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Devoto P, Flore G, Saba P, Frau R, Gessa G (2015) Selective inhibition of dopamine-beta-hydroxylase enhances dopamine release from noradrenergic terminals in the medial prefrontal cortex. Brain Behav 5:e00393. doi: 10.1002/brb3.393

Summary: Dopamine-beta-hydroxylase (DBH) is a neuronal enzyme that is a potential target for the treatment of cocaine abuse, alcohol dependence, and eating disorders. Here the authors administered 5 μg of icv Anti-DBH-SAP (Cat. #IT-03) to rats, and assessed the effect of the dopaminergic lesion on levels of extracellular dopamine. Mouse IgG-SAP (Cat. #IT-18) and saporin (Cat. #PR-01) were used as controls. Extracellular levels of dopamine were significantly increased in both lesioned animals and those treated with the DBH inhibitor nepicastat. Clonadine could reverse the nepicastat effect, but not the effect of Anti-DBH-SAP treatement. The data demonstrate a mechanism for the synergistic effect of cocaine on nepicastat-induced dopamine release.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18), Saporin (Cat. #PR-01)

Araldi D, Ferrari L, Levine J (2015) Repeated mu-opioid exposure induces a novel form of the hyperalgesic priming model for transition to chronic pain. J Neurosci 35:12502-12517. doi: 10.1523/JNEUROSCI.1673-15.2015

Summary: Repeated administration of mu-opioid receptor agonists can lead to persistent mechanical hyperalgesia. One current hypothesis is that a form of hyperalgesic priming is triggered by the repeated activation of these receptors. Classic hyperalgesic priming is associated with signaling via protein kinase Cε (PKε), which is mediated by isolectin-B4+ (IB4) nociceptors. In this work the authors eliminated the IB4+ nociceptors with a 3.2 μg intrathecal injection of recombinant IB4-SAP (Cat. #IT-10). The authors found that hyperalgesic priming induced through the use of DAMGO was dependent on protein kinase A activation rather than activation of PKε. This work demonstrates a novel model for hyperalgesic priming transitioning to chronic pain.

Related Products: IB4-SAP (Cat. #IT-10)

Riazifar H, Sun G, Wang X, Rupp A, Vemaraju S, Ross-Cisneros F, Lang R, Sadun A, Hattar S, Guan M, Huang T (2015) Phenotypic and functional characterization of Bst+/- mouse retina. Dis Model Mech 8:969-976. doi: 10.1242/dmm.018176 PMID: 26035379

Summary: The belly spot and tail mutant mouse strain was first reported on in 1976. Among other phenotypic changes, it carries ocular mutations including retinal colobomas, reduced retinal ganglion cells (RGCs), and axon misrouting. In order to assess the use of this strain as a murine model for stem cell therapies of retinal degenerative diseases the authors performed a number of characterization experiments including electron microscopy, immunohistochemistry, testing of circadian rhythms, and morphological studies. Some of the immunohistochemistry was done using Anti-Melanopsin (Cat. #AB-N38) at a 1:5000 dilution.

Related Products: Melanopsin Rabbit Polyclonal (Cat. #AB-N38)

Gibon J, Buckley S, Unsain N, Kaartinen V, Séguéla P, Barker P (2015) proBDNF and p75NTR control excitability and persistent firing of cortical pyramidal neurons. J Neurosci 35:9741-9753. doi: 10.1523/JNEUROSCI.4655-14.2015 PMID: 26134656

Summary: Principal neurons in the entorhinal cortex (EC) display persistent firing (PF) during working-memory tasks. Much of the communication between the hippocampus and the neocortex passes through the EC, and the EC also receives some cholinergic input from the medial septum and diagonal band of Broca. In this work the authors investigated the role of pro-brain-derived neurotrophic factor (proBDNF) and the p75 receptor in excitability and PF in the EC. The authors propose the proBDNF/p75 system as a regulator for pyramidal neuron excitability and PF in the EC, preventing runaway activity. Some of the western blot and current-clamp data was generated using Anti-p75 (Cat. #AB-N01; no concentration information provided).

Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)

Navratilova E, Xie J, Meske D, Qu C, Morimura K, Okun A, Arakawa N, Ossipov M, Fields H, Porreca F (2015) Endogenous opioid activity in the anterior cingulate cortex is required for relief of pain. J Neurosci 35:7264-7271. doi: 10.1523/JNEUROSCI.3862-14.2015

Summary: There are a number of neuronal circuits involved in the processing of pain, including those that control somatosensory, affective, and cognitive aspects of pain perception. Opioid signaling in the anterior cingulate cortex (ACC) plays a part in pain modulation – this area has also been implicated in the encoding of pain aversiveness. In order to examine the neuronal mechanisms of pain relief and the following reward, the authors of this paper administered 48 ng of Dermorphin-SAP (Cat. #IT-12) into the rostral ACC of rats. Saporin (Cat. #PR-01) was used as a control. The results illuminate the opioid pathway during pain treatment, and the dependence of nucleus accumbens dopaminergic transmission on upstream ACC opioid circuits during pain processing.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Saporin (Cat. #PR-01)

Cetas J, McFarlane R, Kronfeld K, Smitasin P, Liu J, Raskin J (2015) Brainstem opioidergic system is involved in early response to experimental SAH. Transl Stroke Res 6:140-147. doi: 10.1007/s12975-014-0378-2

Objective: To determine the cause of poor long-term outcomes after Subarachnoid hemorrhage (SAH).

Summary: Failure of the RVM μ-opioid receptor cells to initiate the compensatory CBF response sets the stage for acute and delayed ischemic injury following SAH.

Usage: To lesion medullary neurons expressing the μ-opioid receptor, Dermorphin–SAP was microinjected as a bilateral dose of 0.5 pmol in 500 nL per side (1 pmol in 1 μL total dose and injection volume). Blank–SAP or vehicle was injected in equal volumes and dose as controls.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Blank-SAP (Cat. #IT-21)