The Effects of Alcohol Intoxication and Withdrawal on Hypothalamic Neurohormones and Extrahypothalamic Neurotransmitters.

The aim of the present study was to determine the effects of alcohol intoxication and withdrawal on hypothalamic neurohormones such as corticotropin-releasing factor (CRF) and arginine vasopressin (AVP), and extrahypothalamic neurotransmitters such as striatal dopamine (DA), amygdalar gamma aminobutyric acid (GABA), and hippocampal glutamate (GLU). In addition, the participation of the two CRF receptors, CRF1 and CRF2, was investigated. For this purpose, male Wistar rats were exposed to repeated intraperitoneal (ip) administration of alcohol every 12 h, for 4 days and then for 1 day of alcohol abstinence. On the fifth or sixth day, intracerebroventricular (icv) administration of selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B was performed. After 30 min, the expression and concentration of hypothalamic CRF and AVP, the concentration of plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT), and the release of striatal DA, amygdalar GABA, and hippocampal GLU were measured. Our results indicate that the neuroendocrine changes induced by alcohol intoxication and withdrawal are mediated by CRF1, not CRF2, except for the changes in hypothalamic AVP, which are not mediated by CRF receptors.

The effects of alcohol on anxiety-like, depression-like, and social behavior immediately and a day after binge drinking.

The aim of the present study was to determine the effects of binge drinking on anxiety-like, depression-like, and social behavior. The participation of the corticotropin-releasing factor (CRF) receptors (CRF1 and CRF2) in these effects was also investigated. Therefore, male C57BL/6 mice were exposed to drinking in the dark, a classical animal model for binge drinking, and treated intracerebroventricularly (icv) with selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B, immediately or 24 h after binge drinking. After 30 min, the animals were investigated in an elevated plus-maze test and a forced swim test for anxiety-like and depression-like signs, respectively. In addition, mice were tested in a three-chamber social interaction arena for sociability and preference for social novelty. Immediately after binge drinking, mice exposed to alcohol expressed anxiolytic and antidepressant effects, which were reduced by astressin2B, but not antalarmin. Moreover, mice exposed to alcohol showed increased sociability and preference for social novelty immediately after binge drinking. In contrast, 24 h after binge drinking mice exposed to alcohol presented anxiety-like and depression-like signs, which were reversed by antalarmin, but not astressin2B. However, mice exposed to alcohol did not show any significant change in social interaction after 24 h. The present study demonstrates that alcohol exerts different effects on anxiety-like, depression-like, and social behavior immediately and a day after binge drinking, and that the anxiolytic and antidepressant effects produced by binge drinking are mediated by CRF2, whereas the anxiety-like and depression-like signs observed the next day are promoted by CRF1.

The effects of CRF and the urocortins on the hippocampal acetylcholine release in rats.

Corticotropin-releasing factor (CRF) and the urocortins (Ucn1, Ucn2 and Ucn3) are structurally related neuropeptides which act via two distinct CRF receptors, CRF1 and CRF2, with putatively antagonistic effects in the brain. CRF and Ucn1 activate both CRF1 and CRF2, while Ucn2 and Ucn3 activate selectively CRF2. The aim of the present study was to investigate the effects of CRF, Ucn1, Ucn2 and Ucn3 on the hippocampal acetylcholine release through which they may modulate cognitive functions, including attention, learning and memory. In this purpose male Wistar rats were used, their hippocampus was isolated, dissected, incubated, superfused and stimulated electrically. The hippocampal slices were first pretreated with selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B, and then treated with non-selective CRF1 agonists, CRF or Ucn1, and selective CRF2 agonists, Ucn2 or Ucn3. The hippocampal acetylcholine release was increased significantly by CRF and Ucn1 and decreased significantly by Ucn2 and Ucn3. The increasing effect of CRF and Ucn1 was reduced significantly by antalarmin, but not astressin2B. In contrast, the decreasing effect of Ucn2 and Ucn3 was reversed significantly by the selective CRF2, but not the selective CRF1 antagonist. Our results demonstrate that CRF and Ucn1 stimulate the hippocampal acetylcholine release through CRF1, whereas Ucn2 and Ucn3 inhibit the hippocampal acetylcholine release through CRF2. Therefore, the present study suggests the existence of two apparently opposing CRF systems in the hippocampus, through which CRF and the urocortins might modulate cholinergic activity and thereby cognitive functions.

Changes in striatal dopamine release and locomotor activity following acute withdrawal from chronic nicotine are mediated by CRF1, but not CRF2, receptors.

The aim of the present study was to investigate the participation of corticotropin-releasing factor (CRF) receptors (CRF1 and CRF2) in the alterations of the dorsal and ventral striatal dopamine release and the vertical and horizontal locomotor activity observed in rats following chronic nicotine treatment and consequent acute withdrawal. In this purpose, male Wistar rats were exposed to repeated intraperitoneal (ip) injection with nicotine or saline solution for 7 days. On the 8th day or the 9th day the rats were injected intracerebroventricularly (icv) with selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B or saline solution. Thirty minutes after the icv injection the changes of the horizontal and vertical locomotor activity were recorded in an in vivo conducta system. Immediately after the behavioral recordings the changes of the dorsal and ventral striatal dopamine release were determined in an in vitro superfusion system. On the 8th day, the horizontal and vertical locomotor activities and the dorsal and ventral striatal dopamine releases increased significantly in nicotine-treated rats, compared to the saline-treated ones. On the 9th day, the horizontal locomotor activity and the dorsal striatal dopamine release increased significantly, whereas the vertical locomotor activity and the ventral striatal dopamine release decreased significantly in nicotine-treated rats, compared to the saline-treated ones. All the changes observed were attenuated significantly by antalarmin, but not astressin2B. The present study demonstrates that the changes of striatal dopamine release and locomotor activity observed following chronic nicotine treatment and consequent acute withdrawal are mediated by CRF1, but not CRF2, receptor.

[Ileal duplication: challenging differential diagnosis caused by a rare abnormality. Case report]. / Ileum duplex: egy ritka elváltozás okozta differenciáldiagnosztikai kihívás.

Gastrointestinal tract duplications (GSD) are rare congenital abnormalities. Eighty percent of GSDs are diagnosed before the age of two. These lesions can be seen anywhere from the oral cavity to the anus, but ileum is the most commonly affected site. Their clinical presentation is widely variable and unspecific, making the differential diagnosis really hard. Thus despite performing a long line of radiological scans, the diagnosis can be made during a surgery and by the pathologist. A 23-year-old female patient presented at the emergency room (ER) with abdominal cramps. Examinations revealed an unidentified intraabdominal mass. This could not been identified through the next years despite having tons of examinations: intravaginal and abdominal ultrasonographies, CT and MRI scans, colonoscopies, laparoscopies, surgical, gynecological and gastroenterological visits. Amongst the diagnoses were: ovarian cyst, bowel enlargement, Crohn's disease. Due to the latter, she received therapy which temporarily eased her symptoms. But after these, because of abdominal pain, fever and an ultrasonography that showed an intramural abscess in her abdomen, she went through a surgery having an ileocecal resection. Pathological examination showed a duplication of the ileum that might have caused her symptoms all through the years. Despite facing this rare abnormality, it is important to keep this in mind in differentiating abdominal symptoms. It is true that in no case there could be a diagnosis made without surgery, it raises attention to the importance of precise medical history taking and also cooperation between specialties. Orv Hetil. 2018; 159(52): 2217-2221.

Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice.

The aim of the present study was to investigate the effects of the selective agonists of the corticotropin-releasing factor (CRF) 2 receptor, urocortin 2 (UCN 2) and urocortin 3 (UCN 3), on the anxiety- and depression-like signs induced by acute nicotine withdrawal in mice. In order to do so, male CFLP mice were exposed for 7 days to repeated intraperitoneal (IP) injection with nicotine or saline solution and 1day of acute withdrawal and then a single intracerebroventricular (ICV) injection with UCN 2, UCN 3 or saline solution. After 30min the mice were observed in an elevated plus-maze test or a forced swim test, for anxiety- and depression-like behavior. After 5min of testing, the plasma corticosterone concentration reflecting the activity of the hypothalamic-pituitary-adrenal (HPA) axis was also determined by a chemo-fluorescent method. Half of the animals were treated ICV and evaluated on the 8th day, the other half on the 9th day. On the 8th day, nicotine-treated mice presented signs of anxiolysis and depression, but no significant elevation of the plasma corticosterone concentration. On the 9th day, nicotine-treated mice exhibited signs of anxiety and depression and a significant increase of the plasma corticosterone levels. Central administration of UCN 2 or UCN 3 ameliorated the anxiety- and depression-like state including the hyperactivity of the HPA axis, developed during acute withdrawal following chronic nicotine treatment. The present study suggests that selective CRF2 receptor agonists could be used as a therapy in nicotine addiction.