Replicating the Role of the Human Retina for a Cortical Visual Neuroprosthesis

Author(s):  
Samuel Romero ◽  
Christian Morillas ◽  
Antonio Martínez ◽  
Begoña del Pino ◽  
Francisco Pelayo ◽  
...  

Neuroengineering is an emerging research field combining the latest findings from neuroscience with developments in a variety of engineering disciplines to create artificial devices, mainly for therapeutical purposes. In this chapter, an application of this field to the development of a visual neuroprosthesis for the blind is described. Electrical stimulation of the visual cortex in blind subjects elicits the perception of visual sensations called phosphenes, a finding that encourages the development of future electronic visual prostheses. However, direct stimulation of the visual cortex would miss a significant degree of image processing that is carried out by the retina. The authors describe a biologically-inspired retina-like processor designed to drive the implanted stimulator using visual inputs from one or two cameras. This includes dynamic response modeling with minimal latency. The outputs of the retina-like processor are comparable to those recorded in biological retinas that are exposed to the same stimuli and allow estimation of the original scene

2013 ◽  
pp. 1532-1551
Author(s):  
Samuel Romero ◽  
Christian Morillas ◽  
Antonio Martínez ◽  
Begoña del Pino ◽  
Francisco Pelayo ◽  
...  

Neuroengineering is an emerging research field combining the latest findings from neuroscience with developments in a variety of engineering disciplines to create artificial devices, mainly for therapeutical purposes. In this chapter, an application of this field to the development of a visual neuroprosthesis for the blind is described. Electrical stimulation of the visual cortex in blind subjects elicits the perception of visual sensations called phosphenes, a finding that encourages the development of future electronic visual prostheses. However, direct stimulation of the visual cortex would miss a significant degree of image processing that is carried out by the retina. The authors describe a biologically-inspired retina-like processor designed to drive the implanted stimulator using visual inputs from one or two cameras. This includes dynamic response modeling with minimal latency. The outputs of the retina-like processor are comparable to those recorded in biological retinas that are exposed to the same stimuli and allow estimation of the original scene.


2021 ◽  
Vol 9 (3) ◽  
pp. 24
Author(s):  
Brian Heubel ◽  
Anja Nohe

The osteogenic effects of Bone Morphogenetic Proteins (BMPs) were delineated in 1965 when Urist et al. showed that BMPs could induce ectopic bone formation. In subsequent decades, the effects of BMPs on bone formation and maintenance were established. BMPs induce proliferation in osteoprogenitor cells and increase mineralization activity in osteoblasts. The role of BMPs in bone homeostasis and repair led to the approval of BMP2 by the Federal Drug Administration (FDA) for anterior lumbar interbody fusion (ALIF) to increase the bone formation in the treated area. However, the use of BMP2 for treatment of degenerative bone diseases such as osteoporosis is still uncertain as patients treated with BMP2 results in the stimulation of not only osteoblast mineralization, but also osteoclast absorption, leading to early bone graft subsidence. The increase in absorption activity is the result of direct stimulation of osteoclasts by BMP2 working synergistically with the RANK signaling pathway. The dual effect of BMPs on bone resorption and mineralization highlights the essential role of BMP-signaling in bone homeostasis, making it a putative therapeutic target for diseases like osteoporosis. Before the BMP pathway can be utilized in the treatment of osteoporosis a better understanding of how BMP-signaling regulates osteoclasts must be established.


1991 ◽  
Vol 125 (4) ◽  
pp. 348-353 ◽  
Author(s):  
V. Bähr ◽  
J. Hensen ◽  
O. Hader ◽  
T. Bölke ◽  
W. Oelkers

Abstract. Arginine vasopressin stimulates the secretion of adrenocorticotropin. A direct stimulatory effect of AVP on cortisol as well as aldosteron secretion has been postulated by several investigators. To study the possible role of a direct stimulatory action of AVP on the adrenal cortex, normal volunteers were treated with incremental injections of ACTH or with incremental infusions of AVP which raised plasma AVP levels to a maximum of 256±16 pmol/l. In both situations, a significant (p<0.001) linear correlation between plasma ACTH and plasma cortisol was observed. The regression coefficients were not different (p>0.5). Plasma aldosterone was stimulated by both treatments, but the weakly positive correlation between plasma ACTH and plasma aldosterone was not significant for either stimulus. Thus, in man, a direct stimulatory effect of AVP on cortisol secretion cannot be demonstrated. A direct effect of AVP on aldosterone cannot be definitely excluded, but is certainly of minor importance.


2003 ◽  
Vol 162 (1) ◽  
pp. 113-124 ◽  
Author(s):  
Michael Krauss ◽  
Masahiro Kinuta ◽  
Markus R. Wenk ◽  
Pietro De Camilli ◽  
Kohji Takei ◽  
...  

Clathrin-mediated endocytosis of synaptic vesicle membranes involves the recruitment of clathrin and AP-2 adaptor complexes to the presynaptic plasma membrane. Phosphoinositides have been implicated in nucleating coat assembly by directly binding to several endocytotic proteins including AP-2 and AP180. Here, we show that the stimulatory effect of ATP and GTPγS on clathrin coat recruitment is mediated at least in part by increased levels of PIP2. We also provide evidence for a role of ADP-ribosylation factor 6 (ARF6) via direct stimulation of a synaptically enriched phosphatidylinositol 4-phosphate 5-kinase type Iγ (PIPKIγ), in this effect. These data suggest a model according to which activation of PIPKIγ by ARF6-GTP facilitates clathrin-coated pit assembly at the synapse.


2019 ◽  
Vol 11 ◽  
pp. 84-86
Author(s):  
Kelly L. Collins ◽  
Devapratim Sarma ◽  
Shahin Hakimian ◽  
Jeff J. Tsai ◽  
Jeffrey G. Ojemann

1999 ◽  
Vol 16 (3) ◽  
pp. 541-555 ◽  
Author(s):  
YI ZHANG ◽  
RICHARD D. MOONEY ◽  
ROBERT W. RHOADES

Single-unit recording and micropressure ejection techniques were used to test the effects of norepinephrine (NE) on the responses of neurons in the superficial layers (the stratum griseum superficiale and stratum opticum) of the hamster's superior colliculus (SC). Application of NE suppressed visually evoked responses by ≥30% in 75% of 40 neurons tested and produced ≥30% augmentation of responses in only 5%. The decrement in response strength was mimicked by application of the α2 adrenoceptor agonist, p-aminoclonidine, the nonspecific β agonist, isoproterenol, and the β1 agonist, dobutamine. These agents had similar effects on responses evoked by electrical stimulation of the optic chiasm and visual cortex. The α1 agonist, methoxamine, augmented the light-evoked responses of 53% of 49 SC cells by ≥30%, but had little effect on responses evoked by electrical stimulation of optic chiasm or visual cortex. The effects of adrenergic agonists upon the glutamate-evoked responses of SC cells that were synaptically “isolated” by concurrent application of Mg2+ were similar to those obtained during visual stimulation. Analysis of effects of NE on visually evoked and background activity indicated that application of this amine did not significantly enhance signal-to-noise ratios for most superficial layer SC neurons, and signal-to-noise ratios were in some cases reduced. These results indicate that NE acts primarily through α2 and β1 receptors to suppress the visual responses of SC neurons. Activation of either of these receptors reduces the responses of SC neurons to either of their two major visual inputs as well as to direct stimulation by glutamate, and it would thus appear that these effects are primarily postsynaptic.


2019 ◽  
Vol 20 (22) ◽  
pp. 5599
Author(s):  
Iulia Zoicas ◽  
Johannes Kornhuber

The appropriate display of social behaviors is essential for the well-being, reproductive success and survival of an individual. Deficits in social behavior are associated with impaired N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission. In this review, we describe recent studies using genetically modified mice and pharmacological approaches which link the impaired functioning of the NMDA receptors, especially of the receptor subunits GluN1, GluN2A and GluN2B, to abnormal social behavior. This abnormal social behavior is expressed as impaired social interaction and communication, deficits in social memory, deficits in sexual and maternal behavior, as well as abnormal or heightened aggression. We also describe the positive effects of pharmacological stimulation of the NMDA receptors on these social deficits. Indeed, pharmacological stimulation of the glycine-binding site either by direct stimulation or by elevating the synaptic glycine levels represents a promising strategy for the normalization of genetically-induced, pharmacologically-induced or innate deficits in social behavior. We emphasize on the importance of future studies investigating the role of subunit-selective NMDA receptor ligands on different types of social behavior to provide a better understanding of the underlying mechanisms, which might support the development of selective tools for the optimized treatment of disorders associated with social deficits.


1997 ◽  
Vol 273 (6) ◽  
pp. H2843-H2849 ◽  
Author(s):  
Maurizio Cappelli-Bigazzi ◽  
Giuseppe Ambrosio ◽  
Giovanni Musci ◽  
Carmine Battaglia ◽  
Maria Carmela Bonaccorsi Di Patti ◽  
...  

This study evaluated the effects of ceruloplasmin, the copper-containing blue oxidase of vertebrate plasma, on the relaxation of rabbit aortic rings after endothelial release of nitric oxide (NO). Ceruloplasmin at physiological, i.e., micromolar, concentrations inhibited relaxation of rabbit aorta induced by endothelium-dependent agonists like acetylcholine or ADP, whereas it was ineffective toward vasodilation due to direct stimulation of smooth muscle cells by nitroglycerin. The effect was reversible and specific for native, fully metalated ceruloplasmin, since relaxation was not impaired by the heat-treated or metal-depleted derivatives. A trapping mechanism, involving a direct interaction of NO or other NO-containing species (like nitrosothiols and iron-dinitrosyls) with the copper sites and/or with the free thiol of ceruloplasmin, could be safely excluded on the basis of spectroscopic and chemical analyses of the protein exposed to authentic NO, nitrosothiols, or iron-dinitrosyls. The data presented in this paper constitute the first evidence of impairment of the endothelium-dependent vasodilatation by a plasma protein and may shed some light on the still uncertain physiological role of ceruloplasmin.


2014 ◽  
Vol 223 (1) ◽  
pp. 93-106 ◽  
Author(s):  
R Dobie ◽  
V E MacRae ◽  
C Huesa ◽  
R van't Hof ◽  
S F Ahmed ◽  
...  

The suppressor of cytokine signalling (Socs2−/−)-knockout mouse is characterised by an overgrowth phenotype due to enhanced GH signalling. The objective of this study was to define theSocs2−/−bone phenotype and determine whether GH promotes bone mass via IGF1-dependent mechanisms. Despite no elevation in systemic IGF1 levels, increased body weight in 4-week-oldSocs2−/−mice following GH treatment was associated with increased cortical bone area (Ct.Ar) (P<0.01). Furthermore, detailed bone analysis of male and female juvenile and adultSocs2−/−mice revealed an altered cortical and trabecular phenotype consistent with the known anabolic effects of GH. Indeed, maleSocs2−/−mice had increased Ct.Ar (P<0.05) and thickness associated with increased strength. Despite this, there was no elevation in hepaticIgf1expression, suggesting that the anabolic bone phenotype was the result of increased local GH action. Mechanistic studies showed that in osteoblasts and bone ofSocs2−/−mice, STAT5 phosphorylation was significantly increased in response to GH. Conversely, overexpression of SOCS2 decreased GH-induced STAT5 signalling. Although an increase inIgf1expression was observed inSocs2−/−osteoblasts following GH, it was not evidentin vivo.Igf1expression levels were not elevated in response to GH in 4-week-old mice and no alterations in expression was observed in bone samples of 6-week-oldSocs2−/−mice. These studies emphasise the critical role of SOCS2 in controlling the local GH anabolic bone effects. We provide compelling evidence implicating SOCS2 in the regulation of GH osteoblast signalling and ultimately bone accrual, which maybe via mechanisms that are independent of IGF1 productionin vivo.


1989 ◽  
Vol 67 (1) ◽  
pp. 5-9 ◽  
Author(s):  
S. A. Wandji ◽  
J. R. Seoane ◽  
A. G. Roberge ◽  
L. Bédard ◽  
L. Thibault

Five wethers were surgically prepared with cranial implants to study the role of gabaminergic neural pathways on the hypothalamic control of feeding behaviour in ruminants. In the first experiment, the animals were injected (1 μL) with a physiological Tyrode (0.95%) solution, muscimol (0.5 and 1.0 nmol), GABA (0.5 and 1.0 nmol), and L-glutamic acid (0.5 and 1.0 nmol). Feed intake following injections of muscimol (1.0 nmol) and L-glutamic acid (0.5 and 1.0 nmol) was twice as large as that following the Tyrode solution, at 60-min postinjections. These results, however, were not statistically significant (p = 0.12–0.15). In the second experiment, the animals were injected (1 μL) with saline, muscimol (0.8 nmol), L-glutamic acid (0.8 nmol), and pentobarbital (0.26 μmol). Fifteen minutes after the injections, pentobarbital had induced a significant feeding response when compared with control values (p < 0.01), whereas the effect of L-glutamic acid was not significant. However, 30 min after the injections, feed intake of sheep having received L-glutamic acid was higher than that obtained with the control injections (p < 0.01). The response to pentobarbital was stronger than that to either muscimol or L-glutamic acid. Histological analyses of brain tissue indicated that injections were performed in the ventromedial hypothalamus of four sheep and in the dorsomedial hypothalamus of the other. The data indicate that L-glutamic acid stimulates feed intake by acting either as a precursor of GABA or by a direct stimulation of glutaminergic neural pathways involved in the control of feed intake.Key words: Feeding behaviour, glutamic acid, GABA, sheep.


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