BrainWaves: The Neuroscience Graduate Program Newsletter

Emerging MiNDS

BrainWaves
27.03.15 03:06 PM Comment(s)

Two-point orientation discrimination versus the traditional two-point test for tactile spatial acuity assessment

SUMMARY: Jonathan Tong 

For decades, neurologists have used two-point discrimination (2PD) as a tool for diagnosing neurological dysfunction. 2PD involves stimulating a patient with the tips of a caliper and asking: "were you touched with two points or one?" As the separation between tips decreases to zero, so too should the patient's probability of responding "two-points"; the reasoning for this is that two points  that fall between adjacent touch receptors should not be reliably distinguishable from a single point between these same receptors. Remarkably, many patients are able to reliably distinguish two points from one, even when the two points have zero separation (Johnson & Phillips, 1981). This "hyperacuity" might be explained by the fact that a single receptor neuron fires a greater number of impulses to a single indentation than to a double indentation of the same depth (Vega-Bermudez & Johnson, 1999), thus leading to a magnitude difference that the brain can use to discriminate two points at extremely small spacing. We have designed a new clinical screening test that avoids this "magnitude-cue" confound: by having patients identify the orientation of two-point stimuli (horizontal or vertical) in a two-point orientation discrimination (2POD) task, patients must rely on purely spatial information to discern orientation. As expected for a true measure of spatial acuity, 2POD performance approaches chance levels at zero separation, unlike the 2PD task. We recommend replacing the 2PD task with 2POD in clinical settings.



Effects of MK-801 treatment across several pre-clinical analyses including a novel assessment of brain metabolic function utilizing PET and CT fused imaging in live rats.

SUMMARY: Ritesh Daya 

Functional imaging studies in schizophrenic patients have demonstrated metabolic brain abnormalities during cognitive tasks. This study aimed to 1) introduce a novel analysis of brain metabolic function in live animals to characterize the hypo- and hyperfrontality phenomena observed in schizophrenia and following NMDA antagonist exposure, and 2) identify a robust and representative MK-801 treatment regimen that effectively models brain metabolic abnormalities as well as a range of established behavioural abnormalities representative of schizophrenia. Acute treatment at 0.5 mg/kg disrupted facets of memory measured through performance in the 8-arm radial maze task and generated abnormalities in sensorimotor gating, social interaction and locomotor activity. Furthermore, this treatment regimen induced hyperfrontality (increased brain metabolic function in the prefrontal area) observed via PET/CT fused imaging in the live rat. 
These findings provide insight on the effectiveness of the MK-801 pre-clinical model of schizophrenia and provide an optimal regimen to model schizophrenia. PET/CT fused imaging offers a highly translatable tool to assess hypo- and hyperfrontality in live animals.

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