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G E Martin

Publications and source records attributed to G E Martin.

At least 91 records · Page 5Linked to original sources
PubMed1981

13C-NMR experimental methods for determination of resonance multiplicities: Strychnos alkaloids.

13C-NMR spectral assignments of the Strychnos alkaloids brucine and strychnine have been reported by numerous investigators. One recent report contained several disparities in the assignments that were attributable to incorrect determinations of spin multiplicities. The source of the inaccuracies in the spin-multiplicity determinations of very complex molecules is discussed, and several additional techniques for the determination of these multiplicities are described that are less subject to interpretational errors than the conventional and routinely employed single-frequency off-resonance decoupling methods. These procedures are applied using brucine as a representative example.

Alkaloids↗
PubMed1981

Action of selected serotonin antagonists on hyperthermia evoked by intracerebrally injected beta-endorphin.

Methergoline, an antagonist of cerebral serotonin receptors, has been shown to significantly reduce the rise in rectal temperature (Tre) produced by the intracerebral microinjection of beta-endorphin. In this study the role of serotonin in the increase in Tre elicited by beta-endorphin was further examined using three additional serotonin antagonists. beta-Endorphin was administered twice to rats using a crossover design in which half of the animals were first pretreated with the vehicle solution and half with the antagonist. Serotonin antagonists used were: methergoline, methysergide, cinanserin and cyproheptadine. Although methergoline did cause a marked reduction in the beta-endorphin-induced rise in Tre, neither methysergide, nor cinanserin, nor cyproheptadine produced a marked reduction in the hyperthermia. Since methergoline also interacts with the dopamine receptor, the effect of a dopamine antagonist, haloperidol, on the endorphin-evoked response was also examined. Haloperidol failed to attenuate the rise in Tre. The reason for the apparent discrepancy in the action of these serotonin antagonists is unclear. Further research may reveal distinct subpopulations of serotonin receptors at which these antagonists exert differential effects.

Animals↗
PubMed1980

Hypothermia elicited by the intracerebral microinjection of neurotensin.

Changes in rectal temperature were measured after the intracerebral microinjection of neurotensin (2.5 micrograms/0.5 microliters) at 135 sites in the rat. At 63 of the 135 microinjection sites, the tridecapeptide produced a rapid onset of hypothermia ranging in magnitude from 0.8 to 2.3 degrees C below the baseline rectal temperature. The drop in rectal temperature persisted for 2-4 hours following the microinjection. The greatest concentrations of neurotensin-sensitive sites were found in the medial preoptic region of the hypothalamus and in the periaqueductal gray area, both of which contain relatively large amounts of endogenous neurotensin. Other active sites were found in the ventral thalamus, the dorsomedial hypothalamus, and in the diagonal band of Broca. At no injection site did neurotensin evoke an increase in rectal temperature. These data support the proposition that neurotensin may act endogenously to mediate heat-loss mechanisms in the rat. The data provide further evidence indicating a potent neuromodulatory role for neurotensin.

Animals↗
PubMed1979

Action of intracerebrally injected beta-endorphin on the rat's core temperature.

Microinjected directly into the preoptic anterior hypothalamus (POAH), beta-endorphin (0.74--7.4 nmol) induced an increase in rectal temperature (RT) in the free-moving rat. Whereas the initial phase of the endorphin-induced rise in RT was partially attenuated by naloxone (5 or 20 mg/kg i.p.) or naltrexone (3 mg/kg i.p.), the late phase was completely blocked by the prostaglandin synthetase inhibitor, indomethacin (15 mg/kg i.p.). Pretreatment with a combination of indomethacin and naloxone resulted in an almost total block of the endorphin-induced increase in RT. Furthermore, the central serotonin antagonist, methergoline (1 mg/kg i.p.) antagonized the endorphin-evoked fever indicating serotonin may mediate the rise in RT. In contrast to the fever evoked in the POAH, beta-endorphin (7.4 nmol), given into the lateral cerebral ventricle (LCV), elicited a marked drop in RT, catalepsy, and analgesia which were completely blocked by naloxone (5 mg/kg). Similar to morphine, beta-endorphin elicited a naloxone-reversible hyperthermia when administered into the subarachnoid space surrounding the spinal cord. The similarities between beta-endorphin and morphine in their actions on RT as well as the possible role of serotonin or prostaglandins in beta-endorphin's thermogenic action are discussed.

Animals↗
PubMed1979

Effect on core temperature of restraint after peripherally and centrally injected morphine in the Sprague-Dawley rat.

The changes in core temperature (Tc) evoked by morphine in the Sprague-Dawley rate were altered by restraining the rat. The Tc of the free-moving rat rose after the IP (5, 15, 30, 60 mg/kg) or intracerebral injections (10, 20, 50 micrograms) of morphine. In the restrained rate, however, identical doses of morphine evoked either a hyperthermia of lesser magnitude than in the free-moving rat or a drop in Tc. These findings reemphasize the importance of restraint in determinating the action of morphine on Tc and extend the finding to the Sprague-Dawley rat.

Animals↗
PubMed1978

Contralateral turning evoked by the intranigral microinjection of muscimol and other GABA agonists.

Contraversive turning was evoked by the microinjection of GABAergic agents into the substantia nigra (SN) of the rat. Muscimol, the most potent GABA agonist, evoked contralateral turning when injected into the SN in doses of 0.005, 0.05, 0.5 and 5 microgram, whereas 0.5 microgram of muscimol applied at extranigral sites produced no turning. A shorter lived contraversive turning response was evoked by the intranigral micro-injection of imidazole acetic acid (10 or 50 microgram), ethanolamine-O-sulphate (25 or 50 microgram), or GABA (50 microgram). No increase in GABA-induced turning was produced by local pretreatment with pipecolic acid (5 microgram). When injected into the SN, neither picrotoxin, in doses of 0.1, 0.5, 1.0 or 2.0 microgram, nor bicuculline methiodide (Bm), in doses of 0.1 or 0.2 microgram, elicited a significant amount of turning. Picrotoxin, however, partially blocked the turning evoked by the intranigral injection of muscimol, both via the i.p. and intranigral routes of administration whereas Bm did not. In addition, haloperidol (1 mg/kg i.p.) antagonized the muscimol-induced turning. Hence, we feel GABA mimetic substances injected within the SN might evoke contralateral turning via activation of a heretofore undescribed neural system arising from the SN or by activating the ipsilateral dopaminergic neurons projecting from the SN.

Animals↗
PubMed1978

Hyperthermia evoked by the intracerebral injection of morphine sulphate in the rat: the effect of restraint.

Morphine sulphate (M) was microinjected intracerebrally into 26 sites in the free-moving and 11 sites in the restrained rat. The injections were made into the preoptic-anterior hypothalamic (POAH) region as core temperature (Tc) was measured. A marked increase in Tc was evoked from the free-moving rat following doses of M of 1 (n = 10); 10 (n = 19); 20 (n = 7); or 50 microgram (n = 6). On the other hand, no increase in Tc significantly above the control level was observed in the restrained rat following the intracerebral administration of M in doses of 10 (n = 8), 20 (n = 9), 50 (n = 10), or 70 microgram (n = 4). The control injection of the artificial cerebrospinal fluid (5-ion), used as the drug vehicle, caused a mild hyperthermia about 1.0 degrees C above the baseline level in both the free-moving and restrained rat. We conclude that morphine evokes a hyperthermia by its action on POAH neurons, but the M-induced hyperthermia can be attenuated by restraining the rat.

Animals↗
PubMed1977

Restraint alters the effects of morphine and heroin on core temperature in the rat.

The importance of restraint in determining the magnitude of alteration in the rat's core temperature (Tc) after the administration of morphine sulphate (M) and heroin hydrochloride (H) was investigated. M, in doses of 5, 15 and 30 mg/kg, or H, in doses of 0.1, 1 and 5 mg/kg was administered IP to either the restrained or free-moving rats as Tc was measured. After the administration of 5 mg/kg of H or 30 mg/kg of M to the restrained rat, a marked hypothermia was observed which reached a maximum mean depth of 3.1 and 4.5 degrees C below the baseline Tc, respectively. Conversely, a mean increase in Tc of 1.5 and 1.9 degrees C occurred following the administration of these same doses of M and H in the unrestrained animal. Furthermore, the hypothermic effect of the highest dose of M was not observed when the third of 3 consecutive injections of M, administered at 48-hr intervals, was administered to the restrained rat. On the other hand, when M was repeatedly administered to the free-moving rat, the hyperthermic response was consistently observed. Pretreatment with naloxone hydrochloride (5 mg/kg IP) effectively blocked the opiate-induced hypothermia in the restrained animal, but a total dose of 10 mg/kg was necessary to completely block the hyperthermic response in the free-moving rat. Although the factor of restraint itself did not alter the rat's Tc, it did dramatically alter the action of M and H on the body temperature of the rat.

Animals↗
PubMed1977

High pressure liquid chromatographic determination of saccharin in alcoholic products.

After preliminary cleanup, sodium saccharin can be quantitatively determined in wines and proprietary drugs by using high pressure liquid chromatography. The preliminary cleanup removes materials that cause column deterioration, loss of baseline stability, and interfering peaks. The average experimental error found in analyses of 6 wines for sodium saccharin content was 2.3% and the standard deviation was 0.01. In the analysis of 10 cough medicines and vitamin preparations, the difference between declared and experimental values for sodium saccharin averaged 5.7%. The recovery for the extraction process ranged from 97.8 to 101.6%.

Alcoholic Beverages↗
PubMed1976

Catecholamine release by intracerebral perfusion of 6-hydroxydopamine and desipramine.

The rate of catecholamine release at perfusion sites in the diencephalon of the unanesthetized rat during the perfusion of a solution of 6-hydroxydopamine (6-OHDA) or desipramine (DMI). Endogenous stores of norepinephrine (NE) and dopamine (DA) were first tagged by the cerebral microinjection of 14C- or 3H-labelled NE or DA. After successive control perfusates were collected with a push-pull cannula system, 6-OHDA, in a concentration of 5.0, 0.5, or 0.1 mg/ml, was perfused at 20-23 mul/min through a site in the rat'e brain. The compound induced a dose-related release of both NE and DA. In control experiments, 6-OHDA exerted a non-specific releasing effect on 3H-inulin which was not dose dependent. In addition, DMI, an NE reuptake inhibitor in a concentration of 10.0, 2.0 or 0.5 mg/ml, was perfused through 23 sites in the brain following the injection of labelled NE. DMI enhanced the recovery of NE in the push-pull effluent at the 10.0 mg/ml concentration only. However, an augmented efflux of 3H-inulin was also observed during the perfusion of the highest concentration of DMI. These results support the view that 6-OHDA releases catecholamines from endogenous storage sites, but also indicate a strong non-specific releasing action of this compound possibly at extracellular or non-catecholaminergic loci.

Animals↗
PubMed1976

Dopamine efflux from the brain stem of the rat during feeding, drinking and lever-pressing for food.

To determine whether endogenous dopamine (DA) is involved in the control of feeding and drinking, the cerebral activity of 14C-DA was examined in the rat while the animal consumed food or water. A push-pull guide tube was implanted above sites either adjacent to the third ventricle, the anterior hypothalamus or the substantia nigra in each of 41 rats. After the endogenous stores of DA at specific sites were labelled by a microinjection of 0.5 to 2.0 muCi of 14C-DA, an artificial CSF was perfused at half-hour intervals at a rate of 20-23 mul/min in these sites in the food deprived rat. After a 14C-washout curve of radioactivity in the perfusate was derived for successive control samples, the food-deprived rat was offered food or water which was ingested during the course of one or more perfusions. As the rat consumed food, 14C-DA was released in some experiments from circumscribed sites in the nucleus reuniens and the zona incerta. The efflux of 14C-DA from certain sites in the circumscribed sites in the nucleus reuniens and the zona incerta. The efflux of 14C-DA from certain sites in the ventromedial and dorsomedial hypothalamus as well as from the substantia nigra also was enhanced as the rat depressed a lever to obtain food pellets. Since 14C-DA was also released from the zona incerta, perifornical hypothalamus, and into the third ventricle as the rat drank water, these results suggest that dopaminergic neurons in the brain stem play some part in the motor component of ingestive behavior rather than feeding per se.

Animals↗
PubMed1976

Gas-liquid chromatographic determination of beta-asarone in wines and flavors.

Wine samples containing beta-asarone (cis-2,4,5-trimethoxy-l-propenylbenzene) are distilled; beta-asarone is extracted by hexane and then quantitatively determined by gas-liquid chromatography (GLC), using ethyl palmitate as the internal standard. The GLC procedure is rapid and yields precise and accurate results. Mass spectrometry confirmed the identity of the GLC peak as beta-asarone. The ultraviolet spectra of beta-asarone and its isomer were also determined.

Anisoles↗