We examined effects of stress, depression, and their interaction on sympathetic-parasympathetic responses, including percentage heart rate (PHR), percentage skin conductance (PSC), percentage finger temperature (PTEMP), and percentage respiratory rate (PRESPR). Participants were categorized into normal, low-risk, and high-risk depression groups under stress or no-stress by measuring psychophysiological responses. Stress increased PHR and PSC and decreased PTEMP. Depression negatively correlated with PHR and PTEMP. PSC and PTEMP were significantly dependent on and positively correlated with depression. PTEMP was significantly affected by the stress and depression interaction. Stress affects sympathetic, rather than parasympathetic, activity. Depression and the interaction between stress and depression initially associated with the sympathetic division and are then correlated with parasympathetic activity. A sympathetic-parasympathetic hypothesis and its clinical implications are discussed.

The present study used the preproenkephalin knockout (ppENK) mice to test whether the endogenous enkephalins deficit could facilitate the anxiety- and depressive-like symptoms of posttraumatic stress disorder (PTSD). On Day 1, sixteen wildtype (WT) and sixteen ppENK male mice were given a 3 mA or no footshock treatment for 10 seconds in the footshock apparatus, respectively. On Days 2, 7, and 13, all mice were given situational reminders for 1 min per trial, and the freezing response was assessed. On Day 14, all mice were tested in the open field test, elevated plus maze, light/dark avoidance test, and forced swim test. Two hours after the last test, brain tissues were stained to examine c-fos expression in specific brain areas. The present results showed that the conditioned freezing response was significant for different genotypes (ppENK vs WT). The conditioned freezing effect of the ppENK mice was stronger than those of the WT mice. On Day 14, the ppENK mice showed more anxiety- and depressive-like responses than WT mice. The magnitude of Fos immunolabeling was also significantly greater in the primary motor cortex, bed nucleus of the stria terminalis-lateral division, bed nucleus of the stria terminalis-supracapsular division, paraventricular hypothalamic nucleus-lateral magnocellular part, central nucleus of the amygdala, and basolateral nucleus of the amygdala in ppENK mice compared with WT mice. In summary, animals with an endogenous deficit in enkephalins might be more sensitive to PTSD-like aversive stimuli and elicit stronger anxiety and depressive PTSD symptoms, suggesting an oversensitivity hypothesis of enkephalin deficit-induced PTSD.

How high-risk Internet addiction (IA) abusers respond to different autonomic nervous activities compared with low-risk subjects may be a critical research goal with prevention and treatment implications. The aim of the present study was to address this issue by observing differences between high- and low-risk IA abusers in four physiological assessments when surfing the Internet: blood volume pulse (BVP), skin conductance (SC), peripheral temperature (PTEMP), and respiratory response (RESPR). Forty-two male and ten female participants aged 18-24 years were screened with the Chen Internet Addiction Scale (CIAS, 2003), and then separated into high- and low-risk IA groups. Using psychophysiology equipment, participants encountered a 3-minute adaptation period followed by a 6-minute testing period for surfing the Internet on baseline and testing phases. The present results indicate that: (a) the CIAS scores were positively and negatively correlated with the RESPR and the PTEMP; (b) the PTEMP and RESPR of high-risk IA abusers were respectively weaker and stronger than those of low-risk IA abusers; the BVP and SC of high-risk IA abusers were respectively augmented and decreased relative to low-risk IA abusers. Thus we suggest that four autonomic responses may be differentially sensitive to abusers' potency in terms of the IA hypothesis of autonomic activity. The stronger BVP and RESPR responses and the weaker PTEMP reactions of the high-risk IA abusers indicate the sympathetic nervous system was heavily activated in these individuals. However, SC activates parasympathetic responses at the same time in the high-risk IA abusers. The paradoxical responses between the sympathetic and parasympathetic actions are addressed in the discussion.

RationaleAttention-deficit/hyperactivity disorder (ADHD) is one of the most common neurobehavioural disorders with morphological and functional brain abnormalities. However, there is a growing body of evidence that abnormalities in the immune and endocrine systems may also account for the ADHD pathogenesis.ObjectivesTo test ADHD pathogenesis in neurological, immune and endocrine systems, this study examined the concentrations of cytokines, chemokines, oxidative stress markers, metabolic parameters, steroid hormones and steroidogenic enzymes in the serum and/or tissues of spontaneously hypertensive rats (SHRs, animal model of ADHD) and Wistar Kyoto rats (WKYs, control animals). Moreover, the volume of the medial prefrontal cortex (mPFC) as well as the density of dopamine 2 (D2) receptor-expressing cells and tyrosine hydroxylase (TH)-positive nerve fibres in it was also elucidated.MethodsPeripheral blood, spleen and adrenal gland samples, as well as brain sections collected on day 35 (juvenile) and day 70 (maturating) from SHRs and WKYs, were processed by ELISA and immunohistochemistry, respectively.ResultsThe results show significant increases of serum and/or tissue concentrations of cytokines, chemokines and oxidative stress markers in juvenile SHRs when compared to the age-matched WKYs. These increases were accompanied by a lowered volume of the mPFC and up-regulation of D2 in this brain region. In maturating SHRs, the levels of inflammatory and oxidative stress markers were normalised and accompanied by elevated contents of steroid hormones.ConclusionsSignificant elevations of serum and/or tissue contents of cytokines, chemokines and oxidative stress markers as well as volumetric and neurochemical alterations in the mPFC of juvenile SHRs may suggest the cooperation of neurological and immune systems in the ADHD pathogenesis. Elevated levels of steroid hormones in maturating SHRs may be a compensatory effect involved in reducing inflammation and ADHD symptoms.

This study reexamined Grigson's reward comparison hypothesis (1997), which claimed to have resolved the paradox of addictive, rewarding drugs manifesting an aversive effect in the conditioned taste aversion (CTA) paradigm. Here, the authors compared the conditioned suppression effects of lithium chloride (LiCl) and amphetamine in a series of three experiments. In Experiment 1, the concentrations of saccharin solution (conditioned stimulus [CS]) and the doses of amphetamine or LiCl (unconditioned stimulus [US]) were manipulated. In Experiment 2, the effects of employing backward versus forward pairings of the CS and US were compared. Finally, in Experiment 3, the additivity of amphetamine's reward property and LiCl's aversive property was examined. The results of these experiments, respectively, indicated that: (1) manipulating saccharin solution concentrations does not distinguish the suppression effect caused by rewarding or aversive effects when amphetamine or LiCl served as the US; (2) both backward and forward pairings produced suppression of saccharin solution intake regardless of whether amphetamine or LiCl was used as the US; and (3) combining amphetamine and LiCl did not diminish the suppression effect, as would be expected if they had opposing mechanisms for the effects; instead, an additive effect occurred. Taken together, these results suggest that the drug of abuse amphetamine and the emetic drug LiCl both possess aversive properties in the CTA paradigm. No rewarding effects of amphetamine were detected in our experimental data. In all, our results do not support the Grigson's reward comparison hypothesis (1997) and a new "task-dependent drug effects hypothesis" is proposed.