The Journal of comparative neurology
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The nucleus reuniens (RE) is the largest of the midline nuclei of the thalamus and the major source of thalamic afferents to the hippocampus and parahippocampal structures. Nucleus reuniens has recently been shown to exert powerful excitatory actions on CA1 of the hippocampus. Few reports on any species have examined afferent projections to nucleus reuniens. ⋯ The main sources of input to nucleus reuniens were from the orbitomedial, insular, ectorhinal, perirhinal, and retrosplenial cortices; CA1/subiculum of hippocampus; claustrum, tania tecta, lateral septum, substantia innominata, and medial and lateral preoptic nuclei of the basal forebrain; medial nucleus of amygdala; paraventricular and lateral geniculate nuclei of the thalamus; zona incerta; anterior, ventromedial, lateral, posterior, supramammillary, and dorsal premammillary nuclei of the hypothalamus; and ventral tegmental area, periaqueductal gray, medial and posterior pretectal nuclei, superior colliculus, precommissural/commissural nuclei, nucleus of the posterior commissure, parabrachial nucleus, laterodorsal and pedunculopontine tegmental nuclei, nucleus incertus, and dorsal and median raphe nuclei of the brainstem. The present findings of widespread projections to RE, mainly from limbic/limbic-associated structures, suggest that nucleus reuniens represents a critical relay in the transfer of limbic information (emotional/cognitive) from RE to its major targets, namely, to the hippocampus and orbitomedial prefrontal cortex. RE appears to be a major link in the two-way exchange of information between the hippocampus and the medial prefrontal cortex.
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The propriospinal system is important in mediating reflex control and in coordination during locomotion. Propriospinal neurons (PNs) present varied patterns of projections with ascending and/or descending fibers. Following spinal cord contusion injury (SCI) in the rat, certain supraspinal pathways, such as the corticospinal tract, appear to be completely abolished, whereas others, such as the rubrospinal and vestibuospinal tracts, are only partially damaged. ⋯ While short thoracic propriospinal axons are severely damaged after injury, 5-7% of long descending propriospinal tract (LDPT) projections survive following 50 and 12.5-mm weight drop contusion lesions, respectively, albeit with a reduced intensity of retrograde label. Even though the axons of short thoracic propriospinal cells are damaged, their cell bodies of origin remain intact 2 weeks after injury, indicating that they have not undergone postaxotomy retrograde cell death at this time point. Thus, short PNs may constitute a very attractive population of cells to study regenerative approaches, whereas LDPT neurons with spared axons could be targeted with therapeutic interventions, seeking to enhance recovery of function following incomplete lesions to the spinal cord.
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Presympathetic vasomotor adrenergic (C1) and nonadrenergic (non-C1) neurons in the rostral ventrolateral medulla (RVLM) provide the main excitatory drive to cardiovascular sympathetic preganglionic neurons in the spinal cord. C1 and non-C1 neurons contain cocaine- and amphetamine-regulated transcript (CART), suggesting that CART may be a common marker for RVLM presympathetic neurons. To test this hypothesis, we first used double-immunofluorescence staining for CART and tyrosine hydroxylase (TH) to quantify CART-immunoreactive (-IR) catecholamine and noncatecholamine neurons in the C1 region. ⋯ Six fast (2.8-5.8 m/second, noncatecholamine)-, two intermediate (2.1 and 2.2 m/second)-, and five slow (<1 m/second, catecholamine)-conducting RVLM presympathetic vasomotor neurons were juxtacellularly labeled. After fluorescent detection of CART and biotinamide, all 13 neurons were found to be CART-IR. These results suggest that, in rat RVLM, all catecholamine and noncatecholamine presympathetic vasomotor neurons contain CART.
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This study examined the effect of spinal nerve ligation on different populations of immunohistochemically identified neurons in the dorsal root ganglia (DRG) of the rat. The optical fractionator method was used to count neurons in the ipsilateral L4 and L5 DRG 1-20 weeks after ligation of the L5 and L6 spinal nerves, sham surgery, or no surgery. One week after ligation, neurons in the L5 DRG that were labeled by IB4, a marker of unmyelinated primary afferent neurons, were largely absent. ⋯ However, closer examination revealed a significant decrease in the numbers of large-sized neurons, coupled with an increase in the numbers of small- to medium-sized neurons, and the appearance of a novel population of very small-sized neurons labeled by N52. The numbers and cell size distributions of IB4-labeled, CGRP-like immunoreactive, and N52-labeled neurons were unchanged in the adjacent L4 DRG. Unlike the L5 DRG, injury-induced changes in the expression of various receptors, neurotransmitters and neurotrophic factors in the L4 DRG are not confounded by a change in the immunohistochemical phenotype of primary afferent neurons.
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Alterations in the expression of the neuropeptide galanin were examined in micturition reflex pathways 6 weeks after complete spinal cord transection (T8). In control animals, galanin expression was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the superficial dorsal horn; (3) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (4) the lateral collateral pathway in lumbosacral spinal segments. Densitometry analysis demonstrated significant increases (P < or = 0.001) in galanin immunoreactivity (IR) in these regions of the S1 spinal cord after spinal cord injury (SCI). ⋯ In contrast, NGF expression was only increased in the spinal segments adjacent and rostral to the transection site (T7-T8), whereas spinal segments (T13-L1; L6-S1), distal to the transection site exhibited decreased NGF expression. Changes in galanin expression in micturition pathways after SCI may be mediated by changing neurotrophic factor expression, particularly BDNF. These changes may contribute to urinary bladder dysfunction after SCI.