diff --git a/OMEGA.bib b/OMEGA.bib index 04dff97..2224d9f 100644 --- a/OMEGA.bib +++ b/OMEGA.bib @@ -130,24 +130,6 @@ Year = 2017, url = {papers/Cong_eLife2017.pdf}} -@article{Itzhaki:2016, - Author = {Itzhaki, Ruth F and Lathe, Richard and Balin, Brian J and Ball, Melvyn J and Bearer, Elaine L and Braak, Heiko and Bullido, Maria J and Carter, Chris and Clerici, Mario and Cosby, S Louise and Del Tredici, Kelly and Field, Hugh and Fulop, Tamas and Grassi, Claudio and Griffin, W Sue T and Haas, J{\"u}rgen and Hudson, Alan P and Kamer, Angela R and Kell, Douglas B and Licastro, Federico and Letenneur, Luc and L{\"o}vheim, Hugo and Mancuso, Roberta and Miklossy, Judith and Otth, Carola and Palamara, Anna Teresa and Perry, George and Preston, Christopher and Pretorius, Etheresia and Strandberg, Timo and Tabet, Naji and Taylor-Robinson, Simon D and Whittum-Hudson, Judith A}, - Date-Added = {2018-07-16 21:29:57 +0000}, - Date-Modified = {2018-07-16 21:29:57 +0000}, - Doi = {10.3233/JAD-160152}, - Journal = {J Alzheimers Dis}, - Journal-Full = {Journal of Alzheimer's disease : JAD}, - Mesh = {Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Communicable Diseases; Humans; Microbiota}, - Number = {4}, - Pages = {979-84}, - Pmc = {PMC5457904}, - pmid = {26967229}, - Pst = {ppublish}, - Title = {Microbes and Alzheimer's Disease}, - Volume = {51}, - Year = {2016}, - url = {papers/Itzhaki_JAlzheimersDis2016.pdf}} - @article{Barchini2018, Abstract = {Detection of salient objects in the visual scene is a vital aspect of an animal's interactions with its environment. Here, we show that neurons in the mouse superior colliculus (SC) encode visual saliency by detecting motion contrast between stimulus center and surround. Excitatory neurons in the most superficial lamina of the SC are contextually modulated, monotonically increasing their response from suppression by the same-direction surround to maximal potentiation by an oppositely-moving surround. The degree of this potentiation declines with depth in the SC. Inhibitory neurons are suppressed by any surround at all depths. These response modulations in both neuronal populations are much more prominent to direction contrast than to phase, temporal frequency, or static orientation contrast, suggesting feature-specific saliency encoding in the mouse SC. Together, our findings provide evidence supporting locally generated feature representations in the SC, and lay the foundations towards a mechanistic and evolutionary understanding of their emergence.}, Article_Type = {journal}, @@ -11464,6 +11446,7 @@ CONCLUSIONS: These findings indicate that twitches are not produced randomly but Bdsk-File-2 = {papers/Hohl_Neuron2013a.pdf}, Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.neuron.2013.05.026}} + @article{Lee:2013, Abstract = {Sensory inputs control motor behavior with a strength, or gain, that can be modulated according to the movement conditions. In smooth pursuit eye movements, the response to a brief perturbation of target motion is larger during pursuit of a moving target than during fixation of a stationary target. As a step toward identifying the locus and mechanism of gain modulation, we test whether it acts on signals that are in visual or motor coordinates. Monkeys tracked targets that moved at 15$\,^{\circ}$/s in one of eight directions, including left, right, up, down, and the four oblique directions. In eight-ninths of the trials, the target underwent a brief perturbation that consisted of a single cycle of a 10 Hz sine wave of amplitude $\pm$5$\,^{\circ}$/s in one of the same eight directions. Even for oblique directions of baseline target motion, the magnitude of the eye velocity response to the perturbation was largest for a perturbation near the axis of target motion and smallest for a perturbation along the orthogonal axis. Computational modeling reveals that our data are reproduced when the strength of visual-motor transmission is modulated in sensory coordinates, and there is a static motor bias that favors horizontal eye movements. A network model shows how the output from the smooth eye movement region of the frontal eye fields (FEF(SEM)) could implement gain control by shifting the peak of a visual population response along the axes of preferred image speed and direction.}, Author = {Lee, Joonyeol and Yang, Jin and Lisberger, Stephen G}, @@ -43273,11 +43256,6 @@ CONCLUSIONS: Centrifugal axons in the macaque retina are part of the system of a Bdsk-Url-1 = {http://dx.doi.org/10.1523/JNEUROSCI.1199-07.2007}} - - - - - @article{Belanger:1997, Abstract = {In the embryonic CNS, preformed pathways precede the growth of axonal fasciculi [Katz M. J. and Lasek R. J. (1980) Cell Motil. 1, 141-157; Katz M. J. et al. (1980) Neuroscience 5, 821-833]. What are the developmental events that lead to the elaboration of these preformed pathways? To answer this question, we investigated the organization of the primitive neural tube and more particularly the arrangement of the early-generated cells using [3H]thymidine autoradiography or bromodeoxyuridine. Our data suggest that the position of early-generated cells might be involved in the setting of such pathways. In the brain stem of E12(0) (12 days and 0 h) and E12(15) rat embryos, the first-generated cells were organized into three longitudinal columns associated with glycoconjugate-rich extracellular spaces in the adjacent primitive marginal layer. Also, axons traced with 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) were contiguous to the early-generated cellular columns and represented the primordium of the medial longitudinal fasciculus, the lateral longitudinal tract and the mesencephalic trigeminal tract. Our results show a correlation between the organization of early-generated cells, likely neurons, and the pattern of extracellular spaces in the marginal layer where axons grow. It has been reported in the literature that neurons produce elements of the extracellular matrix such as growth-modulating molecules or space-creating molecules. We therefore suggest that the position of early-generated neurons could be involved in the elaboration of a template for the setting of some major longitudinal tracts during embryonic development of the brainstem.}, Author = {B{\'e}langer, M. C. and Auclair, F. and Bertrand, L. and Marchand, R.}, @@ -43625,23 +43603,6 @@ CONCLUSIONS: Centrifugal axons in the macaque retina are part of the system of a url = {papers/Brecht_CurrOpinNeurobiol2007.pdf}, Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.conb.2007.07.008}} - Abstract = {Earlier studies suggested that while after spinal cord lesions and transplants at birth, the transplants serve both as a bridge and as a relay to restore supraspinal input caudal to the injury (Bregman, 1994), after injury in the adult the spinal cord transplants serve as a relay, but not as a bridge. We show here, that after complete spinal cord transection in adult rats, delayed spinal cord transplants and exogenous neurotrophic factors, the transplants can also serve as a bridge to restore supraspinal input (Fig. 9). We demonstrate here that when the delivery of transplants and neurotrophins are delayed until 2 weeks after spinal cord transection, the amount of axonal growth and the amount of recovery of function are dramatically increased. Under these conditions, both supraspinal and propriospinal projections to the host spinal cord caudal to the transection are reestablished. The growth of supraspinal axons across the transplant and back into the host spinal cord caudal to the lesion was dependent upon the presence of exogenous neurotrophic support. Without the neurotrophins, only propriospinal axons were able to re-establish connections across the transplant. Studies using peripheral nerve or Schwann cell grafts have shown that some anatomical connectivity can be restored across the injury site, particularly under the influence of neurotrophins (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Without neurotrophin treatment, brainstem axons do not enter [figure: see text] the graft (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Similarly, cells genetically modified to secrete neurotrophins and transplanted into the spinal cord influence the axonal growth of specific populations of spinally projecting neurons (Tuszynski et al., 1996, 1997; Grill et al., 1997; Blesch and Tuszynski, 1997). Taken together, these studies support a role for neurotrophic factors in the repair of the mature CNS. The regrowth of supraspinal and propriospinal input across the transection site was associated with consistent improvements in hindlimb locomotor function. Animals performed alternating and reciprocal hindlimb stepping with plantar foot contact to the treadmill or stair during ascension. Furthermore, they acquired hindlimb weight support and demonstrated appropriate postural control for balance and equilibrium of all four limbs. After spinal cord injury in the adult, the circuitry underlying rhythmic alternating stepping movements is still present within the spinal cord caudal to the lesion, but is now devoid of supraspinal control. We show here that restoring even relatively small amounts of input allows supraspinal neurons to access the spinal cord circuitry. Removing the re-established supraspinal input after recovery (by retransection rostral to the transplant) abolished the recovery and abolished the serotonergic fibers within the transplant and spinal cord caudal to the transplant. This suggests that at least some of the recovery observed is due to re-establishing supraspinal input across the transplant, rather than a diffuse influence of the transplant on motor recovery. It is unlikely, however, that the greater recovery of function in animals that received delayed transplant and neurotrophins is due solely to the restoration of supraspinal input. Recent work by Ribotta et al. (2000) suggests that segmental plasticity within the spinal cord contributes to weight support and bilateral foot placement after spinal cord transection. This recovery of function occurs after transplants of fetal raphe cells into the adult spinal cord transected at T11. Recovery of function appears to require innervation of the L1-L2 segments with serotonergic fibers, and importantly, animals require external stimulation (tail pinch) to elicit the behavior. In the current study, animals with transection only did not develop stepping overground or on the treadmill without tail pinch, although the transplant and neurotrophin-treated groups did so without external stimuli. Therefore both reorganization of the segmental circuitry and partial restoration of supraspinal input presumably interact to yield the improvements in motor function observed. It is unlikely that the recovery of skilled forelimb movement observed can be mediated solely by reorganization of segmental spinal cord circuitry. We suggest that the restoration of supraspinal input contributes to the recovery observed. It is likely that after CNS injury, reorganization occurs both within the spinal cord and at supraspinal levels, and together contribute to the recovery of automatic and skilled forelimb function and of locomotion. In summary, the therapeutic intervention of tissue transplantation and exogenous neurotrophin support leads to improvements in supraspinal and propriospinal input across the transplant into the host caudal cord and a concomitant improvement in locomotor function. Paradoxically, delaying these interventions for several weeks after a spinal cord transection leads to dramatic improvements in recovery of function and a concomitant restoration of supraspinal input into the host caudal spinal cord. These findings suggest that opportunity for intervention after spinal cord injury may be far greater than originally envisioned, and that CNS neurons with long-standing injuries may be able to re-initiate growth leading to improvement in motor function.}, - Author = {Bregman, Barbara S. and Coumans, Jean-Valery V. and Dai, Hai Ning and Kuhn, Penelope L. and Lynskey, James and McAtee, Marietta and Sandhu, Faheem}, - Date-Added = {2009-03-25 19:34:04 -0400}, - Date-Modified = {2009-03-25 19:55:27 -0400}, - Issn = {0079-6123}, - Journal = {Prog Brain Res}, - Keywords = {Axons;Research Support, Non-U.S. Gov't;Neuroprotective Agents;Cell Transplantation;Nerve Regeneration;Spinal Cord Injuries;Neuronal Plasticity;Mammals;Research Support, U.S. Gov't, P.H.S.;Forelimb;Locomotion;Animals;24 Pubmed search results 2008;Neurons;review}, - Medline = {22328364}, - Nlm_Id = {0376441}, - Organization = {Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA. bregmanb\@georgetown.edu}, - Pages = {257-73}, - Pubmed = {12440372}, - Title = {Transplants and neurotrophic factors increase regeneration and recovery of function after spinal cord injury}, - Uuid = {30EF16BD-52DD-46D7-AEE7-341B5FCC8679}, - Volume = {137}, - Year = {2002}} - @article{Brenowitz:2003, Abstract = {Many types of neurons release endocannabinoids from their dendrites in response to elevation of intracellular calcium levels. Endocannabinoids then activate presynaptic cannabinoid receptors, thereby inhibiting neurotransmitter release for tens of seconds. A crucial step in understanding the physiological role of this retrograde signaling is to determine its sensitivity to elevations of postsynaptic calcium. Here we determine and compare the calcium dependence of endocannabinoid-mediated retrograde inhibition at three types of synapses onto cerebellar Purkinje cells. Previous studies have shown that Purkinje cell depolarization results in endocannabinoid-mediated retrograde inhibition of synapses received from climbing fibers, granule cell parallel fibers, and inhibitory interneurons. Using several calcium indicators with a range of affinities, we performed a series of in situ and in vitro calibrations to quantify calcium levels in Purkinje cells. We found that postsynaptic calcium levels of approximately 15 microM are required for half-maximal retrograde inhibition at all of these synapses. In contrast, previous studies had suggested that endocannabinoid release could occur with slight elevations of calcium above resting levels, which implies that inhibition should be widespread and continuously modulated by subtle changes in intracellular calcium levels. However, our results indicate that such small changes in intracellular calcium are not sufficient to evoke endocannabinoid release. Instead, because of its high requirement for calcium, retrograde inhibition mediated by calcium-dependent endocannabinoid release from Purkinje cells will occur under more restricted conditions and with greater spatial localization than previously appreciated.}, Author = {Brenowitz, Stephan D. and Regehr, Wade G.}, diff --git a/archiv.bib b/archiv.bib index 5a88d0b..fca93ad 100644 --- a/archiv.bib +++ b/archiv.bib @@ -5591,6 +5591,23 @@ CONCLUSIONS: These results suggest that, in contrast to the situation in adult a url = {papers/Brazelton_Science2000.pdf}} @article{Bregman:2002, + Abstract = {Earlier studies suggested that while after spinal cord lesions and transplants at birth, the transplants serve both as a bridge and as a relay to restore supraspinal input caudal to the injury (Bregman, 1994), after injury in the adult the spinal cord transplants serve as a relay, but not as a bridge. We show here, that after complete spinal cord transection in adult rats, delayed spinal cord transplants and exogenous neurotrophic factors, the transplants can also serve as a bridge to restore supraspinal input (Fig. 9). We demonstrate here that when the delivery of transplants and neurotrophins are delayed until 2 weeks after spinal cord transection, the amount of axonal growth and the amount of recovery of function are dramatically increased. Under these conditions, both supraspinal and propriospinal projections to the host spinal cord caudal to the transection are reestablished. The growth of supraspinal axons across the transplant and back into the host spinal cord caudal to the lesion was dependent upon the presence of exogenous neurotrophic support. Without the neurotrophins, only propriospinal axons were able to re-establish connections across the transplant. Studies using peripheral nerve or Schwann cell grafts have shown that some anatomical connectivity can be restored across the injury site, particularly under the influence of neurotrophins (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Without neurotrophin treatment, brainstem axons do not enter [figure: see text] the graft (Xu et al., 1995a,b; Cheng et al., 1996; Ye and Houle, 1997). Similarly, cells genetically modified to secrete neurotrophins and transplanted into the spinal cord influence the axonal growth of specific populations of spinally projecting neurons (Tuszynski et al., 1996, 1997; Grill et al., 1997; Blesch and Tuszynski, 1997). Taken together, these studies support a role for neurotrophic factors in the repair of the mature CNS. The regrowth of supraspinal and propriospinal input across the transection site was associated with consistent improvements in hindlimb locomotor function. Animals performed alternating and reciprocal hindlimb stepping with plantar foot contact to the treadmill or stair during ascension. Furthermore, they acquired hindlimb weight support and demonstrated appropriate postural control for balance and equilibrium of all four limbs. After spinal cord injury in the adult, the circuitry underlying rhythmic alternating stepping movements is still present within the spinal cord caudal to the lesion, but is now devoid of supraspinal control. We show here that restoring even relatively small amounts of input allows supraspinal neurons to access the spinal cord circuitry. Removing the re-established supraspinal input after recovery (by retransection rostral to the transplant) abolished the recovery and abolished the serotonergic fibers within the transplant and spinal cord caudal to the transplant. This suggests that at least some of the recovery observed is due to re-establishing supraspinal input across the transplant, rather than a diffuse influence of the transplant on motor recovery. It is unlikely, however, that the greater recovery of function in animals that received delayed transplant and neurotrophins is due solely to the restoration of supraspinal input. Recent work by Ribotta et al. (2000) suggests that segmental plasticity within the spinal cord contributes to weight support and bilateral foot placement after spinal cord transection. This recovery of function occurs after transplants of fetal raphe cells into the adult spinal cord transected at T11. Recovery of function appears to require innervation of the L1-L2 segments with serotonergic fibers, and importantly, animals require external stimulation (tail pinch) to elicit the behavior. In the current study, animals with transection only did not develop stepping overground or on the treadmill without tail pinch, although the transplant and neurotrophin-treated groups did so without external stimuli. Therefore both reorganization of the segmental circuitry and partial restoration of supraspinal input presumably interact to yield the improvements in motor function observed. It is unlikely that the recovery of skilled forelimb movement observed can be mediated solely by reorganization of segmental spinal cord circuitry. We suggest that the restoration of supraspinal input contributes to the recovery observed. It is likely that after CNS injury, reorganization occurs both within the spinal cord and at supraspinal levels, and together contribute to the recovery of automatic and skilled forelimb function and of locomotion. In summary, the therapeutic intervention of tissue transplantation and exogenous neurotrophin support leads to improvements in supraspinal and propriospinal input across the transplant into the host caudal cord and a concomitant improvement in locomotor function. Paradoxically, delaying these interventions for several weeks after a spinal cord transection leads to dramatic improvements in recovery of function and a concomitant restoration of supraspinal input into the host caudal spinal cord. These findings suggest that opportunity for intervention after spinal cord injury may be far greater than originally envisioned, and that CNS neurons with long-standing injuries may be able to re-initiate growth leading to improvement in motor function.}, + Author = {Bregman, Barbara S. and Coumans, Jean-Valery V. and Dai, Hai Ning and Kuhn, Penelope L. and Lynskey, James and McAtee, Marietta and Sandhu, Faheem}, + Date-Added = {2009-03-25 19:34:04 -0400}, + Date-Modified = {2009-03-25 19:55:27 -0400}, + Issn = {0079-6123}, + Journal = {Prog Brain Res}, + Keywords = {Axons;Research Support, Non-U.S. Gov't;Neuroprotective Agents;Cell Transplantation;Nerve Regeneration;Spinal Cord Injuries;Neuronal Plasticity;Mammals;Research Support, U.S. Gov't, P.H.S.;Forelimb;Locomotion;Animals;24 Pubmed search results 2008;Neurons;review}, + Medline = {22328364}, + Nlm_Id = {0376441}, + Organization = {Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA. bregmanb\@georgetown.edu}, + Pages = {257-73}, + Pubmed = {12440372}, + Title = {Transplants and neurotrophic factors increase regeneration and recovery of function after spinal cord injury}, + Uuid = {30EF16BD-52DD-46D7-AEE7-341B5FCC8679}, + Volume = {137}, + Year = {2002}} + @article{Brewer:1999, Abstract = {Adult mammalian CNS neurons appear to be terminally differentiated and postmitotic. However, this conclusion may be due to nonpermissive conditions in the brain or in culture media. If embryonic rat hippocampal neurons are cultured in Neurobasal/B27 with FGF2, nearly all neurons proliferated until a maximum density was reached. Similarly, adult neurons can be cultured that fire action potentials and display immunoreactivity for neurofilament, MAP2, tau, and glutamate. Seventy percent of the 3000 isolated adult cells per milligram of brain tissue began to proliferate after 3 days in culture and incorporated BrdU. By 4 days of regeneration in culture, virtually all neuron-like cells with asymmetric processes were glutamate positive and immunoreactive for neurofilament. Immunoreactivity of the intermediate filament stem cell marker nestin increased in adult cells to levels present in freshly isolated embryonic neurons. These are the first studies to demonstrate that over 50\%of adult CNS cells with neuron-like characteristics retain regenerative and proliferative potential.}, @@ -45569,3 +45586,21 @@ CONCLUSIONS: This study provides preliminary evidence to suggest that athletes w url = {papers/Iverson_BrainInj2004.pdf}, Bdsk-Url-1 = {http://dx.doi.org/10.1080/02699050310001617352}} +@article{Itzhaki:2016, + Author = {Itzhaki, Ruth F and Lathe, Richard and Balin, Brian J and Ball, Melvyn J and Bearer, Elaine L and Braak, Heiko and Bullido, Maria J and Carter, Chris and Clerici, Mario and Cosby, S Louise and Del Tredici, Kelly and Field, Hugh and Fulop, Tamas and Grassi, Claudio and Griffin, W Sue T and Haas, J{\"u}rgen and Hudson, Alan P and Kamer, Angela R and Kell, Douglas B and Licastro, Federico and Letenneur, Luc and L{\"o}vheim, Hugo and Mancuso, Roberta and Miklossy, Judith and Otth, Carola and Palamara, Anna Teresa and Perry, George and Preston, Christopher and Pretorius, Etheresia and Strandberg, Timo and Tabet, Naji and Taylor-Robinson, Simon D and Whittum-Hudson, Judith A}, + Date-Added = {2018-07-16 21:29:57 +0000}, + Date-Modified = {2018-07-16 21:29:57 +0000}, + Doi = {10.3233/JAD-160152}, + Journal = {J Alzheimers Dis}, + Journal-Full = {Journal of Alzheimer's disease : JAD}, + Mesh = {Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Communicable Diseases; Humans; Microbiota}, + Number = {4}, + Pages = {979-84}, + Pmc = {PMC5457904}, + pmid = {26967229}, + Pst = {ppublish}, + Title = {Microbes and Alzheimer's Disease}, + Volume = {51}, + Year = {2016}, + url = {papers/Itzhaki_JAlzheimersDis2016.pdf}} +