High potassium-induced, calcium-dependent monoamine release from brain slices of the newborn rat

Anesthetics appear to produce neurodepression by altering synaptic transmission and/or intrinsic neuronal excitability. Propofol, a widely used anesthetic, has proposed effects on many targets, ranging from sodium channels to GABAA inhibition. We examined effects of propofol on the intrinsic excitability of hippocampal CA1 neurons (primarily interneurons) recorded from adult rat brain slices. Propofol strongly depressed action potential production induced by DC injection, synaptic stimulation, or high-potassium solutions. Propofol-induced depression of intrinsic excitability was completely reversed by bicuculline and picrotoxin but was strychnine-insensitive, implicating GABAA but not glycine receptors. Propofol strongly enhanced inhibitory postsynaptic currents (IPSCs) and induced a tonic GABAA-mediated current. We pharmacologically differentiated tonic and phasic (synaptic) GABAA-mediated inhibition using the GABAA receptor antagonist SR95531 (gabazine). Gabazine (20 μM) completely blocked both evoked and spontaneous IPSCs but failed to block the propofol-induced depression of intrinsic excitability, implicating tonic, but not phasic, GABAA inhibition. Glutamatergic synaptic responses were not altered by propofol (≤30 μM). Similar results were found in both interneurons and pyramidal cells and with the chemically unrelated anesthetic thiopental. These results suggest that suppression of CA1 neuron intrinsic excitability, by these anesthetics, is largely due to activation of tonic GABAA conductances; although other sites of action may play important roles in affecting synaptic transmission, which also can produce strong neurodepression. We propose that for some anesthetics, suppression of intrinsic excitability, mediated by tonic GABAA conductances, operates in conjunction with effects on synaptic transmission, mediated by other mechanisms, to depress hippocampal function during anesthesia.

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Somatostatin secretion from the rat neurohypophysis and stalk median eminence (SME) in vitro: Calcium-dependent release by high potassium and electrical stimulation

Metabolism ◽

10.1016/0026-0495(78)90052-5 ◽

1978 ◽

Vol 27 (9) ◽

pp. 1243-1245 ◽

Cited By ~ 10

Author(s):

Yogesh C. Patel ◽

H.H. Zingg ◽

J.J. Dreifuss

Keyword(s):

Electrical Stimulation ◽

Median Eminence ◽

High Potassium ◽

Calcium Dependent ◽

Somatostatin Secretion

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Acute hypoxia induces elevation of ornithine decarboxylase activity in neonatal rat brain slices

Reproduction Fertility and Development ◽

10.1071/rd9950385 ◽

1995 ◽

Vol 7 (3) ◽

pp. 385 ◽

Cited By ~ 2

Author(s):

LD Longo ◽

S Packianathan

Keyword(s):

Rat Brain ◽

Ornithine Decarboxylase ◽

Bovine Serum ◽

Brain Slice ◽

Brain Slices ◽

Neonatal Rat ◽

Newborn Rat ◽

Rat Brain Slice

Recent studies in vivo have demonstrated that ornithine decarboxylase (ODC) activity in the fetal rat brain is elevated 4-5-fold by acute maternal hypoxia. This hypoxic-associated increase is seen in the rat brain in both the newborn and the adult. Because of the intimate involvement of ODC in transcription and translation, as well as in growth and development, it is imperative that the manner in which hypoxia affects the regulation of this enzyme be better understood. In order to achieve this, a brain preparation in vitro was required to eliminate the confounding effects of the dam on the fetal and newborn brain ODC activity in vivo. Therefore, brain slices from 3-4-day-old (P-3) newborn rats were utilized to test the hypothesis that ODC activity increases in response to hypoxia in vitro. Cerebral slices from the P-3 rat pups were allowed to equilibrate and recover in artificial cerebrospinal fluid (ACSF) continuously bubbled with a mixture of 95% O2 and 5% CO2 for 1 h before beginning hypoxic exposures. Higher basal ODC activities were obtained by treating the slices with 0.03% fetal bovine serum (FBS) and 0.003% bovine serum albumin (BSA), rather than with ACSF alone. Hypoxia was induced in the slices by replacing the gas with 40%, 21%, 10%, or 5% O2, all with 5% CO2 and balance N2. With FBS and BSA treatment, ODC activity was maintained at about 0.15-0.11 nM CO2 mg-1 protein h-1 throughout the experiment, which was 2-3-fold higher than that without FBS and BSA. ODC activity increased significantly and peaked between 1 h and 2 h after initiation of hypoxia. For instance, with 21% O2, ODC activity increased approximately 1.5-fold at 1 h and approximately 2-fold at 2 h. These studies demonstrate that: (1) the hypoxic-induced increases observed in vivo in the fetal and newborn rat brain ODC activity can be approximated in a newborn rat brain slice preparation in vitro; (2) newborn rat brain slice preparations may provide an alternative to methods in vivo or cell culture methods for studying the regulation of acute hypoxic-induced enzymes; and (3) high, stable baseline ODC activities in brain slices suggest that the cells in the slice are capable of active metabolism if FBS and BSA are available to mimic conditions in vivo.

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Depolarization-induced release of [3H]histamine by high potassium concentrations, electrical stimulation and veratrine from rat brain slices after incubation with the radiolabelled amine

Neurochemistry International ◽

10.1016/0197-0186(83)90031-1 ◽

1983 ◽

Vol 5 (3) ◽

pp. 291-297 ◽

Cited By ~ 7

Author(s):

Arie H. Mulder ◽

Ronald G.M. van Amsterdam ◽

Myranda Wilbrink ◽

Anton N.M. Schoffelmeer

Keyword(s):

Electrical Stimulation ◽

Rat Brain ◽

Brain Slices ◽

High Potassium

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Spontaneous Neural Network Oscillations in Hippocampus, Cortex, and Locus Coeruleus of Newborn Rat and Piglet Brain Slices

Isolated Central Nervous System Circuits - Neuromethods ◽

10.1007/978-1-62703-020-5_11 ◽

2012 ◽

pp. 315-356 ◽

Cited By ~ 13

Author(s):

Chase Kantor ◽

Bogdan Panaitescu ◽

Junya Kuribayashi ◽

Araya Ruangkittisakul ◽

Igor Jovanovic ◽

...

Keyword(s):

Neural Network ◽

Locus Coeruleus ◽

Brain Slices ◽

Newborn Rat ◽

Network Oscillations

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Mechanistic Insight into the Attenuation of Initial Pilocarpine-Induced Seizures in Young Rats by a Non-Convulsive MSO Dose

10.20944/preprints202107.0706.v1 ◽

2021 ◽

Author(s):

Marek J. Pawlik ◽

Blanca I. Aldana ◽

Lautaro F. Belfiori-Carrasco ◽

Marta Obara-Michlewska ◽

Mariusz P. Popek ◽

...

Keyword(s):

Brain Slices ◽

Gas Chromatography Mass Spectrometry ◽

Methionine Sulfoximine ◽

Final Phase ◽

High Potassium ◽

Young Rats ◽

Mrna Content ◽

Pcr Techniques ◽

Insight Into

Pretreatment with non-convulsive dose of methionine sulfoximine (MSO) attenuated lithi-um-pilocarpine-induced (Li-Pilo) seizures in young rats [1]. We hypothesized that the effect of MSO results from a) glutamine synthetase block-mediated inhibition of conversion of Glu/Gln precursors to neurotransmitter Glu, and/or from b) altered synaptic Glu release. Pilo was admin-istered 60 min prior to sacrifice, MSO at 75 mg/kg, i.p., 2.5 h earlier. [1,2-13C]acetate and [U-13C]glucose were i.p.-injected either together with Pilo (onset) or 15 min before sacrifice (final phase). Their conversion to Glu and Gln in hippocampus and entorhinal cortex was followed us-ing [13C] gas chromatography-mass spectrometry. Release of in vitro loaded [3H]D-Asp from ex vi-vo brain slices was measured in continuously collected superfusates. Protein and mRNA expres-sion were measured by Western Blot and real-time PCR techniques, respectively. At no time point nor brain region did MSO modify incorporation of [13C] to Glu or Gln in Pilo-treated rats. MSO pretreatment decreased by ~37% high potassium-induced [3H]D-Asp release and reduced by ~50% the synaptic vesicular Glu transporter VGLUT1 protein, but not mRNA content in the hippo-campus. The results indicate that MSO at non-convulsive dose mitigates the initial Pilo-induced seizures by interfering with synaptic Glu-release but not with neurotransmitter Glu recycling.

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