The striatum is a site of integration of neural pathways involved in reinforcement learning. Traditionally, inputs from cerebral cortex are thought to be reinforced by dopaminergic afferents signaling the occurrence of biologically salient sensory events. Here, we detail an alternative route for short-latency sensory-evoked input to the striatum requiring neither dopamine nor the cortex. Using intracellular recording techniques, we measured subthreshold inputs to spiny projection neurons (SPNs) in urethane-anesthetized rats. Contralateral whole-field light flashes evoked weak membrane potential responses in approximately two-thirds of neurons. However, after local disinhibitory injections of the GABA A antagonist bicuculline into the deep layers of the superior colliculus (SC), but not the overlying visual cortex, strong, light-evoked, depolarizations to the up state emerged at short latency (115 Ϯ 14 ms) in all neurons tested. Dopamine depletion using ␣-methyl-para-tyrosine had no detectable effect on striatal visual responses during SC disinhibition. In contrast, local inhibitory injections of GABA agonists, muscimol and baclofen, into the parafascicular nucleus of the thalamus blocked the early, visual-evoked up-state transitions in SPNs. Comparable muscimol-induced inhibition of the visual cortex failed to suppress the visual responsiveness of SPNs induced by SC disinhibition. Together, these results suggest that short-latency, preattentive visual input can reach the striatum not only via the tecto-nigro-striatal route but also through tecto-thalamo-striatal projections. Thus, after the onset of a biologically significant visual event, closely timed short-latency thalamostriatal (glutamate) and nigrostriatal (dopamine) inputs are likely to converge on striatal SPNs, providing depolarizing and neuromodulator signals necessary for synaptic plasticity mechanisms.

The seawater tolerance of Atlantic salmon (Salmo salar) smolts reared under identical hatchery conditions was assessed in two Norwegian strains: AquaGen and Imsa. Plasma ion levels were disrupted in both strains following seawater exposure, but these disruptions were more profound in the AquaGen fish. To investigate the mechanisms underlying these differences, we measured gill Na+,K+-adenosine triphosphatase (ATPase) activity and mRNA levels of Na+,K+-ATPase α-subunit and two isoforms of the cystic fibrosis transmembrane conductance regulator (CFTR). Gill Na+,K+-ATPase activity rose significantly in both strains following seawater exposure. Both Na+,K+-ATPase α-subunit and CFTR I mRNA levels were significantly elevated for the entire 2-week period following seawater exposure, whereas CFTR II levels were transiently elevated during the first 24 h only. There were no differences in enzyme activity or gene expression between strains, with the exception of CFTR II, which was significantly lower in the Imsa strain 2 weeks following seawater exposure. This suggests that although changes in mRNA and protein expression for these genes are associated with seawater transfer, they are not the basis of observed physiological differences between strains.

No abstract

No abstract

These results suggest that the short-term memory impairment of ethanol-exposed rats 1) can be improved slightly by an increase in encoding time and 2) is related to a decrease in c-Fos expression in the hippocampus.

No abstract

Spontaneously hypertensive rats (SHR) were used as an animal model of attention deficit hyperactivity disorder (ADHD). This study investigated whether, in comparison with its progenitor strain, Wistar-Kyoto rats (WKY), SHR would show deficits in spatial short-term memory in the delayed-matching-to-place (DMP) version of the Morris water maze and be more distracted by exposure to a novel stimulus during recall trials. It also addressed whether dietary supplementation with long-chain polyunsaturated fatty acids (LCPUFA) during development would increase brain docosahexaenoic acid (DHA) and improve SHR behavioral performance. Beginning at weaning (21 days), male SHR and WKY were fed either a control or LCPUFA supplemented diet [0.5% arachidonic acid (AA) and 0.9% DHA], and behavioral testing began at 8 weeks. The first three tasks comprised a series of problems, each consisting of an initial search trial and subsequent recall trials. The intertrial interval (ITI) between the search and recall trial was either 60 s or 60 min. Surprisingly, in contrast to SHR, WKY did not appear to use a spatial short-term memory strategy to solve the problem. Notwithstanding, the performance of both strains was affected by the delay, such that they showed longer path lengths at the long compared with the short ITI. There was no effect of dietary supplementation on DMP performance. SHR fed the control diet were less responsive to a novel stimulus introduced on the first recall trial than WKY, and this tended to increase with supplementation. Analysis of brain fatty acid composition indicated that supplementation did increase DHA in the phosphatidylethanolamine fraction in WKY; however, in SHR, there was either no change (phosphatidylethanolamine) or paradoxical decreases (phosphatidylcholine and phosphatidyserine/phosphatidylinositol). Further research is needed to determine whether SHR are an appropriate model for studying a possible relationship between dietary LCPUFA and the behavioral symptoms of ADHD.

No abstract