A behavioral model of mild stress also produced mechanical hyperalgesia, which was blocked by inactivation of either the DMH or the RVM. The neuropeptide cholecystokinin (CCK) acts in the RVM to enhance nociception and is abundant in the DMH. Using a retrograde tracer and immunohistochemical labeling, we determined that CCK-expressing neurons in the DMH are the only significant supraspinal source of CCK in the RVM. However, not all neurons projecting from the DMH to the RVM contained CCK, and microinjection of the CCK2 receptor
antagonist YM022 in the RVM did not interfere with SIH, suggesting that selleck chemical transmitters in addition to CCK play a significant role in this connection during acute stress. While the RVM has
a well-established role in facilitation of nociception, the DMH, with its well-documented role in stress, may also be engaged in a number of chronic or abnormal pain states. Taken as a whole, these findings establish PD173074 an anatomical and functional connection between the DMH and RVM by which stress can facilitate pain. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Functional disconnectivity during the resting state has been observed in subjects with major depressive disorder (MDD), and in subjects at high genetic risk for major depression during task performance. It is hypothesized that functional impairments in certain brain areas are present in patients with MDD and in their first-degree relatives. To test this hypothesis, an analysis of regional Selleck AZD8186 homogeneity (ReHo) of the whole brain was performed on 45 subjects. Compared with the control group, subjects with MDD and those at high risk for MDD exhibited significantly decreased ReHo in the right
insula and in the left cerebellum. These abnormalities may play an important role in the pathophysiology of depression. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“In the current study the link among the gamma-hydroxybutyrate (GHB)/pentylenetetrazole (PTZ)-induced absence-like seizures and concomitant decreases in the core temperature, as well as electroencephalographic (EEG) activity during rewarming from deep hypothermia produced by a drug-free protocol were investigated. During the rewarming period after deep cooling, most Wistar rats suffered from bilaterally synchronous spike and waves with no or mild behavioral correlates. Spike and wave seizures were temperature-dependent and were initially registered when body temperature (T-b) reached 25-27 degrees C, but mostly during the mild hypothermia of 0.3-1.3 degrees C (T-b of 36.3-37.3 degrees C). In chemical absence models, spike and wave discharges were also closely accompanied by mild systemic hypothermia, as both PTZ- and GHB-induced temperature decreases ranged from about 1-1.4 degrees C respectively, together with EEG markers of absence activity.