Brain research
-
Clinical Trial
Affective modulation of somatosensory-evoked potentials elicited by tactile stimulation.
The present investigation was aimed to evaluate the influence of emotional valence on brain correlates of non-painful somatosensory processing. For this purpose, we examined changes on the somatosensory-evoked potentials (SEP) elicited by frequent and deviant tactile stimuli (probability 14%) when subjects were viewing affective pictures. Twenty healthy volunteers aged between 19 and 47 years old participated in the study. ⋯ Furthermore, larger SEP amplitudes were obtained in response to the deviant than to the frequent stimuli. In addition, unpleasant pictures elicited larger P200 amplitudes of the VEP than pleasant. Data suggest that affective stimuli may modulate the early processing of somatosensory information in the brain, probably reflecting the existence of an adaptive perceptual/attentional mechanism to motivationally relevant stimuli.
-
Previous studies using non-specific serotonergic agonists and antagonists have shown the importance of serotonergic inhibitory mechanisms in the lateral parabrachial nucleus (LPBN) for controlling sodium and water intake. In the present study, we investigated whether the serotonergic 5-HT(1A) receptor subtype in the LPBN participates in this control. Male Holtzman rats had cannulas implanted bilaterally into the LPBN. ⋯ Injections of 8-OH-DAPT (0.1 microg/0.2 microl) into the LPBN also increased 0.3 M NaCl intake induced by 24-h sodium depletion (furosemide, 20 mg/kg bw plus 24 h of sodium-free diet). Serotonin (5-HT, 20 mug/0.2 mul) injected alone or combined with 8-OH-DPAT into the LPBN reduced 24-h sodium depletion-induced 0.3 M NaCl intake. Therefore, the activation of serotonergic 5-HT(1A) receptors in the LPBN increases stimulated hypertonic NaCl and water intake, while 5-HT injections into the LPBN reduce NaCl intake and prevent the effects of serotonergic 5-HT(1A) receptor activation.
-
Recently accumulating evidence demonstrates the presence of very slow activity (< 0.5 Hz) in structures of the visual system of the brain. It was found in our laboratory earlier that specific and significant alterations of this activity (mainly in the domain of seconds) occurred in the visual system in response to illumination changes. The present study was performed in order to test the hypothesis that potentials in the domain of seconds reflect specific and direct interactions of the lateral geniculate nucleus (LGN) and the primary visual cortex (V1) during neural processing of sensory information. ⋯ Significant responses were detected in the both LGN and V1 multisecond activities (pre- vs. post-stimulus recordings). The changes were opposite in direction in the LGN and V1. The obtained results support the conclusion that very slow activity in the domain of seconds reflects specific mechanisms of forward and backward interactions within the LGN-V1 thalamic-cortical-thalamic system, while multisecond activity relates to global neuronal activity fluctuations.
-
Mild hypothermia improves survival and neurological outcome after cardiac arrest, as well as increasing activation of the extracellular-signal-regulated kinase (ERK) in hippocampus. ERK signaling is involved in neuronal growth and survival. We tested the hypothesis that the beneficial effects of hypothermia required ERK activation. ⋯ However, survival, neurological score and histology did not differ between U0126 and vehicle-treated rats after cardiac arrest. Therefore, a dose of U0126 sufficient to inhibit biochemical markers of ERK signaling in hippocampus does not alter the beneficial effects of hypothermia induced after resuscitation in rats and did not affect recovery of normothermia-treated rats. These results suggest that hypothermia-induced improvement in outcomes does not require ERK activation.
-
Comparative Study
Antinociception following application of DAMGO to the basolateral amygdala results from a direct interaction of DAMGO with Mu opioid receptors in the amygdala.
Previous studies from our laboratory have shown that application of the mu opioid agonist DAMGO into the basolateral region of the amygdala (BLA) suppresses the radiant heat tail flick (TF) reflex in anesthetized rats. This antinociceptive effect can be blocked by lesions of brainstem regions such as the periaqueductal gray (PAG) or the rostral ventromedial medulla (RVM) or by functional inactivation of neurons in these regions, suggesting the activation of brainstem-descending antinociceptive systems from the amygdala. However, little is known about the direct interaction of DAMGO with mu receptors in the amygdala. ⋯ Rats pretreated with the non-selective opioid antagonist naltrexone (1.25-3.75 microg/0.25 microl per side) or the G protein inhibitor pertussis toxin (0.25 microg) failed to show inhibition of TF reflexes following infusion of DAMGO (0.168-0.50 microg), indicating that DAMGO works through G-protein-coupled opioid receptors in the BLA. Furthermore, pretreatment with the mu antagonist beta-FNA (1.00-2.00 microg) attenuated antinociception induced by DAMGO injection, suggesting DAMGO's action on mu receptors in the BLA. Accordingly, we confirm a direct interaction of DAMGO with G-protein-coupled mu receptors in the BLA contributing to induction of opioid antinociception in the amygdala.