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C A Marsden

Publications and source records attributed to C A Marsden.

239 records · Page 14Linked to original sources
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Effects of BOC-CCK-4 and L 365.260 on cortical 5-HT release in guinea-pigs on exposure to the elevated plus maze.

The elevated plus maze is a well-established model of anxiety, with previous results showing that guinea-pigs handled daily from birth exhibit behaviour in this test similar to rats. In the present microdialysis study exposure of the guinea-pig to the elevated plus maze increased extracellular 5-HT in the lateral prefrontal cortex. The CCK-B receptor agonist BOC-CCK-4 (10 micrograms/kg) produced 'anxious' behaviour and potentiated the rise in 5-HT observed on exposure to the X-maze. The basal release of cortical extracellular 5-HT was not affected by BOC-CCK-4. Pretreatment with the selective CCK-B antagonist L 365.260 (100 micrograms/kg) antagonized both the 'anxious' behaviour and the neurochemical changes induced by BOC-CCK-4 while L 365.260 alone produced 'anxiolytic' behaviour, decreased basal extracellular 5-HT and prevented the increase in extracellular 5-HT seen when the guinea-pigs were exposed to the X-maze. Our results show that CCK-B receptor stimulation and blockade induce changes in central extracellular 5-HT levels associated with 'anxious' and 'anxiolytic' behaviour, respectively.

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Unchanged sensitivity to electric shock in L-tryptophan treated rats.

Injections of L-tryptophan (50, 100 and 200 mg/kg) i.p. in rats resulted in dose dependent increases in brain concentrations of tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. Sensitivity to electric shock as measured by flinch and jump thresholds was not changed by L-tryptophan 100 and 200 mg/kg. The results indicate that increased 5-HT turnover does not influence sensitivity to electric shock.

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Alterations in core body temperature, locomotor activity, and corticosterone following acute and repeated social defeat of male NMRI mice.

Repeated social defeat of male NMRI mice, coupled with the stress of continuously living opposite a dominant animal, induces a citalopram-reversible increase in anxiety. The experiments reported in the present paper were performed in an attempt to further validate this paradigm by studying the effects of acute and repeated social defeat on corticosterone and the circadian rhythms of core body temperature and locomotor activity, measured by telemetry. Acute social defeat induced a large (controls: 37.14+/-0.29 degrees C; subordinates: 39.79+/-0.33 degrees C) increase in core body temperature and corticosterone (controls: 30.14+/-2.70 ng/ml; subordinates: 89.62+/-9.25 ng/ml). Repeated social defeat (24 defeats) induced a chronic elevation in core body temperature across 24-h (controls: 36.62+/-0.04 degrees C; subordinates: 37.11+/-0.16 degrees C) in subordinate animals and a very large increase in corticosterone (controls: 28.60+/-1.27 ng/ml; subordinates: 441.52+/-8.86 ng/ml). These results illustrate that the chronic social defeat procedure described in this paper induces a state of chronic stress in the subordinate animals. Further studies are warranted to ascertain if the chronic hyperthermia and increases in corticosterone observed in the subordinate animals could be attenuated by chronic antidepressant treatment, thus further extending the predictive validity of this model.

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Detection of salicylate and its hydroxylated adduct 2,3-dihydroxybenzoic acid in glutamate neurotoxicity and the effects of verapamil and ryanodine in rats.

It has been suggested that salicylate hydroxylation can be used to detect hydroxyl radical formation in vivo. In the present study we investigated the effects of verapamil and or ryanodine on salicylate (SA) and its hydroxylated adduct; 2,3-dihydroxybenzoic acid (2,3-DHBA) levels in glutamate induced neurotoxicity of whole rat brains. To detect SA and 2,3-DHBA, an HPLC-EC/UV method was used. Retention time was found to be 3.9 min for 2,3-DHBA and 12.0 min for SA. Verapamil at 10(-5) and 10(-7) and ryanodine at 10(-5) M concentrations were found to have a significant decreasing effect on this degradation induced by glutamate. This was the highest dose for ryanodine tested. As an L-type voltage dependent calcium channel blocker, verapamil was found ineffective at 10(-4), 10(-6) and 10(-8) M concentrations. Surprisingly, none of the combined application groups (verapamil + ryanodine) was found effective on SA hydroxylation. As a result, ryanodine was effective only at the highest dose, while verapamil exerts its effect in a dose dependent fashion as reported before in the literature.

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