Parvalbumin-containing neurons mediate the feedforward inhibition of rat rubrospinal neurons

Abstract

The calcium-binding protein, parvalbumin and glutamic acid decarboxylase immunohistochemistry were used to locate candidate neurons mediating the inhibition of rat rubral neurons. A group of cells with small to medium-sized cell bodies that reacted positively to both were found in the red nucleus and its immediate vicinity. At the caudal nuclear level, these neurons gathered in the reticular formation, the pararubral area dorsolateral to the nucleus. As the nucleus expanded in size rostrally these neurons started to incorporate into the nucleus at about the anterior half of the middle nucleus and were all located within the rostral nucleus. Since these neurons were spatially segregated from the caudal nucleus we tested their connection by applying anterograde tracer to the pararubral area at the caudal red nuclear level. Labeled fibers with bouton-like swellings were found to enter the caudal nucleus and closely apposed rubrospinal neuronal cell bodies. These findings are consistent with our earlier observation that stimulating the pararubral area elicited a monosynaptic gamma-aminobutyric-acid(A) receptor-mediated inhibition on rubrospinal neurons in brainstem slices. In addition, the present study also shows that these inhibitory neurons remained unaltered in rats subjected to unilateral upper cervical rubrospinal tractotomy, suggesting that the reduction of pararubral stimulus-induced inhibition on rubrospinal neurons following spinal axonal injury resulted from causes other than the loss of these inhibitory neurons. In the rats, sensorimotor cortical fibers are known to reach the rostral red nucleus and the pararubral area but not the caudal nucleus. This prompted us to propose that neocortical inputs inhibit rubrospinal neurons through the activation of these PV-containing neurons. The proposed feedforward inhibitory circuit enables the cerebral cortex to disynaptically modulate the rubrospinal control over flexor motor execution.

Asynchronous Transmitter Release from Cholecystokinin-Containing Inhibitory Interneurons Is Widespread and Target-Cell Independent

“…The properties of PV-containing interneurons are particularly well suited to imposing temporal precision (Freund, 2003) and PV-containing or fast-spiking interneurons are the main mediators of feedforward inhibition in many brain areas (Liu et al, 2002; Mallet et al, 2005; Daw et al, 2007). Maintaining synchrony of release throughout trains of presynaptic activity is clearly vital for carrying out this function.…”

The efficacy of end‐to‐end and end‐to‐side nerve repair (neurorrhaphy) in the rat brachial plexus

“…It condensed into a gluey ball at the end of the micropipette immediately (Tseng et al. 1996; Liu et al. 2002) and applied into the C7–T1 DRGs of animals (Table 1) 7 days before they were sacrificed.…”

“…For application, the tracer, which was flaky when dry, was applied by touching it to the tip of micropipette moisturized with water vapor, for instance, over hot water, as it was highly hygroscopic. It condensed into a gluey ball at the end of the micropipette immediately (Tseng et al 1996;Liu et al 2002) and applied into the C7-T1 DRGs of animals (Table 1) 7 days before they were sacrificed.…”

The proximity of the lesion to cell bodies determines the free radical risk induced in rat rubrospinal neurons subjected to axonal injury

“…In an additional analysis aimed at demonstrating the variability of the nNOS expressed in the axotomized neurons over time, the ratio of the OD of each neuron to the mean of the contralateral control neurons of the same section was sorted into several categories from low to high and compared. To evaluate the effect of l-NAME treatment on brainstem-axotomized RS neurons, neurons with identifiable nuclei in the injured and the contralateral control RN in Cresyl violet-stained sections of the caudal RN were counted since this area contained exclusively RS neurons (Tseng et al 1995(Tseng et al , 1996aLiu et al 2002). In our hands, the identification of shrunk-axotomized RS neurons was straightforward because they were retrogradely labeled in all C2-and T10-axotomized animals studied while in brainstem-axotomized animals, glial markers were used to distinguish between neurons and glial cells (Liu et al 2003).…”

“…Data are means€SE. Note that the percentages of RS neurons surviving the axotomy are from a preceding study (Liu et al 2003); the data for survival ratio in the 4 days and 8 weeks columns are from animals 2 days and 10 weeks following lesion In this study we found that almost all RS neurons, 95% and 97% of those in the caudal RN (Liu et al 2002) respectively, increased their nNOS expression following C2 and brainstem axonal injury. The intensity of nNOS expression appeared to be axotomy distance-dependent, for in general L-RS neurons expressed higher levels of nNOS than C-RS neurons following C2 tractotomy, which might also reflect the fact that the C2 lesion removed longer segments of the axons of L-RS neurons than C-RS neurons (Tseng et al 1996a).…”