GAT-1 is a sodium-coupled neurotransmitter transporter responsible for moving g-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.
We have constructed a conjugate between an antibody to an extracellular domain of GAT-1 and saporin, the ribosome- inactivating protein. This construct, GAT1-SAP (Cat. #IT-32) has been used to specifically remove GABAergic neurons of the anterior bed nucleus of the stria terminalis (1) and the medial septum and diagonal band of rats (2). Figure 1 shows the specificity of the targeted toxin, with parvalbumin-positive neurons being drastically reduced, while most cholinergic neurons are spared.
Coming soon is our vesicular GABA transporter-saporin construct to increase the ability to eliminate specific populations of GABAergic neurons.
1. Radley JJ, Gosselink KL, Sawchenko PE. (2009) A discrete GABAergic relay mediates medial prefrontal cortical inhibition of the neuroendocrine stress response. J Neurosci 29(22):7330-40.
2. Pang KC, Jiao X, Sinha S, Beck KD, Servatius RJ. (2010) Damage of GABAergic neurons in the medial septum impairs spatial working memory and extinction of active avoidance: Effects on proactive interference. Hippocampus. Epub, May 17.
GAT1-SAP, Cat. #IT-32
available in these sizes: 25 micrograms, 100 micrograms, and 250 micrograms