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2 edition of Actions of ketamine and pentobarbital on excitatory amino-acid currents. found in the catalog.

Actions of ketamine and pentobarbital on excitatory amino-acid currents.

Zeke Zivojin Miljkovic

Actions of ketamine and pentobarbital on excitatory amino-acid currents.

by Zeke Zivojin Miljkovic

  • 242 Want to read
  • 7 Currently reading

Published .
Written in English


The Physical Object
Pagination88 leaves
Number of Pages88
ID Numbers
Open LibraryOL19539760M

This balance control is only possible due to the excitatory action of glutamate (GLUT) (another amino acid neurotransmitter). Both transmitters (GABA and GLUT) are able of producing changes in the. An excitatory amino acid receptor agonist, or glutamate receptor agonist, is a chemical substance which agonizes one or more of the glutamate receptors.. Examples include: AMPA; Glutamic acid; Ibotenic acid; Kainic acid; N-Methyl-D-aspartic acid; Quisqualic acid; See also. Excitatory amino acid receptor antagonist; Excitatory amino acid reuptake inhibitor.

Ketamine is a cyclohexanone derivative with analgesic and anesthetic properties. Although its mechanism of action is not well understood, ketamine appears exerts complex pharmacological actions including inhibition of biogenic amine uptake, binding to opioid receptors, and inhibition of N-methyl D-aspartate e of the involvement of spinal NMDA receptors in the process of central.   Ketamine has an inhibiting action on some cytochromes belonging to P complex, and this could partly explain the tachyphylaxis observed during the repeated use of the molecule S(+) isomer demethylation is superior to that of R(−) isomer, which explains a 22% higher clearance compared to R(−)ketamine

An excitatory amino acid receptor antagonist, or glutamate receptor antagonist, is a chemical substance which antagonizes one or more of the glutamate receptors.. Examples include: AP5; Barbiturates; Dextromethorphan; Dextrorphan; Dizocilpine; Ethanol; Ibogaine; Ifenprodil; Ketamine; Kynurenic acid; Memantine; Nitrous oxide.   Ketamine Treatment Effects on Synaptic Plasticity in Depression The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government.


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Actions of ketamine and pentobarbital on excitatory amino-acid currents by Zeke Zivojin Miljkovic Download PDF EPUB FB2

Loo P, Braunwalder A, Lehmann J, Williams M. Radioligand binding to central phencyclidine recognition sites is dependent on excitatory amino acid receptor agonists.

Eur J Pharmacol. Apr 29; (3)– MacDonald JF, Miljkovic Z, Pennefather P. Use-dependent block of excitatory amino acid currents in cultured neurons by by:   Anesthetic agents have different actions on the myocardium. Pentobarbital sodium is the most widely used anaesthetic with the cardiodepressive effect of reducing heart rate (HR), stroke index and cardiac index in male rats and mice.

1 This drug is used in doses from 30 mg/kg to mg/kg of body weight in many experiments. The depressive action of pentobarbital (P) has been shown to be Cited by: 9. ischemia and min of reperfusion in rats using pentobarbital, ketamine–pentobarbital or ketamine–xylazine anaesthesia.

A total of 30 rats were randomly divided into three groups. In group P, pentobarbital (60mg/kg, intraperitoneally [IP]) was used solely; in group K–P, ketamine and pentobarbital (50 and 30mg/kg, respect. MacDonald JF, Milkjovic Z, Pennefather P () Use-dependent blockade of excitatory amino acid currents by ketamine.

J Neurophysiol – Google Scholar Morris ME () General anesthetics and intracellular free calcium by: 3. Abstract. The excitatory amino acids, and in particular L-glutamic acid (L-GlU), have long been considered possible transmitters in the mammalian CNS (Nistri and Constanti, ; Puil, ; Fagg and Foster, ).However, only recently have advances in the availability of the appropriate pharmacological tools, such as specific antagonists, stimulated a renewed interest in identification of Author: J.

MacDonald, Z. Miljkovic, J. Schneiderman. Ketamine’s metabolism proceeds primarily via N-demethylation by CYP3A4 to produce norketamine, an active metabolite, with minor contributions by CYP2B6 [16,22] ().Hydroxylation of carbons of the cyclohexane ring on either ketamine or norketamine produces the hydroxynorketamine (HNK) series, some of which are active, such as dehydronorketamine (DHNK).

K etamine e More mechanisms of action than just NMD A blockade. amino acid currents in cultured neurons by ketamine. ketamine and pentobarbital on noradrenaline release from the medial pre. After the membrane currents elicited by a series of the test pulses were recorded, either of the ketamine isomers at a concentration of micro Meter was applied and the membrane currents were recorded after the inward current elicited by a test pulse to 0 mV reached a steady level (.

To know about Ketamine mechanism of action we need to know that Ketamine is a non-competitive antagonist to the phencyclidine site of N-methyl-d-aspartate (NMDA) receptor for glutamate, though Ketamine mechanism of action has effects that are mediated by interaction with many others receptors.

N-Methyl-D-Aspartate Receptor Antagonism: NMDA receptors are ligand-gated ion channels that are. Clinical studies have demonstrated that a single sub-anesthetic dose of the dissociative anesthetic ketamine induces rapid and sustained antidepressant actions.

Role of NMDAR inhibition in ketamine action. We compared the antidepressant-like effects of ketamine and the classical tricyclic antidepressant desipramine in the mouse forced-swim test (FST) at 1 hour (acute) and 24 hours (sustained) after administration (Fig.

1a).A 10mg/kg dose of ketamine resulted in acute and long-lasting dose-dependent antidepressant effects in the FST. It is unclear whether general anesthetics induce enhancement of neural inhibition and/or attenuation of neural studied the effects of pentobarbital (5 x mol/L), propofol (5 x mol/L), ketamine ( mol/L), halothane ( vol%), and isoflurane ( vol%) on both excitatory and inhibitory synaptic transmission in rat hippocampal slices.

The block by ketamine of excitatory amino acid currents is highly voltage dependent. Concentrations of ketamine that had little effect on outward current responses at depolarized potentials were quite effective at blocking inward current responses at hyperpolarized potentials.

As we observed for trichloroethanol, trifluoroethanol inhibited excitatory amino acid‐activated currents in a concentration‐dependent manner. Trifluoroethanol inhibited current activated by NMDA with an IC 50 value of 28± m m, and current activated by kainate with an IC 50 value of 35± m m (P.

Repeated corticosterone and single ketamine injections do not influence basic membrane properties and excitability of DRN projection neurons.

(a 1) Response of a representative putative serotonergic neuron to a depolarizing current pulse and (a 2) a single action potential of this cell at an extended timescale, with the “notch” on the descending phase marked with an asterisk. Sawada S, Yamamoto C. Blocking action of pentobarbital on receptors for excitatory amino acids in the guinea pig hippocampus.

Exp Brain Res. ; 59 (2)– Watkins JC, Krogsgaard-Larsen P, Honoré T. Structure-activity relationships in the development of excitatory amino acid receptor agonists and competitive antagonists.

When higher concentrations of ketamine were removed, the residual current increased before returning to the baseline, suggesting that ketamine possessed a low-affinity blocking action (Fig.

3A). This apparent block by ketamine at higher concentrations resembled the direct action of pentobarbital on GABA A receptors. Drugs that antagonize excitatory amino acid function are consistently neuroprotective in preclinical models of stroke, and many are now entering clinical trials.

Summary Antagonists of the N -methyl- d -aspartate (NMDA) receptor are furthest advanced in clinical development for stroke. The N-methyl-d-aspartate subtype of glutamate receptor (NMDAR) serves critical functions in physiological and pathological processes in the.

excitatory transmitter receptors, the acetylcholine receptor [29]. In common with other anaesthetic agents, ketamin e also enhance s and prolongs GABA A currents [9, 30]. The present study was undertaken to test the hypothesis that actions on amino acid receptors other than NMDA receptors, specifically glutamate non-NMDA and GABA A receptors.

ketamine (Ketamine, through antagonism of NMDA-excitatory receptors, prevents the action of excitatory glutamate; therefore, some neurons are inhibited and others are excited.

The primary site of CNS action of ketamine seems to be the thalamoneocortical projection system. A study conducted by Finch et al found that topical ketamine 10% did not result in any systemic absorption and appeared safe.

33 There are no published data on the safety of topical ketamine above 10%. There is only one documented case report of topical ketamine causing systemic effects; in this case the mother of an month-old patient.Surprisingly, the two anesthetics also differed regarding the effects of transmembrane voltage on anesthetic action.

Both Kv and Delta C currents were inhibited in a voltage-dependent fashion by halothane, whereas the reduction of current by ketamine was independent of membrane potential.