Motor IOR revealed for reaching.

Inhibition of return (IOR) is a spatial phenomenon that is thought to promote visual search functions by biasing attention and eye movements toward novel locations. Considerable research suggests distinct sensory and motor flavors of IOR, but it is not clear whether the motor type can affect responses other than eye movements. Most studies claiming to reveal motor IOR in the reaching control system have been confounded by their use of peripheral signals, which can invoke sensory rather than motor-based inhibitory effects. Other studies have used central signals to focus on motor, rather than sensory, effects in arm movements but have failed to observe IOR and have concluded that the motor form of IOR is restricted to the oculomotor system. Here, we show the first clear evidence that motor IOR can be observed for reaching movements when participants respond to consecutive central stimuli. This observation suggests that motor IOR serves a more general function than the facilitation of visual search, perhaps reducing the likelihood of engaging in repetitive behavior.

Motor inhibition of return can affect prepared reaching movements.

Inhibition of return (IOR) is a widely studied phenomenon that is thought to affect attention, eye movements, or reaching movements, in order to promote orienting responses toward novel stimuli. Previous research in our laboratory demonstrated that the motor form of saccadic IOR can arise from late-stage response execution processes. In the present study, we were interested in whether the same is true of reaching responses. If IOR can emerge from processes operating at or around the time of response execution, then IOR should be observed even when participants have fully prepared their responses in advance of the movement initiation signal. Similar to the saccadic system, our results reveal that IOR can be implemented as a late-stage execution bias in the reaching control system.

Saccadic inhibition of return can arise from late-stage execution processes.

Inhibition of return (IOR) is thought to improve the efficiency of visual search behaviour by biasing attention, eye movements, or both, toward novel stimuli. Previous research suggests that IOR might arise from early sensory, attentional or motor programming processes. In the present study, we were interested in determining if IOR could instead arise from processes operating at or during response execution, independent from effects on earlier processes. Participants made consecutive saccades (from a common starting location) to central arrowhead stimuli. We removed the possible contribution of early sensory/attentional and motor preparation effects in IOR by allowing participants to fully prepare their responses in advance of an execution signal. When responses were prepared in advance, we continued to observe IOR. Our data therefore provide clear evidence that saccadic IOR can result from an execution bias that might arise from inhibitory effects on motor output neurons, or alternatively from late attentional engagement processes.

Synchronous auditory nerve activity in the carboplatin-chinchilla model of auditory neuropathy.

Two hallmark features of auditory neuropathy (AN) are normal outer hair cell function in the presence of an absent/abnormal auditory brainstem response (ABR). Studies of human AN patients are unable to determine whether disruption of the ABR is the result of a reduction of neural input, a loss of auditory nerve fiber (ANF) synchrony, or both. Neurophysiological data from the carboplatin model of AN reveal intact neural synchrony in the auditory nerve and inferior colliculus, despite significant reductions in neural input. These data suggest that (1), intact neural synchrony is available to support an ABR following carboplatin treatment and, (2), impaired spike timing intrinsic to neurons is required for the disruption of the ABR observed in human AN.

Delayed administration of a potent cyclin dependent kinase and glycogen synthase kinase 3 beta inhibitor produces long-term neuroprotection in a hypoxia-ischemia model of brain injury.

We compared the neuroprotective efficacy of a potent and CNS-penetrant cyclin dependent kinase (CDK) and glycogen synthase kinase 3 beta (GSK3beta) inhibitor (Compound 1) in juvenile (postnatal day 21; P21) and adult C57Bl/6 mice (postnatal day 60; P60) using a model of hypoxic-ischemic brain injury (HI). Neuronal cell counts and density measures from brain sections stained with Cresyl Violet revealed that exposure of P21 mice to 60 min of HI resulted in extensive damage to the ipsilateral cornu ammonis 1 (CA1) region of the hippocampus (40% cell loss) and striatum (30% cell loss) 7 days later. Exposure of P60 mice to 40 min of HI produced a similar pattern of cell loss. Intraperitoneal administration of Compound 1 (3 mg/kg) 1, 5 and 9 h after 60 min of HI did not reduce brain injury in P21 mice relative to vehicle controls. By contrast, in P60 mice, this treatment significantly decreased cell loss in the ipsilateral hippocampus (10% cell loss) and striatum (15% loss) relative to vehicle controls. Terminal uridine deoxynucleotidyl transferase (TUNNEL) positive cell counts and infarct volume were also substantially reduced in P60 mice treated with Compound 1. A motor coordination test performed twice weekly until 5 weeks post-HI confirmed that Compound 1 produced long lasting functional recovery. Our results indicate that Compound 1 produced long lasting neuroprotective effects in adult but not juvenile mice suggesting that inhibition of the CDKs and GSK3beta plays a distinct neuroprotective role in the juvenile and adult brain.