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PubMed2002

Transmission through the dorsal spinocerebellar and spinoreticular tracts: wakefulness versus thiopental anesthesia.

BACKGROUND: Most of what is known regarding the actions of injectable barbiturate anesthetics on the activity of lumbar sensory neurons arises from experiments performed in acute animal preparations that are exposed to invasive surgery and neural depression caused by coadministered inhalational anesthetics. Other parameters such as cortical synchronization and motor ouflow are typically not monitored, and, therefore, anesthetic actions on multiple cellular systems have not been quantitatively compared. METHODS: The activities of antidromically identified dorsal spinocerebellar and spinoreticular tract neurons, neck motoneurons, and cortical neurons were monitored extracellularly before, during, and following recovery from the anesthetic state induced by thiopental in intact, chronically instrumented animal preparations. RESULTS: Intravenous administration of 15 mg/kg, but not 5 mg/kg, of thiopental to awake cats induced general anesthesia that was characterized by 5-10 min of cortical synchronization, reflected as large-amplitude slow-wave events and neck muscle atonia. However, even though the animal behaviorally began to reemerge from the anesthetic state after this 5-10-min period, neck muscle (neck motoneuron) activity recovered more slowly and remained significantly suppressed for up to 23 min after thiopental administration. The spontaneous activity of both dorsal spinocerebellar and spinoreticular tract neurons was maximally suppressed 5 min after administration but remained significantly attenuated for up to 17 min after injection. Peripheral nerve and glutamate-evoked responses of dorsal spinocerebellar and spinoreticular tract neurons were particularly sensitive to thiopental administration and remained suppressed for up to 20 min after injection. CONCLUSIONS: These results demonstrate that thiopental administration is associated with a prolonged blockade of motoneuron output and sensory transmission through the dorsal spinocerebellar and spinoreticular tracts that exceeds the duration of general anesthesia. Further, the blockade of glutamate-evoked neuronal responses indicates that these effects are due, in part, to a local action of the drug in the spinal cord. The authors suggest that this combination of lumbar sensory and motoneuron inhibition underlies the prolonged impairment of reflex coordination observed when thiopental is used clinically.

Afferent Pathways↗

PubMed1988

Comparison of propofol and thiopental for the induction of anesthesia.

We compared the safety, efficacy, and side effects of induction of anesthesia with propofol (2.5 mg/kg), a new intravenous agent, and thiopental (4.0 mg/kg) in 62 patients in American Society of Anesthesiologists class I or II. There was no significant difference between induction times for the propofol (40.0 +/- 2.0 sec) and thiopental (44.0 +/- 4.0 sec) groups. Propofol administration produced a significant fall (P less than .05) in systolic blood pressure (SBP), from 134.1 +/- 2.6 mm Hg before injection to 128.3 +/- 2.4, 118.2 +/- 2.7, and 114.4 +/- 2.8 mm Hg one, two, and three minutes after injection, respectively. Diastolic blood pressure (DBP) fell significantly (P less than .05) during the three postinjection periods. Heart rate (HR) rose significantly (P less than .05), from 78.6 +/- 3.1 beats per minute before injection to 89.4 +/- 3.4 beats per minute one minute after injection. In patients given thiopental, SBP fell significantly (P less than .05), from 131.7 +/- 2.7 mm Hg before induction to 126.4 +/- 3.4 and 126.9 +/- 4.0 mm Hg two and three minutes after injection, respectively. The DBP did not change significantly in the thiopental group, but the HR rose significantly (P less than .05), from 73.3 +/- 2.8 beats per minute before injection to 83.9 +/- 3.0, 90.1 +/- 2.3, and 84.2 +/- 2.4 beats per minute one, two, and three minutes after injection, respectively. In 94% of patients given propofol, there were apneic periods of more than 60 seconds, compared to 50% in the thiopental group (P less than .05). There was a significant difference (P less than .05) between groups for the incidence of pain on injection; 31% of the patients receiving propofol had pain, compared to 3% of those receiving thiopental.

Adolescent↗

PubMed1995

Brain tumors do not affect thiopental dosing requirements.

We used the biphasic electroencephalographic (EEG) response to increasing concentrations of thiopental to measure regional brain responses to thiopental. Eight patients with cortical parietal brain tumors, 3.3 (SD 1.3) cm in diameter, and eight control patients with lung cancer and normal brain computed tomography scans received thiopental by infusion (50-75 mg/min) until burst suppression (50% isoelectric activity) on the EEG occurred. Infusion lasted 10.7 (SD 2.4) min, and the average dose of thiopental administered was 810 (SD 170) mg [11.2 (SD 1.9) mg/kg]. During infusion the EEG was continuously recorded from the F3, F4, P3, and P4 electrodes. On-line power spectral analysis was performed, and data were saved for later analysis. Four EEG parameters [log beta (15-30 Hz) power, percent beta power, spectral edge 95% and spectral edge 70%] were plotted against calculated brain concentration of thiopental [using an assumed plasma-effect site rate constant (ke0) of 0.58] for each individual. Three points were measured on each curve (50% upslope, peak, and zero intercept) to quantitate the EEG response. Statistical comparisons were performed between the following sets of data: EEG response at electrode closest to brain tumor versus electrode farthest from tumor (in the same patient); and electrodes closest to brain tumors (parietal P3 and P4) versus same electrode pair in control patients (patients with thoracic tumors) using analysis. No differences were found in any comparison. Thus, the presence of a brain tumor does not affect the response of the brain in this region to thiopental as measured using EEG.

Aged↗

PubMed1990

Thiopental binding to human serum albumin in the presence of halothane.

In vitro thiopental binding (substrate concentration 0.04.10(-3) M = 10 micrograms/ml) to 1% human serum albumin (HSA) increased significantly from 40.2% (= control) to 47.3% in the presence of 1.18.10(-3) M = 2.84 vol% halothane. A 4-fold higher halothane concentration (4.71.10(-3) M) had an even greater effect with an increase in the thiopental fraction bound to 55.5%. With a constant HSA concentration (1% or 5%) and thiopental concentrations in the range 0.01-1.5.10(-3) M or 0.01-0.38.10(-3) M, respectively, the halothane effect (increase in thiopental binding) was always evident, as well as in other experiments with constant thiopental concentration (0.04.10(-3) M) and variation in the HSA concentration (0.5-10%). Two classes of binding sites for thiopental were apparent at the HSA molecule. In the control experiments the following binding parameters were found: n1 = 0.01, k1 = 181.10(3) M-1; n2 = 45.73, k2 = 0.08.10(3) M-1, K = 5.47.10(3) M-1. In the presence of halothane the binding parameters changed as follows: n1 = 0.14, k1 = 29.4.10(3) M-1; n2 = 11.68, k2 = 0.42.10(3) M-1, K = 9.02.10(3) M-1.

Binding Sites↗

PubMed1994

The effect of thiopental on cerebral blood flow, and its relation to plasma concentration, during simulated induction of anaesthesia in a porcine model.

The reversible effect of an induction dose of thiopental on the cerebral blood flow (CBF) was characterized by repeated 133Xe washout measurements during stable physiological conditions in anaesthetized pigs. A thiopental effect corresponding to induction of light and transient anaesthesia was confirmed by electroencephalography (EEG). The concentration (arterial plasma) -effect (-% CBF) relationship of thiopental was estimated using a sigmoidal Emax model. The injection caused a rapid 36 +/- 4.5% (mean +/- s.d.) drop in CBF, with return to baseline by 80 min. According to the pharmacodynamic model, the maximal effect of thiopental (Emax) in this experimental set-up was a 58% lowering of the CBF and the concentration at half-maximal effect (EC50) was 25 micrograms.ml-1. This study provides a complete characterization of the effect of thiopental on the CBF, including the time-course and concentration-effect relationship. A comparison to limited data in the literature suggests that the findings in the pigs constitute a fair approximation of the action of thiopental during the clinical induction of anaesthesia.

Anesthesia, Intravenous↗

PubMedDate not supplied

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in atropinized cats. Effect of increasing inhalant concentrations.

The effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide, and the combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, on both enflurane-induced electroencephalographic (EEG) spike activity and convulsive behavior were measured quantitatively in atropinized cats receiving enflurane with controlled ventilation. Pretreatments with thiopental, ketamine, and diazepam reduced both EEG spike frequency and amplitude at 2.5% to 4.5% inspired enflurane but did not abolish spike activity. Nitrous oxide (66% of inspired gas) did not significantly alter spike frequency or amplitude during 2.5% to 4.5% inspired enflurane, but the combination of thiopental-nitrous oxide or ketamine-nitrous oxide reduced EEG spike activity during 2.5% inspired enflurane. Enflurane-induced convulsive score was markedly suppressed by thiopental and ketamine and was significantly reduced by diazepam, xylazine and nitrous oxide. The combinations of thiopental-nitrous oxide and ketamine-nitrous oxide greatly reduced behavioral-convulsive responses induced by 2.5% to 4.5% inspired enflurane.

Anesthesia, Inhalation↗

PubMed1998

Effects of thiopental on contractile and electrophysiological properties of single canine left ventricular cells.

The effects of thiopental on contraction, membrane potential and membrane ionic currents were studied in single canine left ventricular cells. Thiopental 10(-5) and 10(-4) mol/l reduced the cell-shortening from 7.02 +/- 0.64 microns to 5.66 +/- 1.39 and 3.48 +/- 0.64 microns respectively (mean +/- S.D., N = 10, 0.5 Hz). This effect was enhanced in higher (> 1.0 Hz) electrical stimulation frequencies. Also, thiopental decreased the plateau phase and shortened the duration of action potential. On the other hand, voltage clamp experiment revealed that thiopental 10(-6), 10(-5), and 10(-4) mol/l reduced peak Ca2+ current from 520 +/- 48 pA to 387 +/- 60 pA, 261 +/- 84 pA, and 84 +/- 36 pA respectively (mean +/- S.D., N = 8), and showed a use-dependent block of Ca2+ current. However, only a high dose of thiopental (10(-4) mol/l) inhibited the Na+ current. We conclude that the negative inotropic effect of thiopental on the heart is mediated mainly via inhibition of the Ca2+ current.

Animals↗

PubMed1987

Renal and renin effects of sodium thiopental in rabbits.

Unilateral renal arterial infusion of sodium thiopental on renal function and renin secretion were investigated in unanesthetized rabbits. Sodium thiopental infusion in doses of less than 0.3 mg/kg/min into unilateral renal artery caused dose-dependent increases in urine flow, urinary excretion of electrolytes, fractional excretion of sodium and free water clearance with no changes in systemic blood pressure and clearance of p-aminohippuric acid (renal blood flow). An anesthetic dose of sodium thiopental administered intravenously caused decreases in systemic blood pressure, renal hemodynamics, urine flow and free water clearance during the early period of anesthesia followed by increases in urinary excretion of sodium and fractional excretion of sodium. Unilateral renal arterial infusion of sodium thiopental decreased the renin secretion rate and plasma norepinephrine concentration in renal vein, whereas an anesthetic dose of sodium thiopental administered intravenously increased the renin secretion rate. These observations suggest that the diuretic, natriuretic and renin suppressive effects of sodium thiopental may be due to an inhibition of intrarenal sympathetic nervous system or due to a direct tubular action.

Animals↗

PubMedDate not supplied

Brain blood flow and metabolism after global ischemia and post-insult thiopental therapy in monkeys.

We measured total and regional cerebral blood flow (CBF, rCBF) and cerebral metabolic rate (CMR) of oxygen (O2), glucose (G), and lactate (L) levels for 4 h after 16 min global brain ischemia in rhesus monkeys with and without post-insult thiopental therapy. Eleven monkeys weighing 4-5 kg anesthetized with 1 percent halothane, 66 percent nitrous oxide and 33 percent oxygen, were subjected to 16 min global brain ischemia by a combination of trimethaphan hypotension (to a mean arterial pressure of 50 torr) and a high pressure (1500 torr) neck tourniquet. Post-ischemia, 7 monkeys were untreated (controls) and 4 received thiopental 90 mg/kg infused intravenously over 60 min, beginning at 5 min post-ischemia. Total CBF and rCBF were measured by continuous monitoring of cerebral venous (torcula) and parietal-occipital (external scintillation) 133Xe activity, respectively, after intra-innominate artery injection of 500 micronCi 133Xe in saline. In control monkeys, hyperemia in rCBF, but not in total CBF was observed at 6-7 min post-ischemia, whereas both total CBF and rCBF increased in thiopental treated monkeys. The hyperemia in thiopental treated monkeys coincided with an increase in CMRG without a proportional increase in CMRO2 or lactate levels. Indeed, CMRO2 was depressed in the first 30 min post-ischemia. At 30 min post-ischemia, CMRO2 rose to twofold greater than pre-ischemia in control monkeys, but only to pre-ischemic levels in thiopental treated monkeys. The data suggest that thiopental therapy improves distribution of brain blood flow and brain glucose uptake early post-ischemia and depresses CMRO2 later post-ischemia.

Animals↗

PubMed1993

Comparative myocardial depressive effects of propofol and thiopental.

To compare the direct myocardial effects of thiopental and propofol, concentration-contractility curves were determined by using an isolated guinea pig left atrial preparation. Contractility was measured as peak twitch tension, maximum rate of contraction (dT/dt), and maximum rate of relaxation (-dT/dt). Drug concentrations ranged from 56 microM (10 micrograms/mL) to 2800 microM (500 micrograms/mL) propofol and 3.8 microM (1 microgram/mL) to 190 microM (50 micrograms/mL) thiopental. Data were fitted to a sigmoidal inhibitory pharmacodynamic model in which an increasing incremental drug concentration is needed to cause a consistent incremental effect. Comparisons were then made of the drug concentrations at which a 50% inhibition in contractility was noted (IC50). To compare drugs on an equi-anesthetic basis, comparisons also were made between IC50 values normalized to anesthetic concentrations needed to produce anesthesia (67.8 microM and 28.1 microM for thiopental and propofol, respectively). Data from seven atrial preparations for thiopental and seven atrial preparations for propofol were analyzed. The IC50 (microM) for peak twitch tension were 20.9 +/- 6.3 and 96.6 +/- 10.1 (P < 0.05), for dT/dt were 21.1 +/- 5.9 and 86.9 +/- 8.3 (P < 0.05), and for -dT/dt were 21.0 +/- 6.1 and 84.3 +/- 9.2 (P < 0.05) for thiopental and propofol, respectively. When the normalized IC50 were compared, the differences between anesthetics became greater. For guinea pig left atria in vitro, thiopental is a more potent myocardial depressant than propofol, especially when compared relative to anesthetic potencies; neither anesthetic preferentially affects peak twitch tension, maximum rate of contraction, or maximum rate of relaxation.

Animals↗

PubMed1994

Comparison of propofol and thiopental for rapid anesthesia induction in infants.

We compared the hemodynamic response to laryngoscopy and intubation, as well as emergence and recovery times, when propofol or thiopental were used for rapid intravenous induction of anesthesia in 59 infants undergoing repair of inguinal hernia. An intravenous catheter was inserted under N2O analgesia and atropine 0.01 mg/kg was administered to all patients. Subsequent induction with propofol (3 mg/kg), thiopental (5 mg/kg), or halothane (2%) was followed with succinylcholine (2 mg/kg) and tracheal intubation. Ventilation was manually assisted during surgery, and tracheas were extubated when patients were completely awake. Infants who received propofol showed less hypertensive response to intubation than those who received thiopental or halothane. In the 1- to 6-mo age group, emergence (extubation) time was significantly longer for infants who received thiopental (10.2 +/- 1.4 min) than for those who received propofol or halothane (5.5 +/- 2.5 and 6.2 +/- 1.3 min, respectively). Infants who received thiopental induction had a higher incidence of perioperative airway complications than all others. There was no significant difference in the recovery and discharge times among the three groups. We conclude that when rapid intravenous induction is required for infants, propofol is more effective than thiopental in obtunding the hypertensive response to intubation, and in young infants (1-6 mo) it results in more prompt emergence after short surgical procedures.

Anesthesia, Intravenous↗

PubMed1995

The protective effects of thiopental on brain stem ischemia.

Thiopental, a barbiturate anesthetic, which at high doses suppresses cortical electroencephalogram activity, was evaluated as a neuroprotective agent in a dog model of reversible, hindbrain ischemia. Fourteen dogs were exposed to 20 minutes of isolated brain stem ischemia after pretreatment with 35 mg per kg of thiopental or placebo. Brain stem auditory evoked potentials (BAEPs) and regional cerebral blood flow were measured before and during the ischemia and for 5 hours after reperfusion. During the ischemic period, both control and thiopental-treated animals experienced dramatic declines in the BAEPs to less than 10% of baseline. On reperfusion for 30 minutes, the BAEPs increased in both groups to near 40% of baseline. In the thiopental-treated animals, the BAEPs continued to recover variably to a mean of 70% of baseline by 5 hours of reperfusion. In contrast, untreated animals showed a decline in BAEPs after 30 minutes of reperfusion. The improved recovery of BAEPs in the thiopental-treated animals suggests that thiopental may be of some value as a cerebroprotective agent, although the mechanism remains unclear. The variability in recovery in this group implies that other factors play a significant role in mediating functional recovery from ischemic brain stem damage.

Anesthetics, Intravenous↗

PubMed1984

Comparison of sodium thiopental and methohexital for high-dose barbiturate anesthesia.

High-dose sodium thiopental is frequently used in neuroanesthesia. The authors performed a study to compare a shorter-acting barbiturate, methohexital, to sodium thiopental in producing high-dose barbiturate anesthesia. In two groups of five mongrel dogs each, regional cerebral blood flow (CBF) was determined using the radioactive-microsphere technique, and cardiovascular parameters were measured before, during, and 1 hour after a 1 1/2-hour period of deep barbiturate anesthesia with either sodium thiopental or methohexital. Doses of the barbiturates were adjusted to produce electroencephalogram burst suppression of greater than 30 seconds. Both agents produced a similar degree of cardiac depression, reduction in CBF, and decrease in cerebral metabolic rate of oxygen (CMRO2). Changes in cerebral and peripheral vascular resistance indicated that methohexital caused less vasoconstriction than sodium thiopental. When the barbiturate infusions were discontinued, CMRO2 and CBF returned more rapidly toward control values in the methohexital group than in the thiopental group. The more rapid recovery time and decrease in cerebral vascular resistance with methohexital suggest that it may have some advantage over sodium thiopental during certain neurosurgical procedures.

Anesthesia, Intravenous↗

PubMed2005

The effect of pretreatment with thiopental on reducing pain induced by rocuronium injection.

We examined whether pretreatment with a small dose of thiopental was effective in reducing pain induced by the intravenous injection of rocuronium. Withdrawal movement was used to assess pain reduction. Ninety patients were randomly assigned to one of two groups: patients in the control group were pretreated with 2 mL saline, and those in the thiopental group were pretreated with 2 mL (50 mg) thiopental. Thiopental 5 mg/kg was injected intravenously. After a loss of consciousness, the upper arm was compressed with a rubber tourniquet, and the pretreatment drugs were administered. Thirty seconds later the tourniquet was removed and 0.6 mg/kg rocuronium was administered. Withdrawal movement was assessed using a four-grade scale: no movement, movement limited to the wrist, to the elbow or to the shoulder. The frequency of withdrawal movement in the group pretreated with thiopental was lower than in the control group (34 vs. 13, p < 0.05). We concluded that pretreatment with 2 mL (50 mg) thiopental is effective in reducing pain caused by the intravenous injection of rocuronium.

Adult↗

PubMed1999

Stability of thiopental and pentobarbital in human plasma determined with a new easy and specific gas chromatography-mass spectrometry assay.

A gas chromatographic-mass spectrometric (GC-MS) assay for the determination of thiopental and its main metabolite pentobarbital in human plasma is presented in this study. The sample preparation consists only in the addition of the internal standard barbital and an acidic extraction with ethyl acetate. Analytical separation is accomplished on a RTX-1 15 m x 0.25 mm capillary column with a film thickness of 0.5 micron. The effluent is observed by a mass selective detector operating in the single ion monitoring mode. The limits of detection are 5 ng/ml for pentobarbital and 10 ng/ml for thiopental, the intra-day variabilities are 2.2% and 4.0% and the inter-day variabilities are 3.3% and 7.1% at concentrations of 5 micrograms/ml, respectively. Applying this assay, the stability of thiopental and pentobarbital in human plasma was tested at concentrations of 5 micrograms/ml each. Thiopental is stable in human plasma at least over 41 days stored at -20 degrees C and 5 degrees C, respectively. A decay of about 2%/day is observed under storage at ambient temperature (19-20 degrees C). Pentobarbital is stable under all storage conditions. Methanolic solutions of thiopental are stable for 83 days under storage at 5 degrees C. Aqueous solutions of thiopental-sodium are stable for at least 23 days under storage at 5 degrees C or ambient temperature.

Calibration↗

PubMed1999

Thiopental inhibits nitric oxide production in rat aorta.

We studied whether thiopental affects endothelial nitric oxide dependent vasodilator responses and nitrite production (an indicator of nitric oxide production) elicited by acetylcholine, histamine, and A23187 in rat aorta (artery in which nitric oxide is the main endothelial relaxant factor). In addition, we evaluated the barbiturate effect on nitric oxide synthase (NOS) activity in both rat aorta and kidney homogenates. Thiopental (10-100 microg/mL) reversibly inhibited the endothelium-dependent relaxation elicited by acetylcholine, histamine, and A23187. On the contrary, this anesthetic did not modify the endothelium-independent but cGMP-dependent relaxation elicited by sodium nitroprusside (1 nM - 1 microM) and nitroglycerin (1 nM - 1 microM), thus excluding an effect of thiopental on guanylate cyclase of vascular smooth muscle. Thiopental (100 microg/mL) inhibited both basal (87.8+/-14.3%) and acetylcholine- or A23187-stimulated (78.6+/-3.9 and 39.7+/-5.6%, respectively) production of nitrites in aortic rings. In addition the barbiturate inhibited (100 microg/mL) the NOS (45+/-4 and 42.8+/-9%) in aortic and kidney homogenates, respectively (measured as 14C-labeled citrulline production). In conclusion, thiopental inhibition of endothelium-dependent relaxation and nitrite production in aortic rings strongly suggests an inhibitory effect on NOS. Thiopental inhibition of the NOS provides further support to this contention.

Acetylcholine↗

PubMed2000

Propofol-sodium thiopental admixture reduces pain on injection.

BACKGROUND: Propofol injection associated with a high incidence of pain is well known. Propofol and sodium thiopental mixture has recently been reported to be used for cost saving and able to reduce pain on injection. METHODS: This prospective, randomized, double blind trial was designed to compare the efficacy of different percentages of propofol and sodium thiopental mixture in minimizing propofol injection pain. 146 ASA class 1 patients were assigned to seven groups (pure propofol, pure sodium thiopental, and propofol premixed with 10%, 20%, 30%, 40%, and 50% of sodium thiopental). The intensity of pain was graded and recorded as severe, moderate, mild and no pain according to the response of the patients to the injection. RESULTS: The intensity of injection pain was significantly greater for pure propofol than the others while it was not significantly different among the other groups in comparison. CONCLUSIONS: Sodium thiopental, when added to propofol, can significantly reduce propofol injection pain. This attenuation effect was noted even with as low as 10 volume % of sodium thiopental.

Adult↗

PubMed2005

Effects of ketamine and thiopental on ischemia reoxygenation-induced LDH leakage and amino acid release from rat striatal slices.

Increased release of glutamate is thought to contribute to ischemia-induced neuronal damage. Since general anesthetics such as thiopental and ketamine are thought to provide some degree of cerebral protection, this study was intended to 1) compare the effectiveness of ketamine and thiopental on ischemia-induced tissue damage; and, if so, 2) determine whether attenuation of the increased amino acid release is the sole mechanism for the protective effects demonstrated. Striatal slices prepared from Wistar Albino rats were incubated in an ischemic medium for 1 hour followed by 5 hours in a reoxygenation (REO) medium. Ketamine and thiopental were added medium during ischemia and/or REO periods, and the medium was collected at the end of each incubation period for measurement of amino acid release and lactate dehydrogenase (LDH) leakage. Ischemia significantly increased amino acid release without altering LDH leakage. Ischemia-induced increments in glutamate and aspartic acid releases returned to control levels during REO, but LDH leakage increased (P > 0.001) during this period. Although ketamine (100 microM) and thiopental (100 microM) failed to decrease ischemia-induced excitatory amino acid release, they protected the slices against REO-induced LDH leakage. Ketamine, but not thiopental, was effective even if added after ischemia (P < 0.05). These results indicate that ketamine and thiopental protect the slices against REO-induced LDH leakage. However, mechanisms other than attenuation of the enhanced glutamate release might be responsible for their protective effects.

Amino Acids↗