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This Article Full Text Full Text (PDF) All Versions of this Article: 100/3/1343    most recent 01128.2007v2 01128.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ménard, A. Articles by Grillner, S. PubMed PubMed Citation Articles by Ménard, A. Articles by Grillner, S.

Diencephalic Locomotor Region in the Lamprey—Afferents and Efferent Control

Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden

Submitted 12 October 2007; accepted in final form 26 June 2008

In vertebrates, locomotion can be initiated by stimulation of the diencephalic locomotor region (DLR). Little is known of the different forebrain regions that provide input to the neurons in DLR. In the lamprey, it had been shown previously that DLR provides monosynaptic input to reticulospinal neurons, which in turn elicit rhythmic ventral root activity at the spinal level. To show that actual locomotor movements are produced from DLR, we use a semi-intact preparation in which the brain stem is exposed and the head fixed, while the body is left to generate actual swimming movements. DLR stimulation induced symmetric locomotor movements with an undulatory wave transmitted along the body. To explore if DLR is under tonic GABAergic input under resting conditions, as in mammals, GABAergic antagonists and agonists were locally administered into DLR. Injections of GABA agonists inhibited locomotion, whereas GABA antagonists facilitated the induction of locomotion. These findings suggest that GABAergic projections provide tonic inhibition that once turned off can release locomotion. Double-labeling experiments were carried out to identify GABAergic projections to the DLR. Populations of GABAergic projection neurons to DLR originated in the caudoventral portion of the medial pallium, the lateral and dorsal pallium, and the striatal area. These different GABAergic projection neurons, which also project to other brain stem motor centers, may represent the basal ganglia output to DLR. Moreover, electrical stimulation of striatum induced long-lasting plateau potentials in reticulospinal cells and associated locomotor episodes dependent on DLR being intact, suggesting that striatum may act via the basal ganglia output identified here.