title: Lack of Intrinsic GABAergic Connections in the Thalamic Reticular Nucleus of the Mouse.
abstract: It is generally thought that neurons in the thalamic reticular nucleus (TRN) form GABAergic synapses with other TRN neurons and that these interconnections are important for the function of the TRN. However, the existence of such intrinsic connections is controversial. We combine two complementary approaches to examine intrinsic GABAergic connections in the TRN of the mouse. We find that optogenetic stimulation of TRN neurons and their axons evokes GABAergic IPSCs in TRN neurons in mice younger than 2 weeks of age but fails to do so after that age. Blocking synaptic release from TRN neurons through conditional deletion of vesicular GABA transporter has no effect on spontaneous IPSCs recorded in TRN neurons aged 2 weeks or older while dramatically reducing GABAergic transmission in thalamic relay neurons. These results demonstrate that except for a short period after birth, the TRN of the mouse lacks intrinsic GABAergic connections.
  
  
  
  The thalamic reticular nucleus has a critical role in modulating information transfer from the thalamus to the cortex. It has been proposed that neurons in the thalamic reticular nucleus are interconnected through GABAergic synapses and that these connections serve important functions. Our results show that except for the first 2 weeks after birth, the thalamic reticular nucleus of the mouse lacks intrinsic GABAergic connections.
authors.affiliation: The Jackson Laboratory, Bar Harbor, Maine 04609.
authors.forename: Guoqiang
authors.identifier: 0000-0003-3285-7773
authors.initials: G
authors.lastname: Hou
authors.affiliation: The Jackson Laboratory, Bar Harbor, Maine 04609.
authors.forename: Alison G
authors.identifier: 0000-0002-9402-7786
authors.initials: AG
authors.lastname: Smith
authors.affiliation: The Jackson Laboratory, Bar Harbor, Maine 04609 zhongwei.zhang@jax.org.
authors.forename: Zhong-Wei
authors.identifier: 0000-0001-7165-6216
authors.initials: ZW
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000075402:Channelrhodopsins; D004558:Electric Stimulation; D005260:Female; D059330:GABAergic Neurons / Q000502:physiology*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000502:physiology*; D008164:Luminescent Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009415:Nerve Net / Q000378:metabolism / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010320:Parvalbumins / Q000235:genetics; D018408:Patch-Clamp Techniques; D013787:Thalamic Nuclei / Q000166:cytology*; D050495:Vesicular Inhibitory Amino Acid Transport Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D000075402:Channelrhodopsins; D008164:Luminescent Proteins; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D050495:Vesicular Inhibitory Amino Acid Transport Proteins; C492244:Viaat protein, mouse; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1
keywords: GABA; mouse; optogenetics; parvalbumin; reticular nucleus; thalamus