Notes on the Poetics of Serbo-Croatian Folk Lyric

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Intracellular free sodium and potassium, post-carbachol hyperpolarization, and extracellular potassium-undershoot in rat sympathetic neurones

Double-barrelled ion-sensitive microelectrodes were used to record the free intracellular Na+- and K+-concentrations ([Na+]i, [K+]i) and to determine their relation to changes in membrane potential and extracellular K+ ([K+]e) in rat sympathetic ganglia. The application of 50 μmol/l carbachol resulted in an elevation of [K+]e followed by a post-carbachol [K+]e-undershoot. The membrane depolarization of the sympathetic neurones was associated with an increase in [Na+]i and a decrease in [K+]i. A membrane hyperpolarization and a recovery of [K+]i and [Na+]i to their baseline levels were observed during the [K+]e-undershoot. The time course of the [K+]e-undershoot correlated exactly with the duration of the rise in [Na+]i and decrease of [K+]i. No K+-reuptake occurred in the presence of ouabain. These data confirm, by direct measurements of intracellular ion concentration changes, the contribution of the Na+, K+-pump to the post-carbachol membrane hyperpolarization and [K+]e-undershoot

Substances Acting on the Central Nervous System. IV. Derivatives of 2-Ethyl-2-phenylbutyramide

A number of N- and p-substituted 2-ethyl-2-phenylbutyramides have been synthesized for pharma cological evaluation as potential substances acting on t~e central nervous system (CNS)

Substances Acting on the Central Nervous System. IV. Derivatives of 2-Ethyl-2-phenylbutyramide

A number of N- and p-substituted 2-ethyl-2-phenylbutyramides have been synthesized for pharma cological evaluation as potential substances acting on t~e central nervous system (CNS)

Lactate-proton co-transport and its contribution to interstitial acidification during hypoxia in isolated rat spinal roots

Exposure of nervous tissue to hypoxia results in interstitial acidification. There is evidence for concomitant decrease in extracellular pH to the increase in tissue lactate. In the present study, we used double-barrelled pH-sensitive microelectrodes to investigate the link between lactate transport and acid-base homeostasis in isolated rat spinal roots. Addition of different organic anions to the bathing solution at constant bath pH caused transient alkaline shifts in extracellular pH; withdrawal of these compounds resulted in transient acid shifts in extracellular pH. With high anion concentrations (30 mM), the largest changes in extracellular pH were observed with propionate >l-lactate ≈ pyruvate >62; 2-hydroxy-2-methylpropionate. Changes in extracellular pH induced by 10 mMl- andd-lactate were of similar size. Lactate transport inhibitors α-cyano-4-hydroxycinnamic acid and 4,4′-dibenzamidostilbene-2,2′-disulphonic acid significantly reducedl-lactate-induced extracellular pH shifts without affecting propionate-induced changes in extracellular pH. Hypoxia produced an extracellular acidification that was strongly reduced in the presence of α-cyano-4-hydroxycinnamic acid and 4,4′-dibenzamidostilbene-2,2′-disulphonic acid. In contrast, amiloride and 4,4′-di-isothiocyanostilbene-2,2′-disulphonate were without effect on hypoxia-induced acid shifts. The results indicate the presence of a lactate-proton co-transporter in rat peripheral nerves. This transport system and not Na+/H+ or C1−/HCO−3 exchange seems to be the dominant mechanism responsible for interstitial acidification during nerve hypoxia

eIF2α Phosphorylation Bidirectionally Regulates the Switch from Short- to Long-Term Synaptic Plasticity and Memory

SummaryThe late phase of long-term potentiation (LTP) and memory (LTM) requires new gene expression, but the molecular mechanisms that underlie these processes are not fully understood. Phosphorylation of eIF2α inhibits general translation but selectively stimulates translation of ATF4, a repressor of CREB-mediated late-LTP (L-LTP) and LTM. We used a pharmacogenetic bidirectional approach to examine the role of eIF2α phosphorylation in synaptic plasticity and behavioral learning. We show that in eIF2α+/S51A mice, in which eIF2α phosphorylation is reduced, the threshold for eliciting L-LTP in hippocampal slices is lowered, and memory is enhanced. In contrast, only early-LTP is evoked by repeated tetanic stimulation and LTM is impaired, when eIF2α phosphorylation is increased by injecting into the hippocampus a small molecule, Sal003, which prevents the dephosphorylation of eIF2α. These findings highlight the importance of a single phosphorylation site in eIF2α as a key regulator of L-LTP and LTM formation

Differential actions of m and n cholinergic agonists on the brainstem activating system

The differential actions of i.v. arecoline and nicotine were determined on neocortical and limbic system EEG activation in acute rostral and caudal midbrain transected cats. All animals were prepared under diethyl ether anesthesia and after surgery, paralyzed with decamethonium and maintained on artificial respiration. The peripheral effects of these cholinergic agonists were reduced by methyl atropine (250 [mu]g/kg ) and/or trimethidinium (1 mg/kg) pretreatment.In the caudal midbrain transected preparation, nicotine (20-40 [mu]g/kg) induced marked EEG activation in both the neocortex and hippocampus. After bilateral lesions of the midbrain reticular formation in the same preparation, EEG activation was not observed with nicotine in doses up to 100 [mu]g/kg. The EEG effects of nicotine were blocked by atropine (1 mg/kg) and mecamylamine (1 mg/kg) but not trimethidinium (1 mg/kg). In the rostral midbrain transected preparation no EEG activation was noted with nicotine in doses up to 100 [mu]g/kg. Sporadic sharp waves appeared in the hippocampus with the larger doses indicating a convulsant site of action above the level of transection.Arecoline induced dissociation of the EEG in the hippocampus and neocortex in doses of 20-40 [mu]g/kg in the rostral midbrain transected cat. Marked hippocampal slow "arousal" waves with no desynchronization of the neocortical EEG were seen. These effects of arecoline were blocked by atropine. In the caudal midbrain preparation, even after bilateral lesions of the midbrain reticular formation which blocked nicotine activation, arecoline (20-40 [mu]g/kg) still induced hippocampal slow `arousal' waves without neocortical desynchronization. With doses of 100 [mu]g/kg of arecoline both neocortical and hippocampal EEG activation was noted.It is concluded that the site of nicotine on the rostral forebrain activating system is located primarily in the midbrain reticular formation, whereas arecoline acts on the midbrain reticular formation as well as above the level of the mesencephalon.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/33004/1/0000388.pd