Serotonin and protein kinase C-immunocytochemistry of the retina of the skate Raja erinacea.

Item

Title
Serotonin and protein kinase C-immunocytochemistry of the retina of the skate Raja erinacea.
Identifier
AAI9807997
identifier
9807997
Creator
Schuette, Etha R. I.
Contributor
Adviser: Richard L. Chappell
Date
1997
Language
English
Publisher
City University of New York.
Subject
Biology, Neuroscience | Health Sciences, Ophthalmology | Health Sciences, Pharmacology
Abstract
The skate retina contains at least two different classes of bipolar cell, one of which conforms to the rod bipolar cell known in mammalian retinas. A similar cell is also found in the teleost retina. All these cells are believed to belong to the retinal ON channel and there is no indication that the skate is an exception.;The second class of bipolar cell described in my study has biochemical (accumulation of serotonin) and morphological features (axonal ramifications in the outer strata of the IPL) suggesting that this cell belongs to the retinal OFF channel. Glutamate-receptor agonists, however, failed to induce decrease of serotonin-immunoreactivity in these cells, thus indicating important differences between these cells and their counterparts in other retinas.;The serotonin system of the skate retina can be subdivided into two distinct classes of cell with entirely different pharmacologic profiles. Amacrine cells can be depleted of serotonin by exposing the retina to glutamate receptor agonists and appear to be sensitive to the high affinity serotonin transporter blocker fluoxetine. Bipolar cells, in which serotonin release cannot be induced by receptor stimulation, are insensitive to fluoxetine, however their serotonin uptake can be completely blocked by the serotonin uptake inhibitor zimelidine.;The latter two points show that, within the CNS, at least two serotonin systems with markedly different pharmacologic properties may coexist. Blockage of the serotonin transporter in one part of the system may activate the other system and thus cause complex interactions between different populations of serotonergic/serotonin-accumulating cells. These interactions may exceed by far the simplified concept of increasing extracellular serotonin levels as proposed in antidepressant therapies.
Type
dissertation
Source
PQT Legacy CUNY.xlsx
degree
Ph.D.
Item sets
CUNY Legacy ETDs