Author name: Kristen Hartman

Toolbox: vGAT Products

ATS is pleased to present a new product line specific for the vesicular GABA transporter (vGAT) protein. vGAT mediates both the accumulation of GABA into synaptic vesicles and its release from nerve terminals. vGAT is expressed in nerve endings of GABAergic neurons throughout the CNS. The GABAergic system is crucial to the development and functional

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From the President: A Sigh is (Not) Just a Sigh . . .

The fundamental things apply. “The Peptidergic Control Circuit for Sighing,” recently published in the prestigious journal Nature, has made us rethink our fundamental belief that sighs are only “long, deep breaths expressing sadness, relief or exhaustion.” Often prompting someone to say, “What’s wrong?” As it turns out, sighs “also occur spontaneously every few minutes to

From the President: A Sigh is (Not) Just a Sigh . . . Read More »

Cover Article: Cerebral cholinergic lesion reduces operant responses to unpleasant thermal stimuli

by Ronald G. Wiley, M.D., Ph.D., Departments of Neurology and Pharmacology, Vanderbilt University, Nashville, TN  and C. J. Vierck, Department of Neuroscience, McKnight Brain Institute, University of Florida College of Medicine, Gainesville, FL, USA Degeneration of the cholinergic basal forebrain (CBF: medial septum, diagonal band of Broca, nucleus basalis of Meynert/substantia innominata) is a prominent

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Locus coeruleus and tuberomammillary nuclei ablations attenuate hypocretin/orexin antagonist-mediated rem sleep.

Schwartz M, Nguyen A, Warrier D, Palmerston J, Thomas A, Morairty S, Neylan T, Kilduff T (2016) Locus coeruleus and tuberomammillary nuclei ablations attenuate hypocretin/orexin antagonist-mediated rem sleep. eNeuro 3:ENEURO.0018-0016.2016. doi: 10.1523/ENEURO.0018-16.2016 Summary: To examine the mechanism by which the Orexin 1r/Orexin 2r antagonist almorexant decreases wakefulness and increases NREM and REM sleep the authors

Locus coeruleus and tuberomammillary nuclei ablations attenuate hypocretin/orexin antagonist-mediated rem sleep. Read More »

Substituting mouse transcription factor Pou4f2 with a sea urchin orthologue restores retinal ganglion cell development.

Mao C, Agca C, Mocko-Strand J, Wang J, Ullrich-Lüter E, Pan P, Wang S, Arnone M, Frishman L, Klein W (2016) Substituting mouse transcription factor Pou4f2 with a sea urchin orthologue restores retinal ganglion cell development. Proc Biol Sci 283:20152978. doi: 10.1098/rspb.2015.2978 PMID: 26962139 Summary: Pou4f2 is Pou domain transcription factor that is essential for

Substituting mouse transcription factor Pou4f2 with a sea urchin orthologue restores retinal ganglion cell development. Read More »

Dynamics of spinal microglia repopulation following an acute depletion.

Yao Y, Echeverry S, Shi X, Yang M, Yang Q, Wang G, Chambon J, Wu Y, Fu K, De Koninck Y, Zhang J (2016) Dynamics of spinal microglia repopulation following an acute depletion. Sci Rep 6:22839. doi: 10.1038/srep22839 Summary: This study confirms that similar to microglia in the brain, spinal microglia can repopulate rapidly following

Dynamics of spinal microglia repopulation following an acute depletion. Read More »

Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus.

Fei Y, Wang X, Chen S, Zhou Q, Zhang C, Li Y, Sun L, Zhang L (2016) Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus. Neurochem Res 41:1651-1661. doi: 10.1007/s11064-016-1880-6 Summary: The researchers investigated whether the CSF-contacting nucleus contributed to descending pain modulation in normal and neuropathic rats, and

Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus. Read More »

Functional characterization of a mouse model for central post-stroke pain.

Gritsch S, Bali K, Kuner R, Vardeh D (2016) Functional characterization of a mouse model for central post-stroke pain. Mol Pain 12:1744806916629049. doi: 10.1177/1744806916629049 Summary: While clinical evidence has pointed toward central pain pathway dysfunction in central post-stroke pain (CPSP), the underlying mechanisms have not been defined. In this work the authors created a mouse

Functional characterization of a mouse model for central post-stroke pain. Read More »

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