The pedunculopontine nucleus: its role in the genesis of movement disorders

The pedunculopontine nucleus (PPN) is located in the dorso-lateral part of the ponto-mesencephalic tegmentum. The PPN is composed of two groups of neurons: one containing acetylcholine, and the other containing non-cholinergic neurotransmitters (GABA, glutamate). The PPN is connected reciprocally with the limbic system, the basal ganglia nuclei (globus pallidus, substantia nigra, subthalamic nucleus), and the brainstem reticular formation. The caudally directed corticolimbic-ventral striatal-ventral pallidal-PPN-pontomedullary reticular nuclei-spinal cord pathway seems to be involved in the initiation, acceleration, deceleration, and termination of locomotion. This pathway is under the control of the deep cerebellar and basal ganglia nuclei at the level of the PPN, particularly via potent inputs from the medial globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. The PPN sends profuse ascending cholinergic efferent fibers to almost all the thalamic nuclei, to mediate phasic events in rapid-eye-movement sleep. Experimental evidence suggests that the PPN, along with other brain stem nuclei, is also involved in anti-nociception and startle reactions. In idiopathic Parkinson's disease (IPD) and parkinson plus syndrome, overactive pallidal and nigral inhibitory inputs to the PPN may cause sequential occurrences of PPN hypofunction, decreased excitatory PPN input to the substantia nigra, and aggravation of striatal dopamine deficiency. In addition, neuronal loss in the PPN itself may cause dopamine-r esistant parkinsonian deficits, including gait disorders, postural instability and sleep disturbances. In patients with IPD, such deficits may improve after posteroventral pallidotomy, but not after thalamotomy. One of the possible explanations for such differences is that dopamine-resistant parkinsonian deficits are mediated to the PPN by the descending pallido-PPN inhibitory fibers, which leave the pallido-thalamic pathways before they reach the thalamic targets.

Alterations in the thalamic reticular nucleus of rats neonatally treated with thyroxine

En ratas Wistar normales y tratadas neonatalmente con tiroxina, se obtuvieron cortes seriados del tálamo, teñidos con el método de Golgi-Cox en las edades de 12,20 y 30 días. En la zona de núcleo reticular talámico (TRN), se contó el número de neuronas visibles, el área y la máxima extensión transversal del TRN en un total de 120 secciones. Los hallazgos indicaron que con relación al numero de neuronas en los animales tratados con T4, ocurrió un incremento signifiativo inicial de ellas a los 12 días de edad, seguido de un decremento igualmente significativo a los 20 y 30 días postnatales. Con respecto al área y a la máxima extensión transversal del TRN, sólo se observó una reducción progresiva que alcanzó sus valores más bajos a los 30 días de edad, sin ocurrir el incremento inicial que se ha descrito para el tejido neuronal. Los hallazgos sugieren que el tratamiento neonatal con T4, pudiera interferir con el desarrollo neuronal del TRN y, asimismo, a largo plazo, con las funciones modulatorias sensoriales del TRN