The networks that control the initiation of locomotion are situated at a spinal level in vertebrates. Spinal cord injury leads to the irreversible loss of motor function and sensitivity below the site of injury in non-regenerating vertebrates, such as mammals, and an appropriate therapy does not exist so far. In contrast to mammals, lampreys can recover locomotion following a complete transection of the cord. Because of that, lampreys have been used as a model for studying axonal regeneration since the middle of the last century. Glutamate plays an important role in the processing and transmission of the sensory information in the spinal cord as well as in the spinal circuits underlying locomotion. Glutamate is also involved in some mechanisms during development and regeneration of the central nervous system, such as the regulation of the neurite outgrowth. Further, in the first hours following a spinal lesion, glutamate is implicated in the secondary damage which produces spread of the lesion and neuronal and glial cells death. The main objectives of this project are: (1) To characterize the glutamatergic neuronal populations in the spinal cord of the sea lamprey and compare its distribution with that of GABA and glycine, the main inhibitory neurotransmitters in the central nervous system. (2) To investigate the glutamate release and the subsequent response of astrocytes following SCI in lampreys. (3) To analyze the changes in the spinal glutamatergic system during spinal cord regeneration in lampreys.
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