Showing papers on "Cuneate nucleus published in 2014"

Large-scale reorganization of the somatosensory cortex following spinal cord injuries is due to brainstem plasticity

Abstract: Adult mammalian brains undergo reorganization following deafferentations due to peripheral nerve, cortical or spinal cord injuries. The largest extent of cortical reorganization is seen in area 3b of the somatosensory cortex of monkeys with chronic transection of the dorsal roots or dorsal columns of the spinal cord. These injuries cause expansion of intact face inputs into the deafferented hand cortex, resulting in a change of representational boundaries by more than 7 mm. Here we show that large-scale reorganization in area 3b following spinal cord injuries is due to changes at the level of the brainstem nuclei and not due to cortical mechanisms. Selective inactivation of the reorganized cuneate nucleus of the brainstem eliminates observed face expansion in area 3b. Thus, the substrate for the observed expanded face representation in area 3b lies in the cuneate nucleus.

Spatio-temporal skin strain distributions evoke low variability spike responses in cuneate neurons

Abstract: A common method to explore the somatosensory function of the brain is to relate skin stimuli to neurophysiological recordings. However, interaction with the skin involves complex mechanical effects. Variability in mechanically induced spike responses is likely to be due in part to mechanical variability of the transformation of stimuli into spiking patterns in the primary sensors located in the skin. This source of variability greatly hampers detailed investigations of the response of the brain to different types of mechanical stimuli. A novel stimulation technique designed to minimize the uncertainty in the strain distributions induced in the skin was applied to evoke responses in single neurons in the cat. We show that exposure to specific spatio-temporal stimuli induced highly reproducible spike responses in the cells of the cuneate nucleus, which represents the first stage of integration of peripheral inputs to the brain. Using precisely controlled spatio-temporal stimuli, we also show that cuneate neurons, as a whole, were selectively sensitive to the spatial and to the temporal aspects of the stimuli. We conclude that the present skin stimulation technique based on localized differential tractions greatly reduces response variability that is exogenous to the information processing of the brain and hence paves the way for substantially more detailed investigations of the brain's somatosensory system.

Cytoarchitecture of the Telencephalon in the Coral Reef Multiband Butterflyfish (Chaetodon multicinctus: Perciformes)

Abstract: Detailed neuroanatomical studies of model species are necessary to facilitate comparative experiments which test hypotheses relevant to brain evolution and function. Butterflyfishes (Chaetodontidae) boast numerous sympatric species that differ in social behavior, aggression and feeding ecology. However, the ability to test hypotheses relevant to brain function in this family is hindered by the lack of detailed neural descriptions. The cytoarchitecture of the telencephalon in the monogamous and territorial multiband butterflyfish, Chaetodon multicinctus, was determined with Nissl-stained serial sections and an immunohistochemical analysis of arginine vasotocin (AVT), serotonin, substance P and tyrosine hydroxylase. The ventral telencephalon was similar to that of other perciform fishes studied, with one major difference. A previously undescribed postcommissural region, the cuneate nucleus, was identified and putatively assigned to the ventral telencephalon. While the function of this nucleus is unknown, preliminary studies indicate that it may be part of a behaviorally relevant subpallial neural circuit that is modulated by AVT. The dorsal telencephalon consisted of 15 subdivisions among central, medial, lateral, dorsal and posterior zones. Several regions of the dorsal telencephalon of C. multicinctus differed from many other perciform fishes examined thus far. The nucleus taenia was in a more caudal position, and the central and lateral zones were enlarged. Within the lateral zone, an unusual third, ventral subdivision and a large-celled division were present. One hypothesis is that the enlarged ventral subdivision of the lateral zone (potential hippocampus homolog) relates to an enhancement of spatial learning or olfactory memory, which are important for this coral reef fish. This study provides the neuroanatomical basis for future comparative and evolutionary studies of brain organization and neuropeptide distributions, physiological studies of neural processing and insight into the complex social behavior of butterflyfishes.

The human cuneate nucleus contains discrete subregions whose neurochemical features match those of the relay nuclei for nociceptive information

Abstract: The present paper is aimed at defining distinctive subdivisions of the human cuneate nucleus (Cu), evident from prenatal to old life, whose occurrence has never been clearly formalized in the human brain, or described in other species so far. It extends our early observations on the presence of gray matter areas that host strong substance P (SP) immunoreactivity in the territory of the human Cu and adjacent cuneate fascicle. Here we provide a three-dimensional reconstruction of the Cu fields rich in SP and further identify those areas by means of their immunoreactivity to the neuropeptides SP, calcitonin gene-related peptide, methionine- and leucine-enkephalin, peptide histidine-isoleucine, somatostatin and galanin, to the trophins glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor, and to the neuroplasticity proteins polysialylated neural cell adhesion molecule and growth-associated protein-43. The presence, density and distribution of immunoreactivity for each of these molecules closely resemble those occurring in the superficial layers of the caudal spinal trigeminal nucleus (Sp5C). Myelin and Nissl stainings suggest that those Cu subregions and the Sp5C superficial layers share a similar histological aspect. This work establishes the existence of definite subregions, localized within the Cu territory, that bear the neurochemical and histological features of sensory nuclei committed to the neurotransmission of protopathic stimuli, including pain. These findings appear of particular interest when considering that functional, preclinical and clinical studies show that the dorsal column nuclei, classical relay station of fine somatic tactile and proprioceptive sensory stimuli, are also involved in pain neurotransmission.

Are the mechanisms driving somatosensory reorganization cortical or subcortical

Abstract: It has been long known that somatosensory deafferentation can produce a dramatic reorganization of the somatotopic map, characterized by the retraction of the deafferented body part representation followed by expansion of unaffected body part representations (Pons et al., 1991). Mechanisms driving this phenomenon are not clear, nor is it evident whether they occur within the cortex and/or at subcortical structures (Florence et al., 1998; Jones and Pons, 1998; Jain et al., 2000). The occurrence of anatomical alterations in the cortex after deafferentation (Florence et al., 1998), in addition to the notion that neocortex is a very plastic structure, led to the view that cortical reorganization of sensory maps after lesions is driven, at least in part, by cortical mechanisms. Recent work published by Kambi et al. (2014) contradicts this paradigm. In order to determine the extent to which different sites of somatosensory pathway potentially contribute to cortical plasticity, Kambi and colleagues lesioned the dorsal column in monkeys. They then mapped the hand representation in area 3b during inactivation of the cortical face region or the cuneate nucleus. They showed that transient inactivation of normal chin representation in area 3b did not affect the expanded chin representation, even in the vicinity of the former face/hand boundary. Surprisingly, inactivation of the cuneate nucleus completely abolished responses of the expanded chin representation. These results suggest that after lesions of the dorsal column, reorganization in area 3b is dependent on plastic alterations in the brainstem, and not in the cortex. In fact, cortical reorganization was probably mediated by growth of trigeminal axons into the cuneate nucleus, as previously shown by Jain et al. (2000). The apparent absence of corticocortical mechanisms driving cortical receptive field reorganization in these experiments is very intriguing. Simultaneous recordings from the normal chin and deafferented body representation of S1 demonstrated the expansion of the chin area in animals with dorsal column lesions (Kambi et al., 2014). Based on previous studies, it would be expected that this was due to new corticocortical connections, at least in the vicinity of the face/hand border. Moreover, large-scale sprouting of cortical connections following forelimb deafferentation has already been shown by Florence et al. (1998). This divergence in the results might be related to the type of deafferentation. In Kambi et al. (2014), animals underwent a lesion in the dorsal column, which only interrupts the ascending somatosensory information from the forelimb. Unlike amputees or individuals that suffered complete sectioning of the spinal cord, they could still move their forelimb and consequently, the motor representation of the forelimb was still present. Accordingly, Kambi et al. (2011) has shown that the forelimb motor representation in M1 is substantially preserved after lesion of the dorsal column. Perhaps this is the key difference between models in which cortical mechanisms do or do not contribute to the reorganization of cortical maps. The hand representation in area 3b receives inputs from M1 (Liao et al., 2013). This direct feedback, as well as indirect inputs from other cortical areas, may be a potential source to keep cortical hand region activated during forelimb movements even after lesions of the dorsal column. In this scenario, maintenance of activity by area 3b cortical inputs would preclude production of signals that induce corticocortical sprouting, and so maintain the segregation between face and hand regions. This would explain why large-scale sprouting in area 3b was observed by Florence et al. (1998), but apparently not by Kambi et al. (2014). In that study, animals had amputations and at some point, they lost the motor representation of the missing body part. Accordingly, in humans that have suffered complete spinal cord injury, the reorganization of the somatosensory cortex also results from growth of new lateral connections in the cortex (Henderson et al., 2011). It is possible that depending on the type of deafferentation, the mechanisms driving the functional reorganization in the cortex can be called into action at different levels of the somatosensory system. It would be interesting to explore this question by using the same experimental protocol as Kambi et al. (2014) in amputee animals. Additionally, injections of neurotracers could be done into the deafferented cortical region in order to determine whether or not sprouting occurs after different types of deafferentation. Dendritic spine loss has also been described in deafferented cortical neurons after spinal cord injury (Ghosh et al., 2012). Previous work has shown that alterations in dendritic spine morphology occur after lesions in the central nervous system (Keck et al., 2013) and may differ depending on the site of reorganization and type of sensory deprivation (Whitt et al., 2014). Perhaps synaptic plasticity after lesions of the dorsal column, as performed by Kambi et al. (2014), may induce different cellular responses compared to other types of deafferentation. Additionally, the lack of signal in expanded chin representation after lidocaine infusion in cuneate, but not in area 3b raises the intriguing possibility that these two sites are independently regulated and may present different molecular features in response to lesions. Studies concerning such morphological alterations and the key molecular players behind them would shed light on the location and mechanisms of plastic changes after different types of lesion. Finally, differences in mechanism driving cortical reorganization after deafferentation may also correlate with manifestation of phantom limb pain. It has been proposed that this phenomenon is caused by a maladaptive plasticity in the somatosensory cortex (Ramachandran, 1993). Nevertheless, the occurrence of cortical sprouting, as well as nuances in synaptic plasticity after different types of deafferentation, may account for the development of phantom pain. If so, different types of deafferentation may demand different strategies for treatment. Interestingly, phantom pain is especially common in amputees. Perhaps this is due to specific cortical mechanisms (e.g., cortical sprouting) that are absent in other types of lesion (e.g., lesion of the dorsal column). A better understanding of the differences in mechanisms driving cortical reorganization between different types of deafferentation may provide valuable data for developing therapies to alleviate phantom limb pain.