Effects of electrical stimulation of dorsal raphe nucleus on neuronal response properties of barrel cortex layer IV neurons following long-term sensory deprivation

Abstract: Objective To evaluate the effect of electrical stimulation of dorsal raphe nucleus (DRN) on response properties of layer IV barrel cortex neurons following long-term sensory deprivation. Methods: Male Wistar rats were divided into sensory-deprived (SD) and control (unplucked) groups. In SD group, all vibrissae except the D2 vibrissa were plucked on postnatal day one, and kept plucked for a period of 60 d. After that, whisker regrowth was allowed for 8-10 d. The D2 principal whisker (PW) and the D1 adjacent whisker (AW) were either deflected singly or both deflected in a serial order that the AW was deflected 20 ms before PW deflection for assessing lateral inhibition, and neuronal responses were recorded from layer IV of the D2 barrel cortex. DRN was electrically stimulated at inter-stimulus intervals (ISIs) ranging from 0 to 800 ms before whisker deflection. Results: PW-evoked responses increased in the SD group with DRN electrical stimulation at ISIs of 50 ms and 100 ms, whereas AW-evoked responses increased at ISI of 800 ms in both groups. Whisker plucking before DRN stimulation could enhance the responsiveness of barrel cortex neurons to PW deflection and decrease the responsiveness to AW deflection. DRN electrical stimulation significantly reduced this difference only in PW-evoked responses between groups. Besides, no DRN stimulation-related changes in response latency were observed following PW or AW deflection in either group. Moreover, condition test (CT) ratio increased in SD rats, while DRN stimulation did not affect the CT ratio in either group. There was no obvious change in 5-HT2A receptor protein density in barrel cortex between SD and control groups. Conclusion: These results suggest that DRN electrical stimulation can modulate information processing in the SD barrel cortex

Data for: Apelin-13 ameliorates cognitive impairments in 6-OHDA-inducedunilateral rat model of Parkinson's disease.

- Tracing images of rat movement within the Morris Water Maze (Q=qaderant). The animals in 6-OHDA-treated group often searched for the platform in an inappropriate way which was improved by apelin-13 treatment

Spinal protein kinase A and phosphorylated extracellular signal-regulated kinase signaling are involved in the antinociceptive effect of phytohormone abscisic acid in rats

Objective: The phytohormone abscisic acid (ABA) as a signaling molecule exists in various types of organisms from early multicellular to animal cells and tissues. It has been demonstrated that ABA has an antinociceptive effect in rodents. The present study was designed to assess the possible role of PKA and phosphorylated ERK (p-ERK) on the antinociceptive effects of intrathecal (i.t.) ABA in male Wistar rats. Methods: The animals were cannulated intrathecally and divided into different experimental groups (n=6�7): Control (no surgery), vehicle (received ABA vehicle), ABA-treated groups (received ABA in doses of 10 or 20 µg/rat), ABA plus H.89 (PKA inhibitor)-treated group which received the inhibitor 15 min prior to the ABA injection. Tail-flick and hot-plate tests were used as acute nociceptive stimulators to assess ABA analgesic effects. p-ERK was evaluated in the dorsal portion of the spinal cord using immunoblotting. Results: Data showed that a microinjection of ABA (10 and 20 µg/rat, i.t.) significantly increased the nociceptive threshold in tail flick and hot plate tests. The application of PKA inhibitor (H.89, 100 nM/rat) significantly inhibited ABA-induced analgesic effects. Expression of p-ERK was significantly decreased in ABA-injected animals, which were not observed in the ABA+H.89-treated group. Conclusions: Overall, i.t. administration of ABA (10 µg/ rat) induced analgesia and p-ERK down-expression likely by involving the PKA-dependent mechanism. © 2020 Associacao Arquivos de Neuro-Psiquiatria. All rights reserved

The effect of oral ascorbic acid pretreatment on feeding changes following injection in nucleus accumbens shell in adult male rats

Background: Ascorbic acid (AA) is not synthesized in the brain but it is actively transported through blood-brain barrier by SVCT2 cotransporter and it is stored in high concentrations with heterogeneous distribution in areas such as nucleus accumbens shell (AcbSh) in the mammalian brain. Previous studies have shown that Ascorbic acid injection into AcbSh decreases feeding therefore, in the present study we evaluated the effects of oral Ascorbic acid pretreatment on changes in feeding upon its injection in AcbSh in adult male rats. Methods: Sixty-three adult male rats (220-280 g) were divided into five treatment and five pretreatment groups. The treatment groups included the control (intact) group, sham-operated Ascorbic acid group that received normal saline as vehicle, and three other groups that received different doses of ascorbic acid (10, 50 and 250 µg/rat) by injection into AcbSh for four days. The pretreatment groups received Ascorbic acid (100 mg/kg) for 15 days via gastric gavage before receiving the aforementioned doses in treatment groups into intra nucleus AcbSh. Feeding measurement was repeated every 12 hours by automatic metabolic cage. Results: The results indicated that all injected doses of Ascorbic acid (10, 50 and 250 µg/rat) into nucleus accumbens shell decrease food intake (P<0.05) in rats and oral Ascorbic acid pretreatment had no effects in this regard. Conclusion: Our findings show that ascorbic acid is an effective factor in feeding regulation. Oral pretreatment seems to have no influence on the central effects of ascorbic acid in the nucleus accumbens shell