(C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“The serotonin(1B) receptor (5-HT1BR) plays a role in cognitive processes that also involve glutamatergic neurotransmission via amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors. Accumulating experimental evidence

also highlights the involvement of 5-HT(1B)Rs in several neurological disorders. Consequently, the 5-HT1BR is increasingly implicated as a potential therapeutic target for intervention in cognitive dysfunction. Within the hippocampus, a brain region critical to cognitive processing, populations of pre- and post-synaptic 5-HT(1B)Rs have been identified. Thus, 5-HT(1B)Rs could have a role in the modulation of hippocampal pre- and post-synaptic conductance. Previously, we demonstrated www.selleckchem.com/products/wzb117.html colocalization of 5-HT(1B)Rs with the N-methyl-D-aspartate (NMDA) receptor subunit NR1 in a subpopulation of granule cell dendrites (Peddie et Selleck MX69 al. [53]). In this study, we have examined the cellular and subcellular distribution of 5-HT(1B)Rs with the AMPA receptor subunit GluR2. Of 5-HT1BR positive profiles, 28% displayed colocalization with GluR2. Of these, 87% were dendrites, corresponding to 41% and 10% of all 5-HT1BR labeled or GluR2 labeled dendrites, respectively. Dendritic labeling was both cytoplasmic and membranous but was not usually associated with synaptic sites. Colocalization within dendritic spines and axons

was comparatively rare. These findings indicate that within the dentate gyrus molecular layer, dendritic 5-HT(1B)Rs are expressed predominantly on GluR2 negative granule cell processes. However, a subpopulation of 5-HT(1B)Rs is expressed on GluR2 positive dendrites. Here, it is suggested that activation of the 5-HT1BR may play a role in the modulation of AMPA receptor mediated conductance, further supporting the notion that the 5-HT1BR represents an interesting therapeutic target for modulation of cognitive function. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Locomotor sensitization is the progressive and enduring enhancement of locomotion induced

by stimulants such as drugs, which alter rodent locomotion in a long-standing manner. The dopamine D3 receptor has been reported to play a role Smoothened in morphine addiction. The aim of the present study was to investigate the role of dopamine D3 receptor in the morphine induced locomotor sensitization using dopamine D3 receptor knock-out mice. The dopamine D3 receptor knock-out mice did not display an enhanced behavioral response to acute morphine administration or develop an increased rate of locomotor sensitization to intermittent morphine administration. When 2 mg/kg naloxone was co-administered with 10 mg/kg morphine, morphine-induced locomotion sensitization in wild-type mice was significantly blocked while the locomotion in the D3 receptor knock-out mice was decreased.