RNA content of normal and axotomized retinal ganglion cells of rat and goldfish.

The responses of rat and goldfish retinal ganglion cells to axotomy were examined by a quantitative cytochemical method for RNA and by morphometric measurement 1-60 (rat) and 3-90 (goldfish) days after interruption of one optic nerve or tract intracranially. Unoperated control animals were studied also. The RNA content of axotomized neurons of rat fell 7-60 days postoperatively. Additionally, atrophy of the axotomized somas occurred. Over time, neuronal atrophy approximately paralleled the loss of RNA, and mean cell area and RNA content were reduced by about 25% 60 days after axotomy. Incorporation of 3H-uridine by axotomized neurons declined also. Axotomized retinal ganglion cells of goldfish behaved differently from those of the rat and showed increases in RNA content, most conspicuously 14-60 days postoperatively. Enlargement of axotomized fish neurons occurred but was less proportionately than concomitant increases in RNA content. The nonaxotomized ganglion cells of goldfish displayed statistically significant increases in size and RNA content 14-49 days after unilateral optic nerve or tract lesions. In contrast, alterations in rat retinal ganglion cells contralateral to interruption of one optic nerve were of limited and questionable significance. The contrasting reactions to axotomy by the retinal ganglion cells of these two vertebrates, one of which regenerates optic axons and one of which does not, may support the proposition that the somal response to axon injury has an important bearing upon the success or failure of CNS regeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Viability of retinal ganglion cells after optic nerve crush in adult rats.

The response of retinal ganglion cells to optic nerve crush was examined in the hooded rat. Intracranial nerve crush produces a transient shrinkage of the retinal ganglion cells during the first several weeks postoperatively but partial recovery of cell size then appears to occur. This transient response is considered to be a direct response to axotomy. Retrograde transport of horseradish peroxidase (HRP) is clearly demonstrated at 2 weeks postoperatively. Transport of newly synthesized protein progressively decreases over the first 2 postoperative months. The ganglion cell therefore retains viability for at least the first few weeks after axotomy. Loss of 60% of the neurons in the ganglion cell layer occurs between 3 and 7 months postoperatively. This late occurring retrograde response is considered to result at least in part from loss of sustaining trophic influences rather than as a direct result of the lesion.

Development of angiotensin-induced drinking in the rat.

The suckling rat responds from birth to intraventricular angiotensin, and the drinking behavior elicited by the hormone achieves adult characteristics of reliability and sensitivity at 4--5 days of age. Additional testing of 5-day-old rats injected with a range of doses showed that the threshold dose lies between 0.1--1.0 ng, which is comparable to the adult sensitivity to intraventricular injections. The hormone also increases milk intake in neonates, but the animals choose water over milk as early as 17 days.

Visual discrimination impaired by cutting temporal lobe connections.

An attempt was made to transect the white matter that connects the anterior temporal lobe with dorsal and medial brain areas. Eight monkeys were trained preoperatively on a visual discrimination and tested postoperatively for retention and relearning of the task. They were also tested for Klüver-Bucy symptoms. The two animals that had complete lesions were unable to relearn the visual discrimination. It is suggested that human medial temporal lesions may produce their effects on learning and retention by damage to temporal white matter rather than by destruction of hippocampus.

Partial Klüver-Bucy syndrome produced by destroying temporal neocortex or amygdala.

The temporal neocortex was removed in 4 monkeys, and 5 received amygdala destruction. Four control animals received skin and muscle incisions. The monkeys were compared on a visual pattern discrimination task, a food-non-food discrimination, and a rating scale that measured agonistic and approach behavior. Only the cortical lesion disrupted retention of the visual pattern task and neither lesion disrupted performance of the food-non-food task. Both lesions produced oral behavior, increased reaction to stimuli and decreased emotionality. Thus, the major symptoms of the Klüver-Bucy syndrome are produced by destroying either the temporal neocortex or the amygdala.