A Golgi study of third-layer pyramidal neurons from the corticofrontal cortex of tryptophan-restricted rats was carried out. At 40 days of age, dendritic arborization from treated rats was less profuse than that seen in control rats, and enlargement of dendritic processes, as well as an increase of the number of dendritic spines, were observed in 60-day-old rats. These plastic responses could be mediated either by a decrease in serotonin, which acts on the serotoninergic receptors of pyramidal neurons, or through an indirect mechanism mediated by cortical interneurons, or by serotoninergic modulation of the activity of other cortical neurotransmitters such as acetylcholine. Also, it could represent compensatory mechanisms underlying behavioral performance in some paradigms related to several cognitive processes.
Acute pharmacological studies have shown that the relationship between serotonin and place learning is very unclear and when serotoninergic neurotransmission is manipulated, little or no effect on place learning has been observed. Since tryptophan is the precursor of the serotonin synthesis, female rats were chronically given a tryptophan-restricted diet from the time they were weaned until they were 60 days old and their place learning ability was assessed in the Morris' water maze, during the dark phase and under red lighting. Animals should have solved two 5 attempt blocks separated by a change in diametral position of the goal, at 21, 40 and 60 days of age. Experimental animals took longer distances than control animals, mainly in the second attempt block both at 40 and 60 days of age. Also, a remarkable irregularity on place learning curves of experimental animals was seen, possibly due to an apparent loss of maze solving strategy. These animals were also incapable of efficiently adjusting their external signals-related cognitive map when the goal was moved to a different position and, on the other hand, two different patterns were seen in maze solving at 60 days of age in these same animals. These findings strongly suggest that indirect lowering of brain serotonin levels through chronic restriction of dietary tryptophan may be responsible for the spatial learning deficits observed.
The CA1 hippocampal region is involved in organizing several neuropsychological processes. Pyramidal cell dendritic spines in the CA1 field of rats subjected to chronic tryptophan diet restriction were quantified at 21, 40, and 60 days of age. At 40 days of age, the number of spines in the distal third of the apical dendrite was smaller in experimental animais. The same was true for the medial third of the apical dendrite and the basal dendrite at 60 days of age. The results could be interpreted as a trans-synaptic plastic response due to understimulation of serotoninergic receptors located in the hippocampal Ammon's horn and, particularly, on the CA1 pyramidal neurons as well as on aferences to the hippocampus. Since the present is a model of generalized tryptophan restriction, neurochemical studies are needed to dilucidate this hypothesis.
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