Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling.

γ-aminobutyric acid (GABA) begins as the key excitatory neurotransmitter in newly forming circuits, with chloride efflux from GABA type A receptors (GABARs) producing membrane depolarization, which promotes calcium entry, dendritic outgrowth and synaptogenesis. As development proceeds, GABAergic signaling switches to inhibitory hyperpolarizing neurotransmission. Despite the evidence of impaired GABAergic neurotransmission in neurodevelopmental disorders, little is understood on how agonist-dependent GABAR activation controls the formation and plasticity of GABAergic synapses.

Using an α-bungarotoxin binding site tag to study GABA A receptor membrane localization and trafficking.

It is increasingly evident that neurotransmitter receptors, including ionotropic GABA A receptors (GABAAR), exhibit highly dynamic trafficking and cell surface mobility(1-7). To study receptor cell surface localization and endocytosis, the technique described here combines the use of fluorescent α-bungarotoxin with cells expressing constructs containing an α-bungarotoxin (Bgt) binding site (BBS). The BBS (WRYYESSLEPYPD) is based on the α subunit of the muscle nicotinic acetylcholine receptor, which binds Bgt with high affinity(8,9).

Describing local boards of health: insights from the 2008 National Association of Local Boards of Health Survey.

Objectives: We examined findings from the 2008 National Association of Local Boards of Health Survey to provide information about this understudied entity to the public health community.

Methods: The survey instrument consisted of 196 items covering five parts: (1) demographics; (2) composition and organizational structure; (3) roles, responsibilities, and authorities; (4) telecommunications infrastructure; and (5) concerns and needs. The survey was sent to chairs of local boards of health (LBHs) in 2008 (n = 3,276).