This notion supports the emerging theory that the functional consequences of the distal effects of lesions go beyond simple deafferentation. Specifically, some frontal cortical regions exhibit hypersensitivity to deafferentation that is only detected during behavioral and/or

physiological demand. “
“Cholinergic, GABAergic and glutamatergic projection neurons of the basal forebrain (BF) innervate widespread regions of the neocortex and are thought to modulate learning and attentional processes. Although it is known that neuronal cell types E7080 concentration in the BF exhibit oscillatory firing patterns, whether the BF as a whole shows oscillatory field potential activity, and whether such neuronal patterns relate to components of cognitive tasks, has yet to be determined. To this end, local field potentials (LFPs) were recorded from the BF of rats performing an associative

learning task wherein neutral objects were paired with differently valued reinforcers (pellets). Over time, rats developed preferences for the different objects based on pellet-value, indicating that the pairings had been well learned. LFPs from all rats revealed robust, short-lived bursts of beta-frequency oscillations (∼25 Hz) around the time of object encounter. Beta-frequency LFP events were found to be learning-dependent, with beta-frequency peak amplitudes significantly greater on the first day of the task when ERK inhibitor object–reinforcement pairings were novel than on the last day when pairings were well learned. The findings indicate that oscillatory bursting field potential activity occurs in the BF in freely behaving animals. Furthermore, the temporal distribution of these bursts suggests that they are probably relevant to associative learning. “
“We have shown that delta opioid receptor (DOPR)-mediated analgesia was enhanced in the complete Freund’s adjuvant (CFA) model of inflammation. This effect is thought to originate from translocation of DOPR in the plasma membrane

of dorsal root ganglia and spinal cord neurons. Among the putative mechanisms involved in the regulation of DOPR trafficking, an interaction with substance P (SP) in large dense-core vesicles has been described as an essential event for the externalization of DOPR. As we have previously observed that membrane find more DOPRs were upregulated in small- and medium-sized neurons under inflammatory pain conditions (whereas SP is mainly expressed by small dorsal root ganglia neurons), we raised the hypothesis that an SP-independent mechanism mediates DOPR trafficking and functional emergence in the CFA model. Therefore, we investigated the role of SP in DOPR-mediated analgesia by using preprotachykinin A (precursor of SP) knockout mice (PPTA−/−) in the CFA model of inflammation. First, we confirmed that PPTA−/− mice are not expressing SP and have a similar level of CFA-induced inflammation as wildtype mice.