scholarly journals VII.—On the Physiological Action of Light

1873 ◽  
Vol 27 (1) ◽  
pp. 141-166 ◽  
Author(s):  
James Dewar ◽  
John Gray

Sensory nerves are divided into two classes, those of general sensibility and those of special sense. The nerves of general sensibility are distributed to the skin, muscles, or viscera, and convey influences to the brain which give rise to sensations of touch, heat, &c., or to those vague sensations, not definitely localised, which we include under the name of the muscular sense. The nerves of special sense are endowed with special and individual physiological properties. When a nerve of this order is irritated in any way, either by mechanical, chemical, or electrical stimuli, an influence is conveyed to the brain which gives rise to the same kind of sensation as that produced by the normal stimulus on the terminal organ. For example, pressure on the eyeball, as shown by Newton and Young, electrical stimulation by a continuous current, as demonstrated by Pfaff, Helmholtz Ritter, Purkinje, Du Bois-Reymond, and Schelske, produce many of the phenomena of vision, including not only the perception of light, but the perception of various colours and tints. But while this is the case, it is equally certain that each terminal organ responds to its normal stimulus. Thus the retina, though capable of stimulation by pressure or electricity, is specially fitted by its histological structure for the reception of those minute vibrations of the ether which constitute light. But while the terminal organ is capable of receiving a most delicate action of the normal stimulus, the nerve in connection with it is not so affected. For example, although the retina is affected by light, the optic nerve is not so, as may be proved by Marriotte's well-known experiment, by which it may be demonstrated that when the image of an external object falls on the entrance of the optic nerve, there is no corresponding sensation. The nerve is thus insensible to the normal stimulus of the sense organ, the retina.

2018 ◽  
Vol 28 (4) ◽  
pp. 186-194
Author(s):  
Maria Ioanna Stefanou

In the first half of the 3rd-century BC in Alexandria, the Greek physicians Herophilus of Chalcedon (ca. 330 to ca. 260 BC) and Erasistratus of Chios (ca. 315 to ca. 240 BC) became the first scientists in antiquity to comprehensively study the anatomical underpinnings and the physiological properties of mind processes. Their scientific theories were based on experimental evidence arising from anatomical human dissection studies. Among their neuroscientific achievements were the discovery of the cranial nerves, the meninges, the dural sinuses and the ventricles; the delineation of the motor and sensory nerves; the appraisal of the brain as the seat of consciousness and human intellect; and the attribution of neurological disease to dysfunction of the nervous system. This paper will discuss the short-lived historical circumstances that enabled the ground-breaking progress in the domain of brain sciences during the Hellenistic period. In addition, this paper will examine the intriguing social, political and cultural interplays that determined the resonance of Herophilus and Erasistratus’s work and influenced the course of history of neuroscience.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


Viruses ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 1
Author(s):  
Andréia Veras Gonçalves ◽  
Demócrito de B. Miranda-Filho ◽  
Líbia Cristina Rocha Vilela ◽  
Regina Coeli Ferreira Ramos ◽  
Thalia V. B. de Araújo ◽  
...  

Congenital viral infections and the occurrence of septo-optic dysplasia, which is a combination of optic nerve hypoplasia, abnormal formation of structures along the midline of the brain, and pituitary hypofunction, support the biological plausibility of endocrine dysfunction in Zika-related microcephaly. In this case series we ascertained the presence and describe endocrine dysfunction in 30 children with severe Zika-related microcephaly from the MERG Pediatric Cohort, referred for endocrinological evaluation between February and August 2019. Of the 30 children, 97% had severe microcephaly. The average age at the endocrinological consultation was 41 months and 53% were female. The most frequently observed endocrine dysfunctions comprised short stature, hypothyroidism, obesity and variants early puberty. These dysfunctions occurred alone 57% or in combination 43%. We found optic nerve hypoplasia (6/21) and corpus callosum hypoplasia (20/21). Seizure crises were reported in 86% of the children. The most common—and clinically important—endocrine dysfunctions were pubertal dysfunctions, thyroid disease, growth impairment, and obesity. These dysfunctions require careful monitoring and signal the need for endocrinological evaluation in children with Zika-related microcephaly, in order to make early diagnoses and implement appropriate treatment when necessary.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 717
Author(s):  
Ilenia Savinetti ◽  
Angela Papagna ◽  
Maria Foti

Monocytes play a crucial role in immunity and tissue homeostasis. They constitute the first line of defense during the inflammatory process, playing a role in the pathogenesis and progression of diseases, making them an attractive therapeutic target. They are heterogeneous in morphology and surface marker expression, which suggest different molecular and physiological properties. Recent evidences have demonstrated their ability to enter the brain, and, as a consequence, their hypothetical role in different neurodegenerative diseases. In this review, we will discuss the current knowledge about the correlation between monocyte dysregulation in the brain and/or in the periphery and neurological diseases in humans. Here we will focus on the most common neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and multiple sclerosis.


2018 ◽  
Vol 115 (50) ◽  
pp. E11817-E11826 ◽  
Author(s):  
Nina Milosavljevic ◽  
Riccardo Storchi ◽  
Cyril G. Eleftheriou ◽  
Andrea Colins ◽  
Rasmus S. Petersen ◽  
...  

Information transfer in the brain relies upon energetically expensive spiking activity of neurons. Rates of information flow should therefore be carefully optimized, but mechanisms to control this parameter are poorly understood. We address this deficit in the visual system, where ambient light (irradiance) is predictive of the amount of information reaching the eye and ask whether a neural measure of irradiance can therefore be used to proactively control information flow along the optic nerve. We first show that firing rates for the retina’s output neurons [retinal ganglion cells (RGCs)] scale with irradiance and are positively correlated with rates of information and the gain of visual responses. Irradiance modulates firing in the absence of any other visual signal confirming that this is a genuine response to changing ambient light. Irradiance-driven changes in firing are observed across the population of RGCs (including in both ON and OFF units) but are disrupted in mice lacking melanopsin [the photopigment of irradiance-coding intrinsically photosensitive RGCs (ipRGCs)] and can be induced under steady light exposure by chemogenetic activation of ipRGCs. Artificially elevating firing by chemogenetic excitation of ipRGCs is sufficient to increase information flow by increasing the gain of visual responses, indicating that enhanced firing is a cause of increased information transfer at higher irradiance. Our results establish a retinal circuitry driving changes in RGC firing as an active response to alterations in ambient light to adjust the amount of visual information transmitted to the brain.


2016 ◽  
Vol 10 (1) ◽  
pp. 5-11 ◽  
Author(s):  
Eyyup Karahan ◽  
Ayse Tulin Berk

Aim: To describe the associated ocular, neurologic, and systemic findings in a population of children with optic nerve hypoplasia (ONH) and to evaluate the relationship between ocular signs and neurologic findings. Method: A retrospective chart review of 53 patients with the diagnosis of ONH seen between December 1998 and September 2012 was performed. All neurodevelopmental anomalies, neuroradiologic findings, endocrinologic and systemic findings were recorded. Poor vision was defined as the visual acuity poorer than logMAR 1.0 or inadequate central steady maintained fixation. Results: Thirty (56.6%) of the 53 children with ONH were boys. Mean age at presentation was 56.2±46.8 months (range; 3 months to 18 years). Poor vision defined for the purpose of this study was found in 47.2% of 53 patients. Thirty-three (62.3%) children had nystagmus. Thirty-four (64.2%) children had strabismus. Thirteen (38.2%) of those with strabismus had esotropia, 20 (58.8%) had exotropia. The total number of the children with neurodevelopmental deficit was 22 (41.5%) in our study. Conclusion: The vision of young children with ONH should be monitored at least annually, and any refractive errors should be treated. Neuroimaging of the brain and endocrinologic evaluation is necessary in all cases with ONH.


Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 537-553
Author(s):  
M.A. Wilson ◽  
J.S. Taylor ◽  
R.M. Gaze

The structure of the optic chiasma in Xenopus tadpoles has been investigated by light and electron microscopy. Where the optic nerve approaches the chiasma, a tongue of cells protrudes from the periventricular cell mass into the dorsal part of the nerve. Glial processes from this tongue of cells ensheath fascicles of optic axons as they enter the brain. Coincident with this partitioning, the annular arrangement of axons in the optic nerve changes to the laminar organization of the optic tract. Beyond the site of this rearrangement, all newly growing axons accumulate in the ventral-most part of the nerve and pass into the region between the periventricular cells and pia which we have called the ‘bridge’. This region is characterized by a loose meshwork of glial cell processes, intercellular spaces and the presence of both optic and nonoptic axons. In the bridge, putative growth cones of retinal ganglion cell axons are found in the intercellular spaces in contact with both the glia and with other axons. The newly growing axons from each eye cross in the bridge at the midline and pass into the superficial layers of the contralateral optic tracts. As the system continues to grow, previous generations of axon, which initially crossed in the existing bridge, are displaced dorsally and caudally, forming the deeper layers of the chiasma. At their point of crossing in the deeper layers, these fascicles of axons from each eye interweave in an intimate fashion. There is no glial segregation of the older axons as they interweave within the chiasma.


2020 ◽  
Vol 38 (5) ◽  
pp. 355-368
Author(s):  
Yimeng Lina Du ◽  
Elena G. Sergeeva ◽  
Donald G. Stein

Background: There is growing evidence that the TIR-domain-containing adapter-inducing interferon-β (TRIF) pathway is implicated in the modulation of neuroinflammation following injuries to the brain and retina. After exposure to injury or to excitotoxic pathogens, toll-like receptors (TLR) activate the innate immune system signaling cascade and stimulate the release of inflammatory cytokines. Inhibition of the TLR4 receptor has been shown to enhance retinal ganglion cell (RGC) survival in optic nerve crush (ONC) and in ischemic injury to other parts of the brain. Objective: Based on this evidence, we tested the hypothesis that mice with the TRIF gene knocked out (TKO) will demonstrate decreased inflammatory responses and greater functional recovery after ONC. Methods: Four experimental groups –TKO ONC (12 males and 8 females), WT ONC (10 males and 8 females), TKO sham (9 males and 5 females), and WT sham (7 males and 5 females) –were used as subjects. Visual evoked potentials (VEP) were recorded in the left and right primary visual cortices and optomotor response were assessed in all mice at 14, 30, and 80 days after ONC. GFAP and Iba-1 were used as markers for astrocytes and microglial cells respectively at 7 days after ONC, along with NF-kB to measure inflammatory effects downstream of TRIF activation; RMPBS marker was used to visualize RGC survival and GAP-43 was used as a marker of regenerating optic nerve axons at 30 days after ONC. Results: We found reduced inflammatory response in the retina at 7 days post-ONC, less RGC loss and greater axonal regeneration 30 days post-ONC, and better recovery of visual function 80 days post-ONC in TKO mice compared to WT mice. Conclusions: Our study showed that the TRIF pathway is involved in post-ONC inflammatory response and gliosis and that deletion of TRIF induces better RGC survival and regeneration and better functional recovery in mice. Our results suggest the TRIF pathway as a potential therapeutic target for reducing the inflammatory damage caused by nervous system injury.


Sign in / Sign up

Export Citation Format

Share Document