Neuroscience
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In certain forms of nerve injury and inflammation, noradrenaline augments pain via actions on up-regulated α1-adrenoceptors (α1-ARs). The aim of this study was to use immunohistochemistry to examine α1-AR expression on peripheral neurons, cutaneous blood vessels and keratinocytes after distal tibia fracture and cast immobilization, a model of complex regional pain syndrome type 1. We hypothesized that there would be increased α1-AR expression on neurons and keratinocytes in the injured limb in comparison to the contralateral unaffected limb after distal tibia fracture, in association with inflammatory changes and pain. α1-AR expression was increased on plantar keratinocytes, dermal blood vessels and peripheral nerve fibers at 16weeks after injury both in the fractured and contralateral uninjured limb. ⋯ However, systemic injection of prazosin inhibited behavioral signs of pain, suggesting that fracture and/or casting triggered an up-regulation of α1-ARs in central nociceptive pathways that augmented pain. Together, these findings indicate that α1-AR expression increases in the hind limbs after distal tibia fracture and cast immobilization. However, these peripheral increases do not contribute directly to residual pain.
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Scheduled and restricted access to a palatable snack, i.e. chocolate, elicits a brief and strong anticipatory activation and entrains brain areas related with reward and motivation. This behavioral and neuronal activation persists for more than 7days when this protocol is interrupted, suggesting the participation of a time-keeping system. The process that initiates this anticipation may provide a further understanding of the time-keeping system underlying palatable food entrainment. ⋯ A significant anticipatory activation was observed in the prefrontal cortex on day 3 of entrainment and in the nucleus accumbens on day 5, while the arcuate nucleus and pyriform cortex reached significant activation on day 8. The gradual response observed with this protocol indicates that anticipation of a rewarding food requires repetitive and predictable experiences in order to acquire a temporal estimation. We also confirm that anticipation of palatable food involves diverse brain regions.
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We have studied the performance of a spatial reference memory task, the navigation strategy and the changes in the cytochrome c oxidase activity (COx) in different brain regions in exercised (forced exercise, 10 consecutive days, 15min/day) and non-exercised adult Wistar rats. The spatial learning task was carried out in the radial-arm water maze (RAWM) for four days with six daily trials, and on the fifth day, a probe session was run, in which we rotated the position of the distal cues 90° in a clockwise direction. During the four days of training, the exercised group showed shorter latency and distance traveled to find the platform, as well as fewer memory errors and reduced use of non-appropriate navigation strategies according to the protocol of the task (egocentric). ⋯ Finally, higher COx activity in the cingulate and the retrosplenial cortices, as well as in the dorsal CA1 and CA3 was found in the exercised group. All in all, it seems that the exercise favored the configuration of an efficient and accurate cognitive map of the environment, which was supported by our finding that the rotation of the cues, without altering their overall configuration, did not affect performance. The brain regions with higher COx activity in the exercised group seem to be involved in this function.
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P450 metabolic enzymes are expressed in the human and rodent brain. Recent data support their involvement in the pathophysiology of epilepsy. However, the determinants of metabolic enzyme expression in the epileptic brain are unclear. ⋯ Our data indicate that the effect of acute SE on brain CYP2E1 expression is localized and cell specific. Exposure to selected anti-epileptic drugs could play a role in determining CYP2E1 brain expression. Additional investigation is required to fully reproduce the culprits of P450 enzyme expression as observed in the human epileptic brain.
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Subacute systemic treatment with 3-nitropropionic acid (3-NP) causes specific lesions in the cortex and the striatum, and Huntington's disease behavioral phenotypes in rats. We investigated differentially expressed genes in the striatum, and examined status of a highly expressed huntingtin interacting protein, profilin 2 (Pfn2) in relation to 3-NP-induced striatal neurodegeneration, employing both in vivo animal model and in vitro primary striatal neuronal cultures. Golgi staining of 3-NP-treated rat brain revealed significantly altered dendritic spine morphology and decreased spine density in the cortex and the striatum, as compared to the control. ⋯ Immunoprecipitation assay showed decreased binding of Pfn2 with β-actin, the level of which remained unaffected in the striata and cortices of 3-NP-treated rats. Primary cultures of striatal glutamic acid decarboxylase-65/67 immunopositive GABAergic neurons revealed loss of co-existence of Pfn2 and β-actin in fluorescence imaging studies following 3-NP treatment for 24h. Since Pfn2 is known to regulate dendritic spine dynamics by interacting with β-actin, the reduction in its binding affinity to Pfn2 following 3-NP neurotoxic insult, and the accompanying aberrations of the dendritic spine structure and loss of spine density in striatal neurons suggest that Pfn2 may be involved in neurodegeneration in 3-NP-treated rat model of HD.