GAT-1 is a sodium-coupled neurotransmitter transporter responsible for moving gamma-aminobutyric acid (GABA) across cell membranes. GABA is the predominant inhibitory neurotransmitter in the mammalian central nervous system. GAT-1 is widely distributed in both the central and peripheral nervous systems. GAT-1 and GABA are present in numerous neuronal pathways, some of which are implicated in epilepsy, sleep disorders, neuropathic pain, and attention deficit disorders. GAT1-SAP recognizes cells that express the GABA-1 transporter, GAT-1 in rat. The peptide used as an antigen has 100% sequence homology between rat, human, mouse, and bovine GAT-1.
GAT1-SAP is a chemical conjugate of an affinity-purified rabbit polyclonal antibody against a GAT-1 peptide sequence and the ribosome-inactivating protein, saporin. It specifically eliminates cells expressing GAT-1.
GAT1-SAP is available individually (Cat. #IT-32) or as a kit (Cat. #KIT-32) which includes GAT1-SAP and Rabbit IgG-SAP (Cat. #IT-35).
keywords: GAT-1, GABA-1 transporter, gaba, gamma-aminobutyric acid, γ-aminobutyric acid, Anti-GAT-1, Anti-GAT1, Anti-GABA-1 transporter, Anti-gamma-aminobutyric acid-1 transporter, Anti-γ-aminobutyric acid-1 transporter, saporin, GABAergic neurons, sleeping, wakefulness, pain, brain, neuroscience
Expression of NR2B subunit of the NMDA receptor and spatial long-term memory in medial septal lesioned rats
Kruashvili L, Dashniani M, Beselia G, Chkhikvishvili N (2018) Expression of NR2B subunit of the NMDA receptor and spatial long-term memory in medial septal lesioned rats. FENS 2018 Abstracts F038. Federation of European Neuroscience Societies, Berlin, Germany.
Summary: The present study was designed to investigate the effect of selective immunolesions of cholinergic and GABA- ergic SH projection neurons (using 192 IgG-saporin and GAT-1 saporin, respectively) on spatial memory assessed in water maze and the N-methyl-D-aspartate (NMDA) receptor GluN2B subunit expression in the rat hippocampus. Animals were tested in a standard Morris water maze. We found that immunolesion of medial septal cholinergic neurons did not affect spatial learning as exhibited by a decreased latency to find the hidden platform across the eight training trials. In contrast, rats with immunolesions of medial septal GABAergic neurons did not show a decreased latency across training trials in water maze. Trained control rats spent significantly longer than chance (15 s) performances such as swimming time in test sector (where the hidden platform was located). Moreover, they spent significantly longer in test sector than in the opposite sector, confirming the establishment of long-term memory. In contrast, the preference for test sector was abolished in medial septal immunolesioned rats. Because Saporin treated rats learned the location of the hidden platform during training, the results suggest that saporin treated rats could not remember the training a day later. We found that the expression level of NR2B subunit of NMDA receptor in the hippocampus was decreased significantly in the GAT-1 treated group compared with the control and saporin treated groups. In conclusion, our findings suggest that immunolesion of medial septal GABAergic neurons can interrupt hippocampus-dependent spatial learning, possibly through modulation of NMDA receptor subunit expression in the hippocampus.
Related Products: 192-IgG-SAP (Cat. #IT-01), GAT1-SAP (Cat. #IT-32)
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