Restoration of Motor Defects Caused by Loss of TDP-43 by Expression of the Voltage-Gated Calcium Channel, , in Central Neurons.

Defects in the RNA-binding protein, TDP-43, are known to cause a variety of neurodegenerative diseases, including amyotrophic lateral sclerosis and frontotemporal lobar dementia. A variety of experimental systems have shown that neurons are sensitive to TDP-43 expression levels, yet the specific functional defects resulting from TDP-43 dysregulation have not been well described. Using the TDP-43 ortholog TBPH, we previously showed that TBPH-null animals display locomotion defects as third instar larvae.

Saccade adaptation abnormalities implicate dysfunction of cerebellar-dependent learning mechanisms in Autism Spectrum Disorders (ASD).

The cerebellar vermis (lobules VI-VII) has been implicated in both postmortem and neuroimaging studies of autism spectrum disorders (ASD). This region maintains the consistent accuracy of saccadic eye movements and plays an especially important role in correcting systematic errors in saccade amplitudes such as those induced by adaptation paradigms. Saccade adaptation paradigms have not yet been used to study ASD.

Drosophila gustatory preference behaviors require the atypical soluble guanylyl cyclases.

The intracellular messenger cGMP has been suggested to play a role in taste signal transduction in both vertebrates and invertebrates. In the present study, we have examined the role of the Drosophila atypical soluble guanylyl cyclases (sGCs), Gyc-89Da and Gyc-89Db, in larval and adult gustatory preference behaviors. We showed that in larvae, sucrose attraction requires Gyc-89Db and caffeine avoidance requires Gyc-89Da.

Adaptive modification of saccade size produces correlated changes in the discharges of fastigial nucleus neurons.

Saccade accuracy is known to be maintained by adaptive mechanisms that progressively reduce any visual error that consistently exists when the saccade ends. We used an experimental paradigm known to induce adaptation of saccade size while monitoring the neural correlates of this adaptation. In rhesus monkeys where the medial and lateral recti of one eye were surgically weakened, patching the unoperated eye and forcing the monkey to use the weakened eye induced a gradual increase in saccade size in both eyes until the viewing, weak eye almost acquired the target in one step.

Role of the fastigial nucleus in controlling horizontal saccades during adaptation.

Saccade size was adapted in rhesus monkeys using surgical weakening of the muscles of one eye combined with monocular viewing. Neurons in the caudal fastigial nucleus were recorded during the adaptation. Neuronal discharges changed in a way that could be interpreted as causing the changes in saccade size given our current knowledge of the projections of these neurons to the saccadic burst generator in the brain stem.

Responses of primate caudal parabrachial nucleus and Kölliker-fuse nucleus neurons to whole body rotation.

The caudal aspect of the parabrachial (PBN) and Kölliker-Fuse (KF) nuclei receive vestibular nuclear and visceral afferent information and are connected reciprocally with the spinal cord, hypothalamus, amygdala, and limbic cortex. Hence, they may be important sites of vestibulo-visceral integration, particularly for the development of affective responses to gravitoinertial challenges. Extracellular recordings were made from caudal PBN cells in three alert, adult female Macaca nemestrina through an implanted chamber.

The brainstem burst generator for saccadic eye movements: a modern synthesis.

In the 16 years since we last summarized the behavior of the premotor elements that control saccades, research has revealed shortcomings in previous formulations of the control mechanisms of the brainstem saccadic burst generator. Specifically, complexities in the eye movement plant, a more detailed knowledge of the behaviors of certain bursting neurons, and previously undiscovered anatomical connections have broadened our knowledge but have generated new questions that require rethinking previous concepts. Perhaps the most crucial revelations/insights have come from studies that have implicated the superior colliculus and the midline cerebellum as crucial elements of the burst generator.