Author name: Kristen Hartman

Anxiety-like behavior is modulated by a discrete subpopulation of interneurons in the basolateral amygdala.

Truitt WA, Johnson PL, Dietrich AD, Fitz SD, Shekhar A (2009) Anxiety-like behavior is modulated by a discrete subpopulation of interneurons in the basolateral amygdala. Neuroscience 160:284-294. doi: 10.1016/j.neuroscience.2009.01.083 Summary: It is thought that the basolateral nucleus of the amygdala (BL) is an anxiety regulator. The authors previously demonstrated that SSP-SAP (Cat. #IT-11) lesions of […]

Anxiety-like behavior is modulated by a discrete subpopulation of interneurons in the basolateral amygdala. Read More »

Noradrenergic neurons in the locus coeruleus contribute to neuropathic pain.

Brightwell JJ, Taylor BK (2009) Noradrenergic neurons in the locus coeruleus contribute to neuropathic pain. Neuroscience 160:174-185. doi: 10.1016/j.neuroscience.2009.02.023 Summary: Noradrenergic neurons were eliminated with 5 µg intracerebroventricular injections of anti-DBH-SAP (Cat. #IT-03). Mouse IgG-SAP (Cat. #IT-18) was used as a control. Animals lesioned with anti-DBH-SAP displayed a reduction in behavioral signs of several kinds

Noradrenergic neurons in the locus coeruleus contribute to neuropathic pain. Read More »

Targeting Tools: CTB-SAP

CTB-SAP (Cat. #IT-14) is a conjugate between the cell-binding component of cholera toxin (the B chain) and saporin. CTB binds to GM1 (monosialotetrahexosylganglioside), which is present on the surface of different neurons. It has been suggested to be involved in many problems (besides the most famous in the gut: cholera) of neuronal systems: Parkinson’s, motor

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Targeting Tools: Hug-M-ZAP

This secondary conjugate (molecular weight 210 kDa) recognizes YOUR human monoclonal IgM antibody. Hug-M-ZAP (IT-43) is a chemical conjugate of affinity-purified goat anti-human IgM and the ribosome-inactivating protein, saporin. Hug-M- ZAP uses your primary human monoclonal IgM antibody to target and eliminate cells and can be used to evaluate the potential of a primary antibody

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Cholinergic depletion of the medial septum followed by phase shifting does not impair memory or rest-activity rhythms measured under standard light/dark conditions in rats.

Craig LA, Hong NS, Kopp J, McDonald RJ (2009) Cholinergic depletion of the medial septum followed by phase shifting does not impair memory or rest-activity rhythms measured under standard light/dark conditions in rats. Brain Res Bull 79(1):53-62. doi: 10.1016/j.brainresbull.2008.10.013 Summary: It has been theorized that cognitive decline observed in Alzheimer’s disease is in part due

Cholinergic depletion of the medial septum followed by phase shifting does not impair memory or rest-activity rhythms measured under standard light/dark conditions in rats. Read More »

Featured Article: Deletion of catecholaminergic neurons by anti-DBH-saporin disrupts hypothalamic MAP kinase and CREB activation

Khan AM, Rapp KL, Ponzio TA, Sanchez-Watts G, Watts AG (2009) Featured Article: Deletion of catecholaminergic neurons by anti-DBH-saporin disrupts hypothalamic MAP kinase and CREB activation. Targeting Trends 10(2) Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18) Read the featured article in Targeting Trends. See Also: Khan AM et al. Stimulus-, circuit- and intracellular-level

Featured Article: Deletion of catecholaminergic neurons by anti-DBH-saporin disrupts hypothalamic MAP kinase and CREB activation Read More »

Somatostatin Antibodies

Q: Could you please tell me if the Somatostatin 14 antibody (Cat. #AB-04) will also pick up the Somatostatin 28 residue? A: Yes, it will, because they share the sequence of SS14. However, the Somatostatin-28 antibody (Cat. #AB-05) will not see Somatostatin-14. Related: Anti-Somatostatin-14 (Cat. #AB-04), Anti-Somatostatin-28 (Cat. #AB-05)

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Cover Article: Deletion of Catecholaminergic Neurons by Anti-DBH-Saporin Disrupts Hypothalamic MAP Kinase and CREB Activation

Contributed by Arshad M. Khan, Kimberly L. Rapp, Todd A. Ponzio, Graciela Sanchez-Watts and Alan G. Watts; Dept. of Biological Sciences and Neuroscience Research Institute, University of Southern California, Los Angeles, CA;  and Laboratory for Neurochemistry, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD The brain has evolved adaptive mechanisms for

Cover Article: Deletion of Catecholaminergic Neurons by Anti-DBH-Saporin Disrupts Hypothalamic MAP Kinase and CREB Activation Read More »

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