Topical Application Of Atropine Research Articles

What could this dark lesion on a woman’s eyelid be?

What could this dark lesion on a woman’s eyelid be?

Topical Tacrolimus Progylcosomes Nano-Vesicles As a Potential Therapy for Experimental Dry Eye Syndrome

The present work aimed to evaluate the efficacy of topical tacrolimus (0.01%) loaded propylene glycol (PG) modified nano-vesicles (Proglycosomes Nano-vesicles, PNVs) for the treatment of experimental dry eye syndrome (DES) in rabbits. DES was induced by topical application of atropine (1.0%) and benzalkonium chloride (0.1%) aqueous solution. PNVs treatment (PNV group) was compared with tacrolimus solution 0.01% (TAC group) and untreated group and healthy group were used as controls. PNV treated animals showed improved clinical performance with marked increase in tear production and tear break-up time (TBUT). Further, PNVs also subside ocular inflammation as evident from absence of matrix metalloprotenaise-9 and normal ocular surface temperature (32.3 ± 0.34 °C). Additionally, PNVs have positive effect on ocular and epithelial damage observed through low ocular surface staining score and improved globlet cell density. The PNV treatment was found to more effectively compared to TAC solution and most of the parameters were close to those of healthy animals. In conclusion, tacrolimus PNV formulation (0.01%) could be a potential therapy for treatment of dry eye syndrome.

Retrospective clinical analysis of 118 cases with malignant glaucoma

To study the clinical characteristics and pathogenesis of malignant glaucoma in a 5-year retrospective analysis in Zhongshan Ophthalmic Center (ZOC). Medical records of 5-year malignant glaucoma patients in Zhongshan Ophthalmic Center were reviewed retrospectively. Patients' age, gender, original disease, duration before attack, axial length and the change of depth of anterior chamber, intraocular pressure and visual acuity before and after therapy and at final follow-up were checked and analyzed. One hundred and eighteen cases of malignant glaucoma were hospitalized in ZOC from April 2005 to March 2010, accounts for 2.17% of PACG patients. Average age of malignant glaucoma patients was lower than that of PACG patients. The mean axial length of malignant glaucoma patients was shorter than that of Chinese population. Malignant glaucoma attacked between 1 day and 4.5 years after surgery. Ninety-three percent patients required medication and surgeries. Lens extraction and anterior vitrectomy were more effective than anterior chamber reforming combined with vitreous aspiration. The mean age of failed patient with vitreous cavity suction combined with anterior chamber angioplasty surgery was (43.7 ± 4.8) years, and was significantly younger than succeed patients, (53.7 ± 12.6) years (P < 0.05). Malignant glaucoma are iatrogenic and nine tenths secondary to surgeries of PACG patients. Topical application of atropine is the first choice of medication. Lens extraction combined with anterior vitrectomy has more privileges, however, is not commended especially for younger patients.

Cholinergic afferents to the locus coeruleus and noradrenergic afferents to the medial septum mediate LTP-reinforcement in the dentate gyrus by stimulation of the amygdala

Transient long-term potentiation (E-LTP) can be transformed into a long-lasting LTP (L-LTP) in the dentate gyrus (DG) by behavioral stimuli with high motivational content. Previous research from our group has identified several brain structures, such as the basolateral amygdala (BLA), the locus coeruleus (LC), the medial septum (MS) and transmitters as noradrenaline (NA) and acetylcholine (ACh) that are involved in these processes. Here we have investigated the functional interplay among brain structures and systems which result in the conversion of a E-LTP into a L-LTP (reinforcement) by stimulation of the BLA (BLA-R). We used topical application of specific drugs into DG, and other targets, while following the time course of LTP induced by stimulation of the perforant pathway (PP) to study their specific contribution to BLA-R. One injection cannula, a recording electrode in the DG and stimulating electrodes in the PP and the BLA were stereotactically implanted one week before electrophysiological experiments. Topical application of atropine or propranolol into the DG blocked BLA-R in both cases, but the effect of propranolol occurred earlier, suggesting a role of NA within the DG during an intermediate stage of LTP maintenance. The injection of lidocaine into the LC abolished BLA-R indicating that the LC is part of the functional neural reinforcing system. The effect on the LC is mediated by cholinergic afferents because application of atropine into the LC produced the same effect. Injection of lidocaine inactivating the MS also abolished BLA-R. This effect was mediated by noradrenergic afferents (probably from the LC) because the application of propranolol into the MS prevented BLA-R. These findings suggest a functional loop for BLA-R involving cholinergic afferents to the LC, a noradrenergic projection from the LC to the DG and the MS, and finally, the cholinergic projection from the MS to the DG.

Cholinergic Modulation of Synaptic Transmission and Postsynaptic Excitability in the Rat Gracilis Dorsal Column Nucleus

Somatosensory information, conveyed through the gracilis nucleus (GN), is regulated by descending corticofugal (CF) glutamatergic fibers. In addition, the GN receives cholinergic inputs with still unclear source and functional significance. Using both the in vitro slice and intracellular recording with sharp and patch electrodes and in vivo extracellular single-unit recordings, we analyzed the effects of activation of cholinergic receptors on synaptic, intrinsic, and functional properties of rat GN neurons. The cholinergic agonist carbamilcholine-chloride [carbachol (CCh); 1-10 microM] in vitro (1) induced presynaptic inhibition of EPSPs evoked by both dorsal column and CF stimulation, (2) increased postsynaptic excitability, and (3) amplified the spike output of GN neurons. The inhibition by atropine (1 microM) and pirenzepine (10 microM) of all presynaptic and postsynaptic effects of CCh suggests actions through muscarinic M1 receptors. The above effects were insensitive to nicotinic antagonists. We searched the anatomical origin of the cholinergic projection to the GN throughout the hindbrain and forebrain, and we found that the cholinergic fibers originated mainly in the pontine reticular nucleus (PRN). Electrical stimulation of the PRN amplified sensory responses in the GN in vivo, an effect prevented by topical application of atropine. Our results demonstrate for the first time that cholinergic agonists induce both presynaptic and postsynaptic effects on GN neurons and suggest an important regulatory action of inputs from cholinergic neuronal groups in the pontine reticular formation in the functional control of somatosensory information flow in the GN.

Pupillary constriction in response to light in rodents, which does not depend on central neural pathways

We show here that the widely held belief that reflex constriction of the mammalian pupil in response to light depends exclusively upon neural pathways between eye and brain is in need of revision. We investigated the response of the pupil to light in dark-adapted rodents (golden hamsters; hooded rats; albino rats) subjected to a variety of surgical and pharmacological interventions designed to destroy or block all of the neural pathways and structures through which the reflex could be mediated. The interventions included bilateral intraorbital optic nerve section, or unilateral intracranial optic nerve section with enucleation of the contralateral eye, combined in some cases with bilateral removal of the superior cervical ganglia and/or pinealectomy; topical application of atropine; intraocular injection of tetrodotoxin (TTX). Golden hamsters and hooded rats, but not albino rats, retained an effective constriction of the pupil in response to light after all of these interventions, although the constriction was less and slower than in normal animals. These findings show that hamsters and hooded rats have both a neurally mediated fast light reflex that can be eliminated by severing connections between eye and brain, by blockade of cholinergic transmission to iris smooth muscle, and by blockade of action potentials by TTX; and a local, slower constriction in response to light, which remains after all these procedures. We have also confirmed previous observations of Bito and Turansky (1975) that pupillary constriction in response to light occurs in isolated in vitro anterior chamber preparations of hamster and hooded rat eyes. However, we were not able to demonstrate constriction in identical preparations of albino rat eyes. The data suggest on the basis of both in vivo and in vitro studies, that the hamster and hooded rat, but not the albino rat, possess an autonomous local mechanism for controlling pupillary diameter that is completely independent of the retina or the brain.

Effects of ultraviolet radiation and visible light on hamster pupil

Light does not cause a miotic response in mammals after a topical application of atropine. However, such common sense is based on the pupillary response to visible light. We found ultraviolet (UV) caused slight but evident miosis, even when the patient did not perceive visible light. In order to understand this mechanism further, we conducted in vitro experiments using hamsters. The in vitro hamster iris contracted even when the retina was withdrawn in an incubation solution. The contraction of the hamster pupil caused by visible light was inhibited by procaine, quinacrine, and by the withdrawal of divalent cations, but not by indomethacin, AA861, FPL55712 or autonomic blocking agents. UV-induced miosis was very delayed, continuing after cessation of UV stimuli. Nordihydroguaiaretic acid did not inhibit the miosis induced by UV and/or visible light. The UV-induced miosis was not significantly affected by allopurinol or verapamil, suggesting mechanisms other than neuronal mediation and oxidative stress. This study shows that the isolated hamster iris can react to UV and visible rays. UV-induced miosis is different from the miosis caused by light reflex. To our knowledge, UV-induced miosis has not yet been reported.

On the mechanism of central hypotensive action of clonidine.

The hypotensive effect of clonidine in anaesthetised (pentobarbitone) cat has been analysed with the help of pharmacological tools. Application of clonidine (0.1%) to the exposed ventral surface of medulla oblongata produced hypotension (28.6%) and bradycardia (18%). Similar application of glycine (5%) and GABA (10%) also lowered the blood pressure of cat by 20.3% and 29.3%, respectively. The hypotension as well as the bradycardia owing to clonidine were significantly (p less than 0.01) blocked by similar prior application of atropine methylnitrate (1%) and hemicholinium-3 (HC3, 1%), whereas HC3 pretreatment only insignificantly blocked the hypotension produced by glycine (p greater than 0.80) and GABA (p less than 0.70). Topical application of atropine (1%) also blocked (p less than 0.05) the hypotensive effect of clonidine. Intravenous administration of clonidine (50 microgram/kg) produced hypotension (34.6%) after an initial hypertensive response and bradycardia (38.8%). The hypotension was significantly (p less than 0.01) blocked by pretreatment of the cat with intracerebroventricular atropine (4 mg) or HC3 (0.5 mg). Topical application of atropine (1%) to the ventral surface of medulla also significantly (p less than 0.05) reduced the hypotension and bradycardia resulting from intravenous administration of clonidine. It is concluded that an intact cholinergic link in the brainstem is essential for the hypotensive effect of clonidine.