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Alexa Fluor 594-AffiniPure Donkey Anti-Goat IgG (H+L) antibody

RRID:AB_2340432

Antibody ID

AB_2340432

Target Antigen

Goat IgG (H+L)

Proper Citation

(Jackson ImmunoResearch Labs Cat# 705-585-003, RRID:AB_2340432)

Clonality

polyclonal antibody

Comments

Originating manufacturer of this product

Vendor

Jackson ImmunoResearch Labs Go To Vendor

Cat Num

705-585-003

Astrocytic Activation Generates De Novo Neuronal Potentiation and Memory Enhancement.

  • Adamsky A
  • Cell
  • 2018 Jun 28

Literature context:


Abstract:

Astrocytes respond to neuronal activity and were shown to be necessary for plasticity and memory. To test whether astrocytic activity is also sufficient to generate synaptic potentiation and enhance memory, we expressed the Gq-coupled receptor hM3Dq in CA1 astrocytes, allowing their activation by a designer drug. We discovered that astrocytic activation is not only necessary for synaptic plasticity, but also sufficient to induce NMDA-dependent de novo long-term potentiation in the hippocampus that persisted after astrocytic activation ceased. In vivo, astrocytic activation enhanced memory allocation; i.e., it increased neuronal activity in a task-specific way only when coupled with learning, but not in home-caged mice. Furthermore, astrocytic activation using either a chemogenetic or an optogenetic tool during acquisition resulted in memory recall enhancement on the following day. Conversely, directly increasing neuronal activity resulted in dramatic memory impairment. Our findings that astrocytes induce plasticity and enhance memory may have important clinical implications for cognitive augmentation treatments.

Funding information:
  • Canadian Institutes of Health Research - DP1 DA028871(Canada)

Synaptotagmin 4 Regulates Pancreatic β Cell Maturation by Modulating the Ca2+ Sensitivity of Insulin Secretion Vesicles.

  • Huang C
  • Dev. Cell
  • 2018 May 7

Literature context:


Abstract:

Islet β cells from newborn mammals exhibit high basal insulin secretion and poor glucose-stimulated insulin secretion (GSIS). Here we show that β cells of newborns secrete more insulin than adults in response to similar intracellular Ca2+ concentrations, suggesting differences in the Ca2+ sensitivity of insulin secretion. Synaptotagmin 4 (Syt4), a non-Ca2+ binding paralog of the β cell Ca2+ sensor Syt7, increased by ∼8-fold during β cell maturation. Syt4 ablation increased basal insulin secretion and compromised GSIS. Precocious Syt4 expression repressed basal insulin secretion but also impaired islet morphogenesis and GSIS. Syt4 was localized on insulin granules and Syt4 levels inversely related to the number of readily releasable vesicles. Thus, transcriptional regulation of Syt4 affects insulin secretion; Syt4 expression is regulated in part by Myt transcription factors, which repress Syt4 transcription. Finally, human SYT4 regulated GSIS in EndoC-βH1 cells, a human β cell line. These findings reveal the role that altered Ca2+ sensing plays in regulating β cell maturation.

Funding information:
  • Cancer Research UK - 12183(United Kingdom)
  • NIDDK NIH HHS - R01 DK050203()
  • NIDDK NIH HHS - R01 DK090570()

Innate-like Cytotoxic Function of Bystander-Activated CD8+ T Cells Is Associated with Liver Injury in Acute Hepatitis A.

  • Kim J
  • Immunity
  • 2018 Jan 16

Literature context:


Abstract:

Acute hepatitis A (AHA) involves severe CD8+ T cell-mediated liver injury. Here we showed during AHA, CD8+ T cells specific to unrelated viruses became activated. Hepatitis A virus (HAV)-infected cells produced IL-15 that induced T cell receptor (TCR)-independent activation of memory CD8+ T cells. TCR-independent activation of non-HAV-specific CD8+ T cells were detected in patients, as indicated by NKG2D upregulation, a marker of TCR-independent T cell activation by IL-15. CD8+ T cells derived from AHA patients exerted innate-like cytotoxicity triggered by activating receptors NKG2D and NKp30 without TCR engagement. We demonstrated that the severity of liver injury in AHA patients correlated with the activation of HAV-unrelated virus-specific CD8+ T cells and the innate-like cytolytic activity of CD8+ T cells, but not the activation of HAV-specific T cells. Thus, host injury in AHA is associated with innate-like cytotoxicity of bystander-activated CD8+ T cells, a result with implications for acute viral diseases.

Funding information:
  • Intramural NIH HHS - (United States)

Inferior olivary projection to the zebrin II stripes in lobule IXcd of the pigeon flocculus: A retrograde tracing study.

  • Wylie DR
  • J. Comp. Neurol.
  • 2017 Oct 1

Literature context:


Abstract:

Zebrin II (ZII; a.k.a. aldolase C) is expressed heterogeneously in Purkinje cells (PCs) such that there are sagittal stripes of high expression (ZII+) interdigitated with stripes of little or no expression (ZII-). The pigeon flocculus receives visual-optokinetic information and is important for generating compensatory eye movements. It consists of 4 sagittal zones based on PC complex spike activity (CSA) in response to rotational optokinetic stimuli. There are two zones where CSA responds best to rotation about the vertical axis (VA), interdigitated with two zones where CSA responds best to rotation about an horizontal axis (HA). These optokinetic zones relate to the ZII stripes in folium IXcd of the flocculus, such that an optokinetic zone spans a ZII+/- pair: the HA zones span the P5+/- and P7+/- ZII stripe pairs, whereas the VA zones correspond to ZII stripe pairs P4+/- and P6+/-. In the present study, we used fluorescent retrograde tracing to determine the olivary inputs to the ZII+ and ZII- stripes within the functional pairs. We found that separate but adjacent areas of the medial column of the inferior olive (mcIO) project to the ZII+ and ZII- stripes within each of the functional pairs. Thus, although a ZII+/- stripe pair represents a functional unit in the pigeon flocculus insofar as the CSA of all PCs in the stripe pair encodes similar sensory information, the olivary inputs to the ZII+ and ZII- stripes arise from different, although adjacent, regions of the mcIO.