Neuroreport
-
The acoustic startle response is an important mammalian model for studying the cellular mechanisms of emotions and learning. Lesions in the superior olivary complex have been shown to attenuate the amplitude of the acoustic startle response, thus a substantial contribution of these neurons to the startle response was proposed. ⋯ Glutamate uncaging in the olivary complex excited a subpopulation of olivary neurons but never PnC giant neurons, as shown by patch-clamp recordings. This clearly contradicts an excitatory connection from olivary neurons to PnC giant neurons and thus an involvement of the superior olivary complex in eliciting a startle response.
-
Blinks are known to change the kinematic properties of fast eye movements, probably by changes in the brain stem circuits. To determine whether slow disconjugate (slow vergence) eye movements are affected by blinks under natural viewing conditions, we elicited airpuff-evoked trigeminal blinks randomly during ongoing steady slow vergence eye movements. ⋯ Slow vergence eye movements showed a peak of vergence velocity during the final part of the blink, which depends on the stimulus direction. We propose that the direction-specific blink effect on slow vergence may be caused by changes in brain stem premotor circuits.
-
We have examined the potential role of spinal glial cells in the induction of C fiber-evoked long-term potentiation (LTP) in the spinal cord. Tetanic stimulation of the sciatic nerve induced longterm potentiation of C-fiber-evoked field potentials in the spinal dorsal horn in all rats. ⋯ The effects of fluorocitrate were abolished by kynurenic acid or 2-amino-5-phosphonovaleric acid (AP-5), but not by 6,7-dinitroquinoxaline-2,3-dione (DNQX), picrotoxin or strychnine. These data suggest that spinal glial cells may modulate the central sensitization of nociceptive neurons via NMDA receptors.
-
The present study examined the sleep-wake cycle effects of microinjections of yohimbine, an adrenergic antagonist, and atropine, a cholinergic antagonist, into the cerebral ventricle of clomipramine-induced depressed rats. Yohimbine microinjection caused a significant reduction in the total duration and the number of REM sleep episodes compared to control saline injections. Atropine microinjection caused a significant reduction in the total duration and the number of REM sleep episodes without changing the REM sleep latency compared to control saline microinjection. These results show for the first time that the REM sleep disturbances observed in clomipramine-treatment induced depressed rats can be attenuated by increasing and decreasing the brain noradrenergic and cholinergic activities, respectively.