Abstract
Both, the anterior bed nucleus of the stria terminalis (BNST) and the neuropeptide Y (NPY) system are involved in shaping fear and defensive responses that adapt the organism to potentially life-threatening conditions. NPY is expressed in the BNST but NPY-expressing neurons in this critical hub in the stress response network have not been addressed before. Therefore, we performed whole-cell patch-clamp recordings in acute slices of anterior BNST from Npy-hrGFP transgenic mice to identify and characterize NPY-expressing neurons. We show that NPY-positive and NPY-negative neurons in anterior BNST match the previous classification scheme of type I (Regular Spiking), type II (Low-Threshold Bursting), and type III (fast Inward Rectifying) cells, although the proportion of these physiological phenotypes was similar within both neuronal subpopulations. However, NPY-positive and NPY-negative neurons possessed distinct intrinsic electrophysiological properties. NPY-positive neurons displayed higher input resistance and lower membrane capacitance, corresponding to small cell bodies and shorter less ramified dendrites, as compared to their NPY-negative counterparts. Furthermore, NPY-positive neurons generated higher frequent series of action potentials upon membrane depolarization and displayed significantly lower GABAA receptor-mediated synaptic responsiveness during evoked, spontaneous, and elementary synaptic activity. Taken together, these properties indicate an overall state of high excitability in NPY-positive neurons in anterior BNST. In view of the role of the anterior BNST in anxiety- and stress-related behaviors, these findings suggest a scenario where NPY-positive neurons are preferentially active and responsive to afferent inputs, thereby contributing to adaptation of the organism to stressful environmental encounters.
Highlights
Neuropeptide Y (NPY) is a 36 amino acid neuropeptide, which exists across all vertebrates (Tatemoto, 1982)
All experiments were performed in acute slices of bed nucleus of the stria terminalis (BNST), prepared from Npy-hrGFP transgenic mice (NPY-green fluorescent protein (GFP) mice), which reliably show hrGFP-expression in neuropeptide Y (NPY)-neurons in various regions of the brain, including arcuate nucleus, dentate gyrus, cortex and striatum, as well as in axons of the hypothalamic paraventricular nucleus (PVN), corpus callosum and the olfactory bulb (Partridge et al, 2009; van den Pol et al, 2009)
Single cell reverse transcriptase reaction (RT)-polymerase chain reaction (PCR) performed in a subpopulation of recorded BNST neurons revealed the presence of NPY in 14 of 18 GFP-positive neurons, while NPY was lacking in almost all (14 of 15) GFP-negative neurons
Summary
Neuropeptide Y (NPY) is a 36 amino acid neuropeptide, which exists across all vertebrates (Tatemoto, 1982). NPY is implicated in mechanisms of fear learning and memory (Heilig, 2004; Tasan et al, 2016). More recently it has been shown that various NPY receptor subtypes contribute to fear memory and extinction (for review see: Tasan et al, 2016). Stimulation of Y2 receptors increases (Bacchi et al, 2006), whilst deletion of Y2 receptors reduces anxiety-like responses (Tasan et al, 2010). By comparison, are controlled by combined action of Y1 and Y2 receptors, as deduced from studies in mice lacking NPY and Y1/Y2 receptors (Verma et al, 2012)
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