Brain research
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Clinical evidence suggests that intrauterine growth restriction (IUGR) can cause persistent changes in the preference for palatable foods. In this study, we compared food preferences, the response to food rewards, and the role of the mesolimbic dopaminergic system in feeding behavior, between IUGR and control rats. Time-mated pregnant Sprague-Dawley rats were randomly allocated to a control group (standard chow ad libitum) or a 50% food restriction (FR) group, which received 50% of the control dams׳ habitual intake. ⋯ These data showed that IUGR rats exhibited a preference for palatable foods, potentially due to alterations in their mesolimbic reward pathway. Additionally, the changes observed in the mesolimbic dopaminergic system of IUGR rats proved to be sex-specific. This article is part of a Special Issue entitled 1618.
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This study examined whether there are neural markers of individual differences in working memory (WM) capacity and whether these differences are only manifest when performing a demanding WM task or at all levels of difficulty. Each subject's WM capacity was estimated using a modified digit span task prior to participation in an N-back task that varied difficulty from 1- to 4-back. While performing the N-back task, subjects wore scalp electrodes that allowed measurement of both event-related potentials (ERP) and event-related synchronization and desynchronization (ERS/ERD). ⋯ In addition, P300 amplitudes and alpha ERD responses were found to correlate with individual WM capacities independent of the task difficulty. These results suggest that there are qualitative neural differences among individuals with different WM capacities when approaching cognitive operations. Individuals with high WM capacities may make more efficient use of neural resources to keep their attention focused on the task-relevant information when performing cognitive tasks.
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The impact of hyperglycemia after traumatic brain injury (TBI), and even the administration of glucose-containing solutions to head injured patients, remains controversial. In the current study adult male Sprague-Dawley rats were tested on behavioral tasks and then underwent surgery to induce sham injury or unilateral controlled cortical impact (CCI) injury followed by injections (i.p.) with either a 50% glucose solution (Glc; 2g/kg) or an equivalent volume of either 0.9% or 8% saline (Sal) at 0, 1, 3 and 6h post-injury. The type of saline treatment did not significantly affect any outcome measures, so these data were combined. ⋯ At 15 days post-surgery the loss of cortical tissue volume (p < 0.001 versus sham) was significantly less in the CCI-Glc group (30.0%; p < 0.05) compared to the CCI-Sal group (35.7%). Counts of surviving hippocampal hilar neurons revealed a significant (~40%) loss ipsilateral to CCI (p < 0.001 versus sham), but neuronal loss in the hippocampus was not different in the CCI-Sal and CCI-Glc groups. Taken together, these results indicate that an early elevation of blood glucose may improve some neurological outcomes and, importantly, the induction of hyperglycemia after isolated TBI did not adversely affect any sensorimotor, cognitive or histological outcomes.
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Positive allosteric modulators (PAMs) for the α7 nicotinic receptor hold promise for the treatment of sensory inhibition deficits observed in schizophrenia patients. Studies of these compounds in the DBA/2 mouse, which models the schizophrenia-related deficit in sensory inhibition, have shown PAMs to be effective in improving the deficit. However, the first published clinical trial of a PAM for both sensory inhibition deficits and related cognitive difficulties failed, casting a shadow on this therapeutic approach. ⋯ However, combining the lowest doses of both PNU-120596 and choline chloride in this mouse model did improve sensory inhibition. We propose here that the difference in efficacy of PNU-120596 between the 2 mouse strains is driven by differences in hippocampal α7 nicotinic receptor numbers, such that C3H Chrna7 heterozygote mice require additional direct stimulation of the α7 receptors. These data may have implications for further clinical testing of putative α7 nicotinic receptor PAMs.
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Traumatic brain injury (TBI) is a major contributor to mortality and morbidity. The pathophysiology involves development of brain edema. Therapeutic options are limited as the mechanisms are not fully understood. ⋯ The total amount of AQP4 protein decreased (-20%). The disruption of the BBB lasted for 4 days while the impact on AQP4 levels disappeared between day 1 and 4. Our findings shows that blunt focal brain injury results in an early development of brain edema involving both cytotoxic and vasogenic components, a persistent BBB breakdown and a temporary decrease in AQP4, and indicates that both types of edemas and mechanisms should be targeted in TBI treatment.