Modulation of the stress response by coffee: an in vivo microdialysis study of hippocampal serotonin and dopamine levels in rat

Extract fromAcanthopanax senticosusHarms (Siberian Ginseng) Activates NTS and SON/PVN in the Rat Brain

“…We have confirmed that ASH increases NA and its turnover, especially in the anterior hypothalamus, 5,9) but alone it did not cause development of gastric erosions. This is clear from the results of a separate experiment in which we measured the gastric erosion index (GEI) to restraint stress (RS) in eight rats per treatment: ASH alone (0), water alone (0), water + RS (56:25 AE 3:82), and ASH + RS (23:75 AE 3:84).…”

“…2) Further, the anti-stress effects of ASH have also been found to mediate some of the substances, syringin 2,3) and chlorogenic acid, 4,5) acting in the brain. We have also previously demonstrated antistress property of ASH and its components, e.g.,…”

Modulation of the hypothalamo–pituitary–adrenocortical axis by caffeine

“…The higher corticosterone and ACTH release induced by the 10 mg/kg caffeine dose, especially in the background (60 dB) noise condition is likely a reflection of the ability of caffeine at this dose to induce HPA axis activation basally, as shown in Experiment 3, but not by reducing the threshold to stressful events. A number of prior results suggested that a low dose of caffeine may produce an attenuation of the HPA axis response to stressful stimuli: first, because of the biphasic effects of caffeine reported in some responses (Svenningsson et al, 1995;Garrett and Holtzman, 1995); second, the finding that a similar low dose (2 mg/kg) attenuated the restraint-induced elevations in hippocampal serotonin and dopamine release (Yamato et al, 2002), despite the fact that caffeine alone elevated these neurotransmitters in the hippocampus (Carter et al, 1995); and finally, the existence of a putative mechanism whereby antagonism at adenosine A2a receptors might produce different effects than antagonism at the A1 receptors (Fredholm et al, 1999), as indicated by the findings that only high doses of caffeine (10 mg/kg and above) induce anxiety in rodents (Lister, 1987;Baldwin et al, 1989;Jain et al, 1995;Bhattacharya et al, 1997), while selective blockade of A1 receptors (Florio et al, 1998) but not A2a receptors (El Yacoubi et al, 2000) was reported to induce anxiety. These central actions of caffeine might have been expected to generalize to regulation of the hypothalamic paraventricular nucleus.…”

“…These doses were employed because traditionally doses of 30 mg/kg and higher have been considered high doses not relevant to human consumption, but doses lower than 20 mg/kg did not activate the HPA axis 2 h following injections but were not studied at earlier time points (Nicholson, 1989). A dose similar to the lowest dose employed (2 mg/ kg) was ascribed a relaxant effect by Yamato et al (2002), and to our knowledge, no other studies have reported effects at doses lower than 2 mg/kg. In a pilot study an additional group was injected with 60 mg/kg caffeine and sacrificed 2 h following injection, but the corticosterone response for this group was not different from the group injected with 30 mg/ kg caffeine.…”

“…Additional evidence also suggests that caffeine may produce biphasic effects related to stress and anxiety. While high doses of caffeine consistently induce anxiety in rodents (Lister, 1987;Baldwin et al, 1989;Jain et al, 1995;Bhattacharya et al, 1997), a low dose of caffeine was ascribed a relaxing effect as indexed by the reduction of some neurotransmitter system activity in response to restraint stress (Carter et al, 1995;Yamato et al, 2002). Such putative anxiolytic or stress reducing effects have not, however, been tested directly using effector systems such as behavioral or neuroendocrine indices.…”