Enhanced Excitability of the Neonatal Rat Hippocampus After Acute Exposure to Ethanol

© 2016, Springer Science+Business Media New York.Enhanced excitability manifested by seizures and epilepsy is one of the characteristic features of the fetal alcohol spectrum disorders (FASD). Here, we examined network excitability using a high-potassium model in the hippocampal slices prepared from the postnatal days of P7–9 rats treated with ethanol. Ethanol was administered at 6 g/kg intraperitoneally 12 h before the slice preparation. The extracellular field potential recordings from the hippocampal slices using multishank silicon probes placed along CA3-CA1 axis were performed in the interface chamber. We found that elevation of the extracellular potassium from 3.5 to 6 mM evoked seizure-like clonic or tonic-clonic discharges in 77 % of the slices from the ethanol-treated animals and only in 15 % of the slices from the control animals. Further elevation of the extracellular potassium to 8.5 mM evoked epileptiform activity in 92 and 69 % of the slices from the ethanol-treated and the control animals, respectively. The current source density profile and the multiple unit activity analysis pointed on the CA3 hippocampal region as a generator of the epileptiform activity. Thus, the hippocampal slices from the ethanol-treated neonatal rats display enhanced excitability and could serve as a FASD model to study the early epileptiform transformations following exposure to ethanol

Enhanced Excitability of the Neonatal Rat Hippocampus After Acute Exposure to Ethanol

© 2016, Springer Science+Business Media New York.Enhanced excitability manifested by seizures and epilepsy is one of the characteristic features of the fetal alcohol spectrum disorders (FASD). Here, we examined network excitability using a high-potassium model in the hippocampal slices prepared from the postnatal days of P7–9 rats treated with ethanol. Ethanol was administered at 6 g/kg intraperitoneally 12 h before the slice preparation. The extracellular field potential recordings from the hippocampal slices using multishank silicon probes placed along CA3-CA1 axis were performed in the interface chamber. We found that elevation of the extracellular potassium from 3.5 to 6 mM evoked seizure-like clonic or tonic-clonic discharges in 77 % of the slices from the ethanol-treated animals and only in 15 % of the slices from the control animals. Further elevation of the extracellular potassium to 8.5 mM evoked epileptiform activity in 92 and 69 % of the slices from the ethanol-treated and the control animals, respectively. The current source density profile and the multiple unit activity analysis pointed on the CA3 hippocampal region as a generator of the epileptiform activity. Thus, the hippocampal slices from the ethanol-treated neonatal rats display enhanced excitability and could serve as a FASD model to study the early epileptiform transformations following exposure to ethanol

Impairments to the Giant Depolarizing Potentials After the Third Trimester Equivalent Ethanol Exposure in the Neonatal Rat

© 2016, Springer Science+Business Media New York.Ethanol exerts multiple adverse effects in the developing hippocampus resulting in the life-long neurological and behavioral deficits. However, the early disturbances in the hippocampal network function after exposure to ethanol remain largely unknown. Here, we examined the properties of the neonatal CA3 hippocampal network-driven giant depolarizing potentials using extracellular recordings of the local field potential and multiple units from the hippocampal slices prepared from the 5–11-day-old rats treated by ethanol in vivo (6 g/kg, intraperitoneally), 12 h before the slice preparation. Activity in hippocampal slices from the ethanol-treated animals displayed several abnormalities including a threefold increase in overall neuronal firing and profound, by nearly sevenfold, reduction of synchronization of CA3 units in giant depolarizing potentials. Thus, alterations in the hippocampal network function emerge shortly after the ethanol exposure and manifest in the enhanced excitation and severe impairments to the giant depolarizing potentials

Enhanced Excitability of the Neonatal Rat Hippocampus After Acute Exposure to Ethanol

© 2016, Springer Science+Business Media New York.Enhanced excitability manifested by seizures and epilepsy is one of the characteristic features of the fetal alcohol spectrum disorders (FASD). Here, we examined network excitability using a high-potassium model in the hippocampal slices prepared from the postnatal days of P7–9 rats treated with ethanol. Ethanol was administered at 6 g/kg intraperitoneally 12 h before the slice preparation. The extracellular field potential recordings from the hippocampal slices using multishank silicon probes placed along CA3-CA1 axis were performed in the interface chamber. We found that elevation of the extracellular potassium from 3.5 to 6 mM evoked seizure-like clonic or tonic-clonic discharges in 77 % of the slices from the ethanol-treated animals and only in 15 % of the slices from the control animals. Further elevation of the extracellular potassium to 8.5 mM evoked epileptiform activity in 92 and 69 % of the slices from the ethanol-treated and the control animals, respectively. The current source density profile and the multiple unit activity analysis pointed on the CA3 hippocampal region as a generator of the epileptiform activity. Thus, the hippocampal slices from the ethanol-treated neonatal rats display enhanced excitability and could serve as a FASD model to study the early epileptiform transformations following exposure to ethanol

Semantico-phonological disorders in patients with Wernicke's aphasia

© Medwell Journals, 2015. The study presents the neurolinguistic analysis of semantic disorders caused by the specific perception of addressed speech by the patients with Wernicke's aphasia provoked by stroke. The sample of patients included 14 people (8 men and 6 women, aged 45-69) with dominant left hemisphere. All of them had lesions (caused by strokes) in Wernicke's area according to the data of MRI. The research was conducted during the acute period. The disorders were revealed by analyzing spontaneous dialogues with patients on matters of their everyday life and with the help of conversation analysis. The baseline neurocognitive tests (Mini-Mental State Examination, Montreal Cognitive Assessment) were used to exclude general cognitive impairment. The research was conducted at the Department of Neurology No. 1 in the Republic Clinical Hospital No. 2 (Kazan, Russia); this hospital is a clinical base of Kazan Federal University

Ethanol-Induced Apoptosis of Interneurons in the Neonatal GAD67-GFP Mouse Hippocampus

© 2016, Springer Science+Business Media New York.Ethanol induces massive neuroapoptosis in the developing brain. However, whether ethanol-induced neuroapoptosis also involves GABA interneurons remains unknown. Here, we addressed this question in the postnatal days (P) P3-P24 GAD67-GFP mouse hippocampus using cleaved caspase-3 staining, a sensitive measure of ethanol-induced apoptotic neurodegeneration combined with DAPI staining to monitor the apoptotic nuclear degradation. We observed that 8 h following ethanol treatment (6 g/kg, intraperiotoneally), significant proportion of GAD67-GFP expressing hippocampal interneurons was stained with cleaved caspase-3 antibodies and displayed chromatin condensation with a formation of the DAPI-stained apoptotic bodies. Maximal number of the cleaved caspase-3 stained interneurons (16.6 % of the total number of GFP expressing neurons and 21.6 % of the total number of caspase-3 stained cells) was observed in the hippocampal slices from P6-9 mice, and minimal damage to interneurons was observed in P3–4 and > P11 mice. While the apoptotic interneurons were found in all hippocampal regions and layers, their highest density was observed in the CA1 region and hilus. Thus, ethanol-induced neuroapoptosis involves hippocampal interneurons that may contribute to the life-long neurobehavioral deficits, increased excitability, and higher incidence of seizures characteristic of the fetal alcohol spectrum disorders

Pharmacodynamics of the Glutamate Receptor Antagonists in the Rat Barrel Cortex

Epipial application is one of the approaches for drug delivery into the cortex. However, passive diffusion of epipially applied drugs through the cortical depth may be slow, and different drug concentrations may be achieved at different rates across the cortical depth. Here, we explored the pharmacodynamics of the inhibitory effects of epipially applied ionotropic glutamate receptor antagonists CNQX and dAPV on sensory-evoked and spontaneous activity across layers of the cortical barrel column in urethane-anesthetized rats. The inhibitory effects of CNQX and dAPV were observed at concentrations that were an order higher than in slices in vitro, and they slowly developed from the cortical surface to depth after epipial application. The level of the inhibitory effects also followed the surface-to-depth gradient, with full inhibition of sensory evoked potentials (SEPs) in the supragranular layers and L4 and only partial inhibition in L5 and L6. During epipial CNQX and dAPV application, spontaneous activity and the late component of multiple unit activity (MUA) during sensory-evoked responses were suppressed faster than the short-latency MUA component. Despite complete suppression of SEPs in L4, sensory-evoked short-latency multiunit responses in L4 persisted, and they were suppressed by further addition of lidocaine suggesting that spikes in thalamocortical axons contribute ∼20% to early multiunit responses. Epipial CNQX and dAPV also completely suppressed sensory-evoked very fast (∼500 Hz) oscillations and spontaneous slow wave activity in L2/3 and L4. However, delta oscillations persisted in L5/6. Thus, CNQX and dAPV exert inhibitory actions on cortical activity during epipial application at much higher concentrations than in vitro, and the pharmacodynamics of their inhibitory effects is characterized by the surface-to-depth gradients in the rate of development and the level of inhibition of sensory-evoked and spontaneous cortical activity

Direct current coupled recordings of cortical spreading depression using silicone probes

© 2017 Nasretdinov, Lotfullina, Vinokurova, Lebedeva, Burkhanova Chernova, Zakharov and Khazipov. Electrophysiological assessment of infraslow ( < 0.1 Hz) brain activities such as cortical spreading depression (SD), which occurs in a number of pathologies including migraine, epilepsy, traumatic brain injury (TBI) and brain ischemia requires direct current (DC) coupled recordings of local field potentials (LFPs). Here, we describe how DC-coupled recordings can be performed using high-density iridium electrode arrays (silicone probes). We found that the DC voltage offset of the silicone probe is large and often exceeds the amplifier input range. Introduction of an offset compensation chain at the signal ground efficiently minimized the DC offsets. Silicone probe DC-coupled recordings across layers of the rat visual and barrel cortices revealed that epipial application of KCl, dura incision or pinprick TBI induced SD which preferentially propagated through the supragranular layers and further spread to the granular and infragranular layers attaining maximal amplitudes of ~−30 mV in the infragranular layers. SD at the superficial cortical layers was nearly two-fold longer than at the deep cortical layers. Continuous epipial KCl evoked multiple recurrent SDs which always started in the supragranular layers but often failed to propagat e through the deeper cortical layers. Intracortical KCl injection into the infragranular layers evoked SD which also started in the supragranular layers and spread to the granular and infragranular layers, further indicating that the supragranular layers are particularly prone to SD. Thus, DC-coupled recordings with silicone probes after offset compensation can be successfully used to explore the spatial—temporal dynamics of SD and other slow brain activities

Pharmacodynamics of the glutamate receptor antagonists in the rat barrel cortex

© 2018 Vinokurova, Zakharov, Lebedeva, Burkhanova, Chernova, Lotfullina, Khazipov and Valeeva. Epipial application is one of the approaches for drug delivery into the cortex. However, passive diffusion of epipially applied drugs through the cortical depth may be slow, and different drug concentrations may be achieved at different rates across the cortical depth. Here, we explored the pharmacodynamics of the inhibitory effects of epipially applied ionotropic glutamate receptor antagonists CNQX and dAPV on sensory-evoked and spontaneous activity across layers of the cortical barrel column in urethane-anesthetized rats. The inhibitory effects of CNQX and dAPV were observed at concentrations that were an order higher than in slices in vitro, and they slowly developed from the cortical surface to depth after epipial application. The level of the inhibitory effects also followed the surface-to-depth gradient, with full inhibition of sensory evoked potentials (SEPs) in the supragranular layers and L4 and only partial inhibition in L5 and L6. During epipial CNQX and dAPV application, spontaneous activity and the late component of multiple unit activity (MUA) during sensory-evoked responses were suppressed faster than the short-latency MUA component. Despite complete suppression of SEPs in L4, sensory-evoked short-latency multiunit responses in L4 persisted, and they were suppressed by further addition of lidocaine suggesting that spikes in thalamocortical axons contribute ~20% to early multiunit responses. Epipial CNQX and dAPV also completely suppressed sensory-evoked very fast (~500 Hz) oscillations and spontaneous slow wave activity in L2/3 and L4. However, delta oscillations persisted in L5/6. Thus, CNQX and dAPV exert inhibitory actions on cortical activity during epipial application at much higher concentrations than in vitro, and the pharmacodynamics of their inhibitory effects is characterized by the surface-to-depth gradients in the rate of development and the level of inhibition of sensory-evoked and spontaneous cortical activity

MERGERS AND ACQUISITIONS: DON'T LOSE THE LOTTERY

Companies use Mergers and acquisitions strategy as a way to diversify and grow their businesses. This complex business process involves combinations of one business with another to form one big business. The acquisition involves buying out another business or portion of it. When looking mergers and acquisitions we should be careful to avoid choosing a firm that might bring more challenges than benefits420-42