Changes in the excitability of hindlimb motoneurons during muscular atonia induced by stimulating the pedunculopontine tegmental nucleus in cats

http://dx.doi.org/10.1016/j.neuroscience.2003.12.016We have previously reported that electrical stimulation delivered to the ventral part of the pedunculopontine tegmental nucleus (PPN) produced postural atonia in acutely decerebrated cats [Neuroscience 119 (2003) 293]. The present study was designed to elucidate synaptic mechanisms acting on motoneurons during postural atonia induced by PPN stimulation. Intracellular recording was performed from 72 hindlimb motoneurons innervating extensor and flexor muscles, and the changes in excitability of the motoneurons following the PPN stimulation were examined. Repetitive electrical stimulation (20–50 μA, 50 Hz, 5–10 s) of the PPN hyperpolarized the membrane potentials of both the extensor and flexor motoneurons by 2.0–12 mV (6.0±2.3 mV, n=72). The membrane hyperpolarization persisted for 10–20 s even after termination of the stimulation. During the PPN stimulation, the membrane hyperpolarization was associated with decreases in the firing capability (n=28) and input resistance (28.5±6.7%, n=14) of the motoneurons. Moreover the amplitude of Ia excitatory postsynaptic potentials was also reduced (44.1±13.4%, n=14). After the PPN stimulation, these parameters immediately returned despite that the membrane hyperpolarization persisted. Iontophoretic injections of chloride ions into the motoneurons reversed the polarity of the membrane hyperpolarization during the PPN stimulation. The polarity of the outlasting hyperpolarization however was not reversed. These findings suggest that a postsynaptic inhibitory mechanism, which was mediated by chloride ions, was acting on hindlimb motoneurons during PPN-induced postural atonia. However the outlasting motoneuron hyperpolarization was not due to the postsynaptic inhibition but it could be due to a decrease in the activity of descending excitatory systems. The functional role of the PPN in the regulation of postural muscle tone is discussed with respect to the control of behavioral states of animals

Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: A new concept for understanding motor disorders in basal ganglia dysfunction

http://dx.doi.org/10.1016/S0306-4522(03)00095-2The present study is designed to elucidate how basal ganglia afferents from the substantia nigra pars reticulata (SNr) to the mesopontine tegmental area of the brainstem contribute to gait control and muscle-tone regulation. We used unanesthetized and acutely decerebrated cats (n=27) in which the striatum, thalamus and cerebral cortex were removed but the SNr was preserved. Repetitive stimulation (50 Hz, 10–60 μA, for 5–20 s) applied to a mesencephalic locomotor region (MLR), which corresponded to the cuneiform nucleus, and adjacent areas, evoked locomotor movements. On the other hand, stimulation of a muscle-tone inhibitory region in the pedunculopontine tegmental nucleus (PPN) suppressed postural muscle tone. An injection of either glutamatergic agonists (N-methyl-Image -aspartic acid and kainic acid) or GABA antagonists (bicuculline and picrotoxin) into the MLR and PPN also induced locomotion and muscle-tone suppression, respectively. Repetitive electrical stimuli (50–100 Hz, 20–60 μA for 5–20 s) delivered to the SNr alone did not alter muscular activity. However stimulating the lateral part of the SNr attenuated and blocked PPN-induced muscle-tone suppression. Moreover, weaker stimulation of the medial part of the SNr reduced the number of step cycles and disturbed the rhythmic alternation of limb movements of MLR-induced locomotion. The onset of locomotion was delayed as the stimulus intensity was increased. At a higher strength SNr stimulation abolished the locomotion. An injection of bicuculline into either the PPN or the MLR diminished the SNr effects noted above. These results suggest that locomotion and postural muscle tone are subject to modulation by GABAergic nigrotegmental projections which have a partial functional topography: a lateral and medial SNr, for regulation of postural muscle tone and locomotion, respectively. We conclude that disorders of the basal ganglia may include dysfunction of the nigrotegmental (basal ganglia–brainstem) systems, which consequently leads to the production of abnormal muscle tone and gait disturbance

Effects of the melatonin and diazepam on eye movement and postural muscle tone in decerebrate cats.

The definitive version is available at www.blackwell-synergy.com authorThe effects of an intravenous application of melatonin upon eye movements and muscular tonus were examined in acute decerebrate cats in order to elucidate whether melatonin can be beneficial as a therapeutic agent for treating sleep disturbance. The results were compared to those produced by an intravenous application of diazepam, one of the benzodiazepines, and from a microinjection of carbachol, a cholinergic agent resistant to cholinesterase, into the pontine reticular formation. The application of melatonin produced neither changes in muscle tone nor in eye movements in cats in which the decerebration was made at the level of precollicular-postmammillary level (mesencephalic cats). However, it did produce rapid eye movements (REM) with muscular atonia in the cats in which the decerebration was performed at the level of precollicular-precollicular-preoptic chiasma level (hypothalamic cats). In the latter preparation, the suprachiasmatic nucleus (SCN) was preserved. Although an application of diazepam abolished muscle tone, it did not change eye movements in either mesencephalic or hypothalamic cats. An intrapontine carbachol injection resulted in muscular atonia associated with REM in the mesencephalic cats. These results suggest that the melatonin application activates SCN neurons, which, in turn, trigger REM sleep generating system in the brainstem. However, muscle tone suppression induced by the diazepam application may not be a result of the activation of the brainstem REM sleep generating system. We propose that melatonin would be a more useful and safe therapeutic agent for treating sleep disturbances than conventional drugs such as benzodiazepines