Involvement of nigrotecto-reticulospinal pathways in the iminodipropionitrile (IDPN) model of spasmodic dyskinesias: a 2-deoxy-D-[1-14C]glucose study in the rat.

Chronic administration of iminodipropionitrile (IDPN) to rats causes a persistent behavioral syndrome characterized by lateral and vertical head twitches, random circling, and increased tactile and acoustic startle responses. In order to identify brain areas which are affected in rats manifesting this syndrome, we used the autoradiographic 2-deoxy-D-[1-14C]glucose ([14C]DG) method to map cerebral glucose utilization in IDPN-treated rats. One day after the development of the dyskinetic syndrome, there were significant decreases in local glucose utilization in the substantia nigra pars reticulata (SNr) and compacta (SNc), the dorsal raphe, the superficial and deep layers of the superior colliculus, the inferior colliculi, the interpeduncular nucleus, the medial and dorsolateral geniculate nuclei, and the superior and lateral vestibular nuclei. There were also significant decreases in layer 2 of the cingulate cortex and in the temporal and occipital cortices. In contrast, there were no changes in the motor cortex, the caudate-putamen, the nucleus accumbens, or the median raphe. These findings suggest that deleterious effects of IDPN on the nigrotectal pathways which affect head and neck movements and circling behaviors via the brainstem reticulospinal tracts may play an important role in the IDPN-induced persistent spasmodic dyskinetic syndrome in rats.