The interaction of Urocortin II and Urocortin III with amygdalar and hypothalamic cotricotropin-releasing factor (CRF) - reflections on the regulation of the hypothalamic-pituitary-adrenal (HPA) axis

Electroosmotic pumps employing silica frits synthesized from potassium silicate as a stationary phase show strong electroosmotic flow velocity and resistance to pressure-driven flow. We characterize these pumps and measure an electroosmotic mobility of 2.5x10(-8) m(2)/V s and hydrodynamic resistance per unit length of 70 x10(17) Pa s/m(4) with a standard deviation of less than 2% even when varying the amount of water used in the potassium silicate mixture. Furthermore, we demonstrate the simple integration of these pumps into a proofof- concept PDMS lab-on-a-chip device fabricated from a 3D-printed template.Funding Agencies|Vetenskapsradet [2007-3983, 2008-7537, 2011-6404]</p

The action of neuropeptide AF on passive avoidance learning. Involvement of neurotransmitters

The evolutionary origins of human handedness are still unknown. The study of lateralized behaviour in our closest relatives, the nonhuman primates, is useful to clarify how this trait appeared and evolved in our species. In the present study, lateralized behaviour was assessed in a population of 32 free-ranging Mexican mantled howler monkeys (Alouatta palliata mexicana) for thirteen spontaneous motor patterns, at individual and group levels, as well as the effect that age, sex and posture have on its strength and direction. The studied population of howler monkeys displayed only few significant lateral biases at the individual level with single motor patterns (Binomial tests, p≤0.05). No biases towards the use of a particular limb or side of the body were found at a population level. Therefore, even though some individuals showed significant limb/side preference with single motor patterns, no signs of task specialization, side specialization, or true handedness were found. Similarly, no effects of sex, age or posture were found on the direction or strength of lateralized behaviour. The general absence of limb/side preferences found in this population may be due to the constraints imposed by the arboreal life and/or the type of diet. Possible causal agents of the few significant individual biases found here may be the presence of handicaps and/or experience. Further research is needed in order to assess whether the lack of human-like handedness reported in this study is only specific to the studied population, a general phenomenon of the genus Alouatta or perhaps of all the Platyrrhini

Ghrelin and nicotine stimulate equally the dopamine release in the rat amygdala.

The orexigenic peptide ghrelin plays a prominent role in the regulation of energy balance and in the mediation of reward processes and reinforcement for addictive drugs, such as nicotine. Nicotine is the principal psychoactive component in tobacco, which is responsible for addiction and relapse of smokers. Ghrelin and nicotine activates the mesolimbicocortical dopaminergic pathways via growth hormone secretagogue receptors (GHS-R1A) and nicotinic acetylcholine receptors (nAchR), respectively, resulting in the release of dopamine in the nucleus accumbens, the amygdala and the prefrontal cortex. In the present study an in vitro superfusion of rat amygdalar slices was performed in order to investigate the direct action of ghrelin and nicotine on the amygdalar dopamine release. Ghrelin increased significantly the dopamine release from the rat amygdala following electrical stimulation. This effect was inhibited by both the selective GHS-R1A antagonist GHRP-6 and the selective nAchR antagonist mecamylamine. Under the same conditions, nicotine also increased significantly the dopamine release from the rat amygdala. This effect was antagonized by mecamylamine, but not by GHRP-6. Co-administration of ghrelin and nicotine induced a similar increase of amygdalar dopamine release. This stimulatory effect was partially reversed by both GHRP-6 and mecamylamine. The present results demonstrate that both ghrelin and nicotine stimulates directly the dopamine release in the amygdala, an important dopaminergic target area of the mesolimbicocortical pathway

Ghrelin Amplifies the Nicotine-Induced Release of Dopamine in the Bed Nucleus of Stria Terminalis (BNST)

Ghrelin is an orexigenic neuropeptide that is known for stimulating the release of growth hormone (GH) and appetite. In addition, ghrelin has been implicated in addiction to drugs such as nicotine. Nicotine is the principal psychoactive component in tobacco and is responsible for the reward sensation produced by smoking. In our previous in vitro superfusion studies, it was demonstrated that ghrelin and nicotine stimulate equally the dopamine release in the rat amygdala, and ghrelin amplifies the nicotine-induced dopamine release in the rat striatum. However, less attention was paid to the actions of ghrelin and nicotine in the bed nucleus of the stria terminalis (BNST). Therefore, in the present study, nicotine and ghrelin were superfused to the BNST of male Wistar rats, and the dopamine release from the BNST was measured in vitro. In order to determine which receptors mediate these effects, mecamylamine, a non-selective nicotinic acetylcholine receptor (nAchR) antagonist, and GHRP-6, a selective growth hormone secretagogue receptor (GHS-R1A) antagonist, were also superfused to the rat BNST. Nicotine significantly increased the release of dopamine, and this effect was significantly inhibited by mecamylamine. Ghrelin increased dopamine release even more significantly than nicotine did, and this effect was significantly inhibited by GHRP-6. Moreover, when administered together, ghrelin significantly amplified the nicotine-induced release of dopamine in the BNST, and this additive effect was reversed partly by mecamylamine and partly by GHRP-6. Therefore, the present study provides a new base of evidence for the involvement of ghrelin in dopamine signaling implicated in nicotine addiction