss of sensory input as well as structural remodeling such that the balance of nociceptive inputs and descending modulation was permanently altered. These changes may contribute to mechanisms rostral to the site of SCI that trigger and maintain neuropathic pain.