Anterior Eye Chamber Of Rats Research Articles

Retrograde transport of horseradish peroxidase in sensory and adrenergic neurons following injection into the anterior eye chamber

Horseradish peroxidase (HRP) was injected into the anterior eye chamber of rats and mice and frozen sections from both superior cervical and trigeminal ganglia were incubated to demonstrate neurons accumulating the tracer by retrograde axonal transport. Labelled cells were observed only in ganglia ipsilateral to the HRP injection. Within the trigeminal ganglion, peroxidase-containing neurons were restricted to the medial ophthalmic area, whereas labelled cells in the superior cervical ganglion were more widely distributed. With the use of a new and more sensitive technique for the demonstration of HRP in neurons, it was possible to show retrograde transport also of small amounts of peroxidase injected into the anterior eye chamber. In addition, this technique enabled identification of the central and peripheral processes of neurons in the trigeminal ganglion and the dendrites and axons of sympathetic ganglion cells. The rate of retrograde HRP transport in rats was calculated to approximately 4--5 mm/h for both sensory and adrenergic nerves, which is consistent with previous estimates for this protein. It differs from the transport rate reported for nerve growth factor (NGF) and macromolecular toxins in sensory and adrenergic nerves of the same species. These rates were, however, obtained with a different method and in a different population of sensory neurons and are, therefore, not directly comparable. After treatment with 6-hydroxydopamine the number of HRP-labelled cells in the superior cervical ganglion was significantly reduced compared to controls. Cell counts from trigeminal ganglia showed no significant difference between controls and treated animals.

Retrograde axonal transport of specific macromolecules as a tool for characterizing nerve terminal membranes.

The uptake of macromolecules by nerve terminals which is followed by retrograde axonal transport seems to occur by two different mechanisms, a specific and a nonspecific one. The nonspecific uptake depends on the presence of macromolecules (e.g., horseradish peroxidase) in the vicinity of the nerve terminals at very high concentrations and is enhanced by neuronal activity. In contrast, the specific uptake and subsequent retrograde axonal transport becomes apparent at much lower concentrations of the appropriate macromolecules, depends on the affinity of these ligands for specific binding sites on the surface of the neuronal membrane, and is independent of neuronal activity. The fact that lectins and some bacterial toxins bind to specific membrane glycoproteins or glycolipids allows conclusions to be drawn regarding qualitative and even quantitative aspects of the composition of the plasma membrane of the nerve terminals. 125I-labelled nerve growth factor (NGF), tetanus toxin, cholera toxin, wheat germ agglutinin (WGA), ricin II, phytohemagglutinin (PHA), and concanavalin A (ConA) were injected into the anterior eye chamber of rats where they were taken up by adrenergic nerve terminals and transported retrogradely to the superior cervical ganglion. The saturation of the uptake-transport found for NGF, WGA, choleragenoid and an atoxic binding-fragment of tetanus toxin indicates that limited numbers of binding sites, which showed also different affinities, are present for each ligand on the membrane of the nerve terminals. Competition experiments showed that the binding sites for the ligands investigated are largely independent. Two different classes of binding sites (high affinity--low capacity and intermediate affinity--intermediate capacity) seem to be involved in the saturable retrograde axonal transport of NGF. In contrast, WGA seems to have only a single class of binding-uptake sites with high capacity and relatively low affinity. Strong evidence for positive cooperativity was obtained for the uptake and subsequent transport of the tetanus toxin fragment.

Degeneration and regeneration of the adrenergic nerves in the rat iris induced by dihydroxytryptamines.

One single injection of 75 μg 5,6- or 5,7-dihydroxytryptamine into the anterior eye chamber of rats induces a loss of catecholamine fluorescence in adrenergic nerves by 6 hours. 2 1÷2 days after application of either drug sprouting of new terminals from non-degenerated preterminal axons located in the iris periphery is observed. This regrowth of adrenergic terminals results in a complete reconstitution of the adrenergic ground plexus in the iris during one month.

The Ultrastructure of Pancreatic Tissue from Duct-Ligated Rats Implanted into Anterior Chamber of Rat Eyes

AbstractPancreatic tissue from rats with ligated pancreatic ducts was implanted into the anterior chamber of the eyes of diabetic and non-diabetic rats, and the ultrastructure of the implants studied afterwards at inervals ranging from 15 min to 4 weeks. During the first, avascular, stage, lasting for 2 days at most, serious damage to a number of the islet cells was noted. During the next, revascularization stage, the ultrastructure, especially in the 2–4-week-old implants, pointed to recovery and/or regeneration of islet cells; on the whole, both the β and α cells in the implants from the non-diabetic hosts showed a normal ultrastructure at this time, whereas in the implants from the diabetic hosts the β cells showed signs of heightened activity. The cells in the excretory ducts showed largely the same changes with the passage of time as the islet cells, but to a less pronounced degree. The ultrastructure of the duct cells at the end of a few weeks exhibited greater signs of activity in the implants from...