Limits...
Miniaturized Technologies for Enhancement of Motor Plasticity.

Moorjani S - Front Bioeng Biotechnol (2016)

Bottom Line: The idea that the damaged brain can functionally reorganize itself - so when one part fails, there lies the possibility for another to substitute - is an exciting discovery of the twentieth century.This is a very significant alteration from our previously static view of the brain and has profound implications for the rescue of function after a motor injury.Presentation of the right cues, applied in relevant spatiotemporal geometries, is required to awaken the dormant plastic forces essential for repair.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Biophysics, and the Washington National Primate Research Center, University of Washington , Seattle, WA , USA.

ABSTRACT
The idea that the damaged brain can functionally reorganize itself - so when one part fails, there lies the possibility for another to substitute - is an exciting discovery of the twentieth century. We now know that motor circuits once presumed to be hardwired are not, and motor-skill learning, exercise, and even mental rehearsal of motor tasks can turn genes on or off to shape brain architecture, function, and, consequently, behavior. This is a very significant alteration from our previously static view of the brain and has profound implications for the rescue of function after a motor injury. Presentation of the right cues, applied in relevant spatiotemporal geometries, is required to awaken the dormant plastic forces essential for repair. The focus of this review is to highlight some of the recent progress in neural interfaces designed to harness motor plasticity, and the role of miniaturization in development of strategies that engage diverse elements of the neuronal machinery to synergistically facilitate recovery of function after motor damage.

No MeSH data available.


Related in: MedlinePlus

Delivery of chondroitinase ABC (ChABC) promotes functional recovery after spinal-cord injury. (A) Descending corticospinal tract (CST) axons calculated as a percentage of the fibres seen 4 mm above the lesion, where the CST was intact. Higher fiber counts were seen in the presence of ChABC (Les + ChABC) compared to treatment with vehicle (Les + veh), but the axon numbers were significantly lower compared to the unlesioned sham controls. Asterisks denote significant difference between vehicle and ChABC treatment. (B) Plot shows the average size of cortical evoked cord dorsum potentials (CDPs) 1 segment above the lesion site and at 1-mm intervals caudal to this site. Data were normalized to the size of the rostral recording. ChABC treatment increased the size of CDPs below the lesion compared to treatment with vehicle, which was abolished by a re-lesion, indicating CST regeneration. (C) Number of forelimb foot slips made when rats crossed a narrow beam or grid. In both the beam and grid tasks, lesioned rats treated with vehicle made significantly more foot-slip errors compared to unlesioned sham controls. By contrast, lesioned rats treated with ChABC made a marked functional recovery on both these tasks over time. Asterisks denote significant difference from sham controls. All data are shown as mean ± standard error of the mean. Les, lesion; Veh, vehicle. Image adapted, with permission, from Bradbury et al. (2002).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4834582&req=5

Figure 5: Delivery of chondroitinase ABC (ChABC) promotes functional recovery after spinal-cord injury. (A) Descending corticospinal tract (CST) axons calculated as a percentage of the fibres seen 4 mm above the lesion, where the CST was intact. Higher fiber counts were seen in the presence of ChABC (Les + ChABC) compared to treatment with vehicle (Les + veh), but the axon numbers were significantly lower compared to the unlesioned sham controls. Asterisks denote significant difference between vehicle and ChABC treatment. (B) Plot shows the average size of cortical evoked cord dorsum potentials (CDPs) 1 segment above the lesion site and at 1-mm intervals caudal to this site. Data were normalized to the size of the rostral recording. ChABC treatment increased the size of CDPs below the lesion compared to treatment with vehicle, which was abolished by a re-lesion, indicating CST regeneration. (C) Number of forelimb foot slips made when rats crossed a narrow beam or grid. In both the beam and grid tasks, lesioned rats treated with vehicle made significantly more foot-slip errors compared to unlesioned sham controls. By contrast, lesioned rats treated with ChABC made a marked functional recovery on both these tasks over time. Asterisks denote significant difference from sham controls. All data are shown as mean ± standard error of the mean. Les, lesion; Veh, vehicle. Image adapted, with permission, from Bradbury et al. (2002).

Mentions: Intrathecal microliter-bolus infusions of chondroitinase ABC (ChABC) have been used for enzymatic degradation of CSPGs to promote recovery of locomotor and proprioceptive behaviors after spinal-cord injury in rats (Figure 5; Bradbury et al., 2002). Alilain and coworkers also employed (nanoliter-volume) ChABC injections in rats for digestion of CSPGs upregulated around phrenic motor neurons, which, in conjunction with a peripheral nerve graft, resulted in functional regeneration of respiratory pathways after spinal-cord injury (Alilain et al., 2011).


Miniaturized Technologies for Enhancement of Motor Plasticity.

Moorjani S - Front Bioeng Biotechnol (2016)

Delivery of chondroitinase ABC (ChABC) promotes functional recovery after spinal-cord injury. (A) Descending corticospinal tract (CST) axons calculated as a percentage of the fibres seen 4 mm above the lesion, where the CST was intact. Higher fiber counts were seen in the presence of ChABC (Les + ChABC) compared to treatment with vehicle (Les + veh), but the axon numbers were significantly lower compared to the unlesioned sham controls. Asterisks denote significant difference between vehicle and ChABC treatment. (B) Plot shows the average size of cortical evoked cord dorsum potentials (CDPs) 1 segment above the lesion site and at 1-mm intervals caudal to this site. Data were normalized to the size of the rostral recording. ChABC treatment increased the size of CDPs below the lesion compared to treatment with vehicle, which was abolished by a re-lesion, indicating CST regeneration. (C) Number of forelimb foot slips made when rats crossed a narrow beam or grid. In both the beam and grid tasks, lesioned rats treated with vehicle made significantly more foot-slip errors compared to unlesioned sham controls. By contrast, lesioned rats treated with ChABC made a marked functional recovery on both these tasks over time. Asterisks denote significant difference from sham controls. All data are shown as mean ± standard error of the mean. Les, lesion; Veh, vehicle. Image adapted, with permission, from Bradbury et al. (2002).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4834582&req=5

Figure 5: Delivery of chondroitinase ABC (ChABC) promotes functional recovery after spinal-cord injury. (A) Descending corticospinal tract (CST) axons calculated as a percentage of the fibres seen 4 mm above the lesion, where the CST was intact. Higher fiber counts were seen in the presence of ChABC (Les + ChABC) compared to treatment with vehicle (Les + veh), but the axon numbers were significantly lower compared to the unlesioned sham controls. Asterisks denote significant difference between vehicle and ChABC treatment. (B) Plot shows the average size of cortical evoked cord dorsum potentials (CDPs) 1 segment above the lesion site and at 1-mm intervals caudal to this site. Data were normalized to the size of the rostral recording. ChABC treatment increased the size of CDPs below the lesion compared to treatment with vehicle, which was abolished by a re-lesion, indicating CST regeneration. (C) Number of forelimb foot slips made when rats crossed a narrow beam or grid. In both the beam and grid tasks, lesioned rats treated with vehicle made significantly more foot-slip errors compared to unlesioned sham controls. By contrast, lesioned rats treated with ChABC made a marked functional recovery on both these tasks over time. Asterisks denote significant difference from sham controls. All data are shown as mean ± standard error of the mean. Les, lesion; Veh, vehicle. Image adapted, with permission, from Bradbury et al. (2002).
Mentions: Intrathecal microliter-bolus infusions of chondroitinase ABC (ChABC) have been used for enzymatic degradation of CSPGs to promote recovery of locomotor and proprioceptive behaviors after spinal-cord injury in rats (Figure 5; Bradbury et al., 2002). Alilain and coworkers also employed (nanoliter-volume) ChABC injections in rats for digestion of CSPGs upregulated around phrenic motor neurons, which, in conjunction with a peripheral nerve graft, resulted in functional regeneration of respiratory pathways after spinal-cord injury (Alilain et al., 2011).

Bottom Line: The idea that the damaged brain can functionally reorganize itself - so when one part fails, there lies the possibility for another to substitute - is an exciting discovery of the twentieth century.This is a very significant alteration from our previously static view of the brain and has profound implications for the rescue of function after a motor injury.Presentation of the right cues, applied in relevant spatiotemporal geometries, is required to awaken the dormant plastic forces essential for repair.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Biophysics, and the Washington National Primate Research Center, University of Washington , Seattle, WA , USA.

ABSTRACT
The idea that the damaged brain can functionally reorganize itself - so when one part fails, there lies the possibility for another to substitute - is an exciting discovery of the twentieth century. We now know that motor circuits once presumed to be hardwired are not, and motor-skill learning, exercise, and even mental rehearsal of motor tasks can turn genes on or off to shape brain architecture, function, and, consequently, behavior. This is a very significant alteration from our previously static view of the brain and has profound implications for the rescue of function after a motor injury. Presentation of the right cues, applied in relevant spatiotemporal geometries, is required to awaken the dormant plastic forces essential for repair. The focus of this review is to highlight some of the recent progress in neural interfaces designed to harness motor plasticity, and the role of miniaturization in development of strategies that engage diverse elements of the neuronal machinery to synergistically facilitate recovery of function after motor damage.

No MeSH data available.


Related in: MedlinePlus