Showing papers on "Cuneate nucleus published in 2020"
TL;DR: Findings indicate that proprioception from forelimb/neck muscle spindles and JCMSs is somatotopically transmitted to the ventromedial floor of the ventrobasal thalamic complex, but not to its rostrodorsal shell.
Abstract: Proprioceptive signals from body muscles have historically been considered to project to the rostrodorsal shell of the ventrobasal thalamic complex [the ventral posterolateral nucleus (VPL) and ventral posteromedial nucleus (VPM)]. However, we have recently found that proprioception from rat jaw-closing muscle spindles (JCMSs) is conveyed via the supratrigeminal nucleus to the caudo-ventromedial edge of the VPM, but not to the rostrodorsal shell of the VPM. Therefore, proprioception from other body muscles may also project to thalamic regions other than the rostrodorsal shell of the VPL. We thus examined the thalamic projection from the rat external cuneate nucleus (ECu), which receives proprioceptive inputs from forelimb and neck muscles. After injection of anterograde tracer into the ECu, axon terminals were contralaterally labeled in the ventromedial part (VPLvm) of the VPL, but not in the rostrodorsal shell of the VPL. After anterograde tracer injection into the cuneate nucleus (Cu), axon terminals were widely labeled in the contralateral VPL including the VPLvm. In the VPLvm, we electrophysiologically confirmed the proprioceptive inputs responsive to electrical stimulation of the ECu or median nerve and to the pressure of forelimb/neck muscles or wrist flexion. After retrograde tracer injection into the VPLvm, neurons were contralaterally labeled in the ECu and Cu. After retrograde tracer injection into the VPL where no such proprioceptive inputs were recorded, no ECu neurons were labeled. These findings indicate that proprioception from forelimb/neck muscle spindles and JCMSs is somatotopically transmitted to the ventromedial floor of the ventrobasal thalamic complex, but not to its rostrodorsal shell.
11 citations
TL;DR: It is shown that adult mice recover tactile and proprioceptive function following a unilateral dorsal column lesion and that detour circuits represent a common blueprint for axonal rewiring after injury.
Abstract: Anatomically incomplete spinal cord injuries can be followed by functional recovery mediated, in part, by the formation of intraspinal detour circuits. Here, we show that adult mice recover tactile and proprioceptive function following a unilateral dorsal column lesion. We therefore investigated the basis of this recovery and focused on the plasticity of the dorsal column-medial lemniscus pathway. We show that ascending dorsal root ganglion (DRG) axons branch in the spinal grey matter and substantially increase the number of these collaterals following injury. These sensory fibers exhibit synapsin-positive varicosities, indicating their integration into spinal networks. Using a monosynaptic circuit tracing with rabies viruses injected into the cuneate nucleus, we show the presence of spinal cord neurons that provide a detour pathway to the original target area of DRG axons. Notably the number of contacts between DRG collaterals and those spinal neurons increases by more than 300% after injury. We then characterized these interneurons and showed that the lesion triggers a remodeling of the connectivity pattern. Finally, using re-lesion experiments after initial remodeling of connections, we show that these detour circuits are responsible for the recovery of tactile and proprioceptive function. Taken together our study reveals that detour circuits represent a common blueprint for axonal rewiring after injury.
7 citations
TL;DR: Investigation of central nervous system and selected peripheral nervous system tissues in Beagle dogs found cuneate, gracile, and cochlear nuclei and the cerebellar white matter were the most common locations for AD, and incidence increased with age.
Abstract: Axonal dystrophy (AD) is a common age-related neurohistological finding in vertebrates that can be congenital or induced by xenobiotics, vitamin E deficiency, or trauma/compression. To understand the incidence and location of AD as a background finding in Beagle dogs used in routine toxicity studies, we examined central nervous system (CNS) and selected peripheral nervous system (PNS) tissues in twenty 18- to 24-month-old and ten 4- to 5-year-old control males and females. Both sexes were equally affected. The cuneate, gracile, and cochlear nuclei and the cerebellar white matter (rostral vermis) were the most common locations for AD. Incidence of AD increased with age in the cuneate nucleus, cerebellar white matter (rostral vermis), trigeminal nuclei/tracts, and lumbar spinal cord. Axonal dystrophy in the CNS was not accompanied by neuronal degeneration/necrosis, nerve fiber degeneration, and/or glial reaction. Axonal dystrophy was not observed in the PNS (sciatic nerve, vagus nerve branches, or gastrointestinal mural autonomic plexuses).
5 citations
TL;DR: Neuroanatomical support is provided for a role for NUCB2/nesfatin‐1 in feeding behaviour and energy balance and in the solitary tract, where altered neurochemistry may contribute to obesity.
Abstract: Feeding is a complex behaviour entailing elaborate interactions between forebrain, hypothalamic and brainstem neuronal circuits via multiple orexigenic and anorexigenic neuropeptides. Nucleobindin-2 (NUCB2)/nesfatin-1 is a negative regulator of food intake and body weight with a widespread distribution in rodent brainstem nuclei. However, its localisation pattern in the human brainstem is unknown. The present study aimed to explore NUCB2/nesfatin-1 immunoexpression in human brainstem nuclei and its possible correlation with body weight. Sections of human brainstem from 20 autopsy cases (13 males, seven females; eight normal weight, six overweight, six obese) were examined using immunohistochemistry and double immunofluorescence labelling. Strong immunoreactivity for NUCB2/nesfatin-1 was displayed in various brainstem areas, including the locus coeruleus, medial and lateral parabrachial nuclei, pontine nuclei, raphe nuclei, nucleus of the solitary tract, dorsal motor nucleus of vagus (10N), area postrema, hypoglossal nucleus, reticular formation, inferior olive, cuneate nucleus, and spinal trigeminal nucleus. NUCB2/nesfatin-1 was shown to extensively colocalise with neuropeptide Y and cocaine- and amphetamine-regulated transcript in the locus coeruleus, dorsal raphe nucleus and solitary tract. Interestingly, in the examined cases, NUCB2/nesfatin-1 protein expression was lower in obese than normal weight subjects in the solitary tract (P = 0.020). The findings of the present study provide neuroanatomical support for a role for NUCB2/nesfatin-1 in feeding behaviour and energy balance. The widespread distribution of NUCB2/nesfatin-1 in the human brainstem nuclei may be indicative of its pleiotropic effects on autonomic, neuroendocrine and behavioural processes. In the solitary tract, a key integrator of energy status, altered neurochemistry may contribute to obesity. Further research is necessary to decipher human brainstem energy homeostasis circuitry, which, despite its importance, remains inadequately characterised.
5 citations