GABA and glycine receptors in rat brain: autoradiographic localization.
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Animals↗
Biomedical subjects
M A Zarbin
Publications and source records attributed to M A Zarbin.
Glycine receptor: light microscopic autoradiographic localization with [3H]strychnine.
Glycine receptors have been localized by autoradiography in the rat central nervous system (CNS) using [3H]strychnine. The gross distribution of receptors is in excellent accord with the distribution determined by filtration binding assays. Specifically, the density of glycine receptors is greatest in the gray matter of the spinal cord and decreases progressively in regions more rostral in the neuraxis. Glycine receptors were found to be associated with both sensory and motor systems in the CNS. Moreover, there is a striking correlation between areas of high strychnine binding site density and areas in which glycine has been found to be electrophysiologically active. Finally, the anatomic localization of strychnine binding sites may help explain many of the signs and symptoms of strychnine ingestion. For example, individuals consuming subconvulsive doses of strychnine frequently experience altered cutaneous and auditory sensation. We have localized strychnine receptors in areas of the acoustic system known to influence discriminative aspects of audition and in areas of the spinal cord and trigeminal nuclei which modulate discriminative aspects of cutaneous sensation. The alteration of visceral functions (e.g., blood pressure and respiratory rate) associated with strychnine ingestion may be accounted for in a similar manner.
Afferent Pathways↗
Muscarinic cholinergic receptors: autoradiographic localization of high and low affinity agonist binding sites.
Previous studies have shown that muscarinic cholinergic agonists bind to 3 distinct receptor sites in brain, each being distinguished by their affinity for the agonists. Antagonists, on the other hand, bind to these sites with the same high affinity. The relative concentrations of the two high and the low affinity agonist sites are known to vary in different brain regions. The goal of this study was to localize separate populations of high and low affinity receptor sites in brain at the light microscopic level. All muscarinic receptors in slide-mounted intact tissue sections were labeled with [3H]N-methyl scopolamine ([3H]NMS), but in some experiments carbachol was added to selectively inhibit the binding of [3H]NMS to the high affinity sites. Autoradiograms of these tissue sections were generated by the apposition of emulsion-coated coverslips. Certain brain areas showed a relatively large displacement of [3H]NMS by carbachol indicating high concentrations of high affinity agonist binding sites. These areas included lamina IV of the cerebral cortex, nucleus tractus diagonalis, some thalamic nuclei, the zona incerta and the dorsal lateral geniculate body.
Animals↗
Opioid receptors undergo axonal flow.
Previous studies have indicated the presence of opiate receptors on axons of the rat vagus nerve and on other small diameter fibers. In examinations of the effect of ligation on the distribution of receptors in the vagus nerve by in vitro labeling light microscopic autoradiography, a large buildup of receptors was found proximal to the ligature. This result indicates an axonal flow of receptors.
Animals↗
Synaptosomal transport: a chloride dependence for choline, GABA, glycine and several other compounds.
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Animals↗
Pathophysiology and management of subretinal hemorrhage.
Subretinal hemorrhage can arise from the retinal and/or choroidal circulation. Significant subretinal hemorrhage occurs in several conditions, but most commonly is associated with age-related macular degeneration, presumed ocular histoplasmosis, high myopia, retinal arterial macroaneurysm, and trauma. Released toxins, outer retinal shear forces, and a diffusion barrier created by subretinal hemorrhage all contribute to photoreceptor damage and visual loss. The use of tissue plasminogen activator and improvements in surgical instrumentation have facilitated surgical drainage and have made it a useful option in the management of selected cases. Mechanisms of subretinal hemorrhage formation, underlying etiologies, diagnostic evaluation, and the histopathology of damage are summarized. Published surgical series are reviewed and surgical advances are summarized. The value of surgically removing subretinal hemorrhages to improve visual outcome remains unestablished, because definitive studies have not been performed. Guidelines for selecting candidates for surgical intervention are proposed.
Animals↗
Morphology of early choroidal neovascularization in age-related macular degeneration: correlation with activity.
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Bruch Membrane↗
Endophthalmitis.
Endophthalmitis is an inflammatory reaction of intraocular fluids or tissues. Infectious endophthalmitis is one of the most serious complications of ophthalmic surgery. Occasionally, infectious endophthalmitis is the presenting feature of an underlying systemic infection. Successful management of infectious endophthalmitis depends on timely diagnosis and institution of appropriate therapy. Recognition of the different clinical settings in which endophthalmitis occurs and awareness of the highly variable presentation it may have facilitate timely diagnosis. Biopsy of intraocular fluid/tissue is the only method that permits reliable diagnosis and treatment. The different presenting clinical settings, a rational approach to diagnosis (i.e., when, what, and how to biopsy), and the treatment of infectious endophthalmitis are reviewed.
Diagnostic Techniques, Ophthalmological↗
Drusen in age-related macular degeneration: pathogenesis, natural course, and laser photocoagulation-induced regression.
Drusen are subretinal pigment epithelial deposits that are characteristic of but not uniquely associated with age-related macular degeneration (AMD). Age-related macular degeneration is associated with two types of drusen that have different clinical appearances and different prognoses. Hard drusen appear as small, punctate, yellow nodules and can precede the development of atrophic AMD. Areolar atrophy of the retinal pigment epithelium (RPE), choriocapillaris, and outer retina develop as the drusen disappear, but drusen can regress without evidence of atrophy. Soft drusen appear as large (usually larger than 63 microm in diameter), pale yellow or grayish-white, dome-shaped elevations that can resemble localized serous RPE detachments. They tend to precede the development of clinically evident RPE detachments and choroidal neovascularization. Drusen characteristics correlated with progression to exudative maculopathy include drusen number (five or more), drusen size (larger than 63 microm in diameter), and confluence of drusen. Focal hyperpigmentation in the macula and systemic hypertension also are associated with an increased risk of developing choroidal new vessels (CNVs). Large drusen are usually a sign of diffuse thickening of Bruch's membrane with basal linear deposit, a vesicular material that probably arises from the RPE, constitutes a diffusion barrier to water-soluble constituents in the plasma, results in lipidization of Bruch's membrane, and creates a potential cleavage plane between the RPE basement membrane and the inner collagenous layer of Bruch's membrane through which CNVs can grow. Disappearance of drusen spontaneously and in areas adjacent to laser photocoagulation scars was first noted by Gass (Gass JD: Arch Ophthalmol 90:206-217, 1973; Trans Am Acad Ophthalmol Otolaryngol 75:580-608, 1971). Subsequent reports have confirmed these observations. Photocoagulation-induced drusen regression might prevent patients with drusen from developing exudative maculopathy. The mechanism for spontaneous drusen regression probably involves RPE atrophy. The mechanism for photocoagulation-induced drusen regression is unknown. If photocoagulation-induced drusen regression is anatomically similar to atrophy-associated drusen regression, then the former will be associated with dissolution of basal linear deposit and a residuum of basal laminar deposit. Sarks and coworkers (Sarks JP, Sarks SH, Killingsworth MC: Eye 11:515-522, 1997) proposed that this in turn will eliminate the potential cleavage plane between the RPE basement membrane and inner collagenous layer of Bruch's membrane through which CNVs grow, thus retarding the growth of CNVs.
Bruch Membrane↗
Age-related macular degeneration: review of pathogenesis.
Age-related macular degeneration is a condition (a) characterized by accumulation of membranous debris on both sides of the retinal pigment epithelium (RPE) basement membrane. Clinical manifestations of drusen, atrophy of the RPE/choriocapillaris, RPE detachment, and choroidal new vessel (CNV) formation occur after age 50 years. A hypothetical pathogenic sequence of events consistent with known data is: 1) RPE dysfunction (e.g., precipitated by an inherited susceptibility and/or environmental exposure); 2) accumulation of intracellular material in the RPE (e.g., accumulation of normal substrate material that is not enzymatically degraded properly vs. abnormal substrate material); 3) abnormal accumulation of extracellular material (basal laminar and basal linear deposit); 4) change in Bruch's membrane composition (e.g., increased lipid deposition and protein crosslinking); 5) change in Bruch's membrane parmeability to nutrients (e.g., impaired diffusion of water soluble plasma constituents across Bruch's membrane); and 6) response of the RPE to metabolic distress (i.e., atrophy vs. CNV growth). Histopathological and clinical studies indicate that areas of choroidal ischemia often are seen near CNVs in AMD patients. In response to decreased oxygen delivery/metabolic "distress", the RPE may elaborate substances leading to CNV growth. Perhaps RPE atrophy, followed by choriocapillaris and photoreceptor atrophy, is a response to decreased nutrients/increasing metabolic abnormalities in areas of excessive accumulation of extracellular debris. Unanswered questions regarding AMD include: 1) is AMD an ocular manifestation of a systemic disease or purely an ocular disease?; 2) what determines whether CNVs vs. atrophy of the RPE-choriocapillaris-photoreceptors develops?; and 3) what induces the maturation of CNVs into an inactive scar, and what limits the growth of most CNVs to the area centralis?
Basement Membrane↗
Central retinal vein occlusion: review of management.
Central retinal vein occlusion is usually a disease of the elderly and is often associated with systemic vascular disease, e.g., hypertension, diabetes mellitus, arteriosclerotic vascular disease. Younger patients, especially those less than 45 years of age, with retinal vein occlusion should be evaluated carefully for the possibility of an underlying thrombotic tendency. The authors describe the ocular manifestations, pathogenesis, associated conditions, patient evaluation, and treatment of patients with central retinal vein occlusion.
Age Factors↗
Central retinal vein occlusion: report of two familial cases.
The authors report a 46-year-old father and 17-year-old son who each presented with unilateral central retinal vein occlusion (CRVO) and bilateral abnormalities of retinal vascular perfusion. The son presented with a nonperfused CRVO in the left eye, developed traction-rhegmatogenous retinal detachment treated with vitreous surgery, and developed prolonged arteriovenous filling in the retina of the fellow eye. The father presented with progressive CRVO in the right eye, developed choroido-vitreal neovascularization following laser treatment to create a chorioretinal anastomosis, underwent vitrectomy for retinal detachment and vitreous hemorrhage in that eye, and developed prolonged arm-eye and retinal arteriovenous circulation times in the fellow eye. An extensive evaluation (including hematological studies and imaging of the major vessels of the neck) failed to reveal a predisposing cause in either patient although echocardiography disclosed a mitral valve thrombus in the father. After institution of coumadin therapy, the circulatory parameters in the fellow eye of each patient improved.
Adolescent↗
Anterior segment ischemia and retinal detachment after vertical rectus muscle surgery.
PURPOSE: The authors describe the clinical course of a woman who developed two complications following vertical strabismus repair: anterior segment ischemia (ASI) and retinal detachment. METHODS: A 62 year-old woman is described. She presented with new onset proptosis and left hypertropia with significant diplopia in all fields of gaze. This presentation, her 15 year history of thyroid disease, and preoperative computed tomography (CT) of the orbits were consistent with Graves' ophthalmopathy. Vertical strabismus repair was carried out by recessing the left superior rectus muscle and resecting the left inferior rectus muscle. RESULTS: The diplopia was eliminated. The patient developed significant postoperative ASI and iatrogenic rhegmatogenous retinal detachment in the left eye due to unsuspected globe perforation. She was treated with systemic corticosteroids and radial scleral buckling. CONCLUSIONS: Severe ASI following strabismus surgery is a well recognized complication, with age, thyroid ophthalmopathy, and manipulation of the vertical rectus muscles as risk factors. The retinal detachment soon after strabismus surgery was difficult to detect, possibly due to diminished visualization of the posterior segment as a result of ASI.
Anterior Eye Segment↗