The Journal of comparative neurology
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Songbirds have a complex vocal repertoire, much of which is learned by imitation. The vocal motor system of songbirds includes a set of telencephalic pathways dedicated to the acquisition and production of learned song. The main vocal motor pathway goes from the high vocal center (HVC) to the robust nucleus of the archistriatum (RA), which in turn innervates mesencephalic and medullary nuclei involved in vocalization. ⋯ We also saw a weaker projection from RA to the medial part of the dorsolateral nucleus of the thalamus (DLM), which is known to project to the lateral portion of the magnocellular nucleus of the anterior neostriatum (IMAN). IMAN is known to project to RA, completing yet another feedback circuit; IMAN is also part of the anterior forebrain pathway, which plays an essential role in song learning. These thalamo-telencephalic circuits are similar to the thalamo-cortical circuits found in mammalian motor systems, and we suggest that the signals carried by these loops may be important for song perception, song learning, song production, and/or the bilateral coordination of vocal motor commands.
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Peripheral nerve section induces sprouting of the central terminals of axotomized myelinated primary afferents outside their normal dorsoventral termination zones in lamina I, III, and IV of the dorsal horn into lamina II, an area that normally only receives unmyelinated C-fiber input. This axotomy-induced regenerative sprouting is confined to the somatotopic boundaries of the injured nerve in the spinal cord. We examined whether intact myelinated sciatic afferents are able to sprout novel terminals into neighbouring areas of the dorsal horn in the adult rat following axotomy of two test nerves, either the posterior cutaneous nerve of the thigh or the saphenous nerve. ⋯ No mediolateral sprouting was seen into those areas of neuropil solely innervated by the test nerve. We conclude that intact myelinated primary afferents do have the capacity to collaterally sprout, but that any resultant somatotopic reorganization of central projections is limited to the dorsoventral plane. These changes may contribute to sensory hypersensitivity at the edges of denervated skin.
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Soman (pinacolymethylphosphonofluoridate), a highly potent, irreversible inhibitor of cholinesterase, causes intense convulsions, neuropathology and, ultimately, death. There is evidence that certain brain structures are selectively vulnerable to the pathological consequences of soman-induced seizures. A working hypothesis is that central nervous system (CNS) structures with the earliest and most severe signs of neuropathology may be key sites for the initiation of the seizures. ⋯ At 8 hours and beyond, Fos expression returned to control levels throughout the CNS except for the piriform cortex and the locus coeruleus which still had robust labeling. By 24 hours, neuropathology was evident throughout the rostral-caudal extent of layer II of the piriform cortex. The rapid induction of Fos in the piriform cortex and the locus coeruleus, taken together with previous anatomical, eletrophysiological and neurochemical studies, suggests that prolonged, excessive exposure to synaptically released acetylcholine and norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex and subsequently in other cortical and subcortical structures.
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Substance P (SP) is implicated in transmission of primary afferent nociceptive signals. In primary neurons, SP is colocalized with calcitonin gene-related peptide (CGRP), which is another neuropeptide marker for small to medium primary neurons. CGRP coreleased with SP augments the postsynaptic effect of SP and thereby modulates the nociceptive transmission. ⋯ The medullary dorsal horn (MDH) and the lateral edge of Vo received convergent CGRP-ir projection from the ipsilateral trigeminal primaries and other neurons. The glossopharyngeal and vagal primaries are candidates for the source of CGRP-ir projection to the Vo and the MDH, while the dorsal root axons supply the MDH with CGRP-ir terminals. In addition, contralateral primary neurons crossing the midline appear to contain CGRP and to terminate in the MDH.
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In order to investigate the existence of anatomical subdivisions within the thalamic reticular nucleus (Rt), the distribution of reticular neurons expressing the calcium binding protein calretinin was investigated in the rat by means of immunocytochemistry. Calretinin immunoreactive (Cr-ir) neurons were mainly distributed in the lateral and ventral regions, and along the medial border of the Rt rostral pole. Caudal to the rostral pole, many neurons were Cr-ir in the more dorsal part of the rostral two-thirds (the "dorsal cap") of the Rt. ⋯ The double-labeling experiments demonstrated that the reticular neurons projecting to the ipsilateral anterodorsal, midline, mediodorsal, and anterior intralaminar nuclei frequently expressed calretinin; by contrast, the majority of the reticular commissural neurons did not express the protein, with the exception of neurons projecting to the contralateral mediodorsal and midline nuclei. The ipsilaterally projecting calretinin-positive neurons were frequently located along the medial edge of the rostral pole and in the dorsal cap of the nucleus, segregated from the commissural calretinin-negative neurons. The combined analysis of calretinin expression patterns and tract tracing data provided further insight in the anatomical organization of the thalamic reticular nucleus, suggesting a different neurophysiological role for the ipsilaterally vs. the contralaterally projecting reticular neurons in the modulation of the synaptic activity of the dorsal thalamus.