Vibration decreases the responsiveness of Ia afferents and spinal motoneurons in humans

Vibration decreased the responsiveness of Ia afferents from the muscle exposed to vibration, and the duration of depressive effect was modulated by the duration and frequency of the vibration: a longer duration and a higher frequency of vibration led to a longer recovery time of the depression. In addition to this presynaptic effect, it also depressed the responsiveness of spinal motoneurons, indicating postsynaptic inhibition through specific circuits triggered by Ia impulses.

Three neurotransmitters regulate diverse inhibitory and excitatory Parvalbumin interneuron circuits in the dorsal horn

Parvalbumin-expressing interneurons (PVINs) in the spinal dorsal horn are found primarily in laminae II inner and III. Inhibitory PVINs (iPVINs) play an important in segregating innocuous tactile input from pain-processing circuits, achieved through presynaptic inhibition of myelinated low-threshold mechanoreceptors and postsynaptic inhibition of distinct spinal circuits. By comparison, relatively little is known of the role of excitatory PVINs (ePVINs) in sensory processing. Here we use neuroanatomical and optogenetic approaches to show that ePVINs comprise a larger proportion of the PVIN population than previously reported, and that both ePVIN and iPVIN populations form synaptic connections amongst (and between) themselves. We find that these cells contribute to neuronal networks that influence activity within several functionally distinct circuits, and that aberrant activity of ePVINs under pathological conditions contributes to the development of mechanical hypersensitivity.

0066 Glycinergic Postsynaptic Inhibition is Responsible for the Suppression of Hypoglossal Motoneuron Activity During Naturally-Occurring REM Sleep

Introduction The present study was undertaken to explore the role of glycinergic postsynaptic inhibition and monoaminergic disfacilitation (a withdrawal of excitatory noradrenergic and serotonergic inputs) in the control of hypoglossal motoneuron activity during REM sleep. Accordingly, glycinergic, noradrenergic and serotonergic antagonists were microinjected into the hypoglossal nucleus, and their effects on the hypoglossal nerve activity during REM sleep were examined in chronically-instrumented, unanesthetized cats. Methods Adults cats were prepared for monitoring behavioral states of sleep and wakefulness, and for extracellular recordings from hypoglossal nerve. Strychnine (a glycinergic antagonist) and a mixture of prazosin (a noradrenergic antagonist) and methysergide (a serotonergic antagonist) were microinjected, separately, into the hypoglossal nucleus during naturally-occurring states of sleep and wakefulness. Results During REM sleep, compared to non-REM sleep, the hypoglossal nerve activity decreased by 17.4±1.5% (n=17) in the control recordings (prior to the injection of strychnine). Following the microinjection of strychnine, there was only a mean decrease of 7.2±1.2% (n=12) in the nerve activity during REM sleep versus NREM sleep. The strychnine effect was statistically significant compared to control (p<0.001; unpaired t-test), which indicates that strychnine blocks REM sleep-related suppression of hypoglossal nerve activity. In contrast, the microinjection of prazosin and methysergide did not significantly reduce the hypoglossal nerve activity during REM sleep (control: 15.9±2.3, n=9 vs. prazosin+methysergide: 12.6±1.4%, n=10, p=0.229, unpaired t-test). Conclusion The present results demonstrate that the microapplication of strychnine, but not prazosin and methysergide, into the hypoglossal nucleus significantly reduces the suppression of the hypoglossal nerve activity during naturally-occurring REM sleep. We therefore suggest that glycinergic postsynaptic inhibition is primarily responsible for the suppression of hypoglossal motoneuron activity during REM sleep. Support 5R01NS094062

Genetic inactivation of mTORC1 or mTORC2 in neurons reveals distinct functions in glutamatergic synaptic transmission

Although mTOR signaling is known as a broad regulator of cell growth and proliferation, in neurons it regulates synaptic transmission, which is thought to be a major mechanism through which altered mTOR signaling leads to neurological disease. Although previous studies have delineated postsynaptic roles for mTOR, whether it regulates presynaptic function is largely unknown. Moreover, the mTOR kinase operates in two complexes, mTORC1 and mTORC2, suggesting that mTOR’s role in synaptic transmission may be complex-specific. To better understand their roles in synaptic transmission, we genetically inactivated mTORC1 or mTORC2 in cultured mouse glutamatergic hippocampal neurons. Inactivation of either complex reduced neuron growth and evoked EPSCs (eEPSCs), however, the effects of mTORC1 on eEPSCs were postsynaptic and the effects of mTORC2 were presynaptic. Despite postsynaptic inhibition of evoked release, mTORC1 inactivation enhanced spontaneous vesicle fusion and replenishment, suggesting that mTORC1 and mTORC2 differentially modulate postsynaptic responsiveness and presynaptic release to optimize glutamatergic synaptic transmission.

The Effects of Two Different Stretching Programs on Balance Control and Motor Neuron Excitability

We examined the effects of training (4d/wk for 6 wks) with static stretching (SS) or contract-relax proprioceptive neuromuscular facilitation (PNF) on static balance time and motor neuron excitability. Static balance time, Hmax/Mmax ratios and H-reflex recovery curves (HRRC) were measured in 28 healthy subjects (SS: n=10, PNF: n=9, control: n=9) before and after training. SS improved static balance time with a trend observed for PNF. Post training, during 150-200-250 msec interstimulus intervals, we observed a reduction in facilitation, but during 500-700-900 msec interstimulus interval; there was an increase in H2/H1 ratio in the PNF group only. Both stretching techniques improved static balance. The Ia afferent inhibitions during the acute exercises were not found after the SS and PNF training programmes. It was concluded that training with contract-relax proprioceptive neuromuscular facilitation may cause some augmentation in supraspinal and postsynaptic inhibition on the motoneuron pool.