Author name: Kristen Hartman

Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin.

Burk JA, Lowder MW, Altemose KE (2008) Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin. Behav Brain Res 195:231-238. doi: 10.1016/j.bbr.2008.09.006 Summary: Attentional processing has been shown to be dependent on basal forebrain cholinergic inputs to the cerebral cortex. In this work the authors wished to specify which components should be used […]

Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin. Read More »

Selective lesion of septal cholinergic neurons in rats impairs acquisition of a delayed matching to position T-maze task by delaying the shift from a response to a place strategy.

Fitz NF, Gibbs RB, Johnson DA (2008) Selective lesion of septal cholinergic neurons in rats impairs acquisition of a delayed matching to position T-maze task by delaying the shift from a response to a place strategy. Brain Res Bull 77:356-360. doi: 10.1016/j.brainresbull.2008.08.016 Summary: It has been theorized that the effect of cholinergic lesions of the

Selective lesion of septal cholinergic neurons in rats impairs acquisition of a delayed matching to position T-maze task by delaying the shift from a response to a place strategy. Read More »

Methylphenidate-induced impulsivity: pharmacological antagonism by beta-adrenoreceptor blockade.

Milstein JA, Dalley JW, Robbins TW (2010) Methylphenidate-induced impulsivity: pharmacological antagonism by beta-adrenoreceptor blockade. J Psychopharmacol 24:309-321. doi: 10.1177/0269881108098146 Summary: In this work bilateral 20 ng intracortical injections of anti-DBH-SAP (Cat. #IT-03) were used to examine the role of noradrenergic neurons in the control of psychostimulant-induced impulsivity. Although β-adrenoreceptor blockade abolished this impulsivity, lesioning noradrenergic

Methylphenidate-induced impulsivity: pharmacological antagonism by beta-adrenoreceptor blockade. Read More »

Neuropathic pain is maintained by brainstem neurons co-expressing opioid and cholecystokinin receptors.

Zhang W, Gardell S, Zhang D, Xie JY, Agnes RS, Badghisi H, Hruby VJ, Rance N, Ossipov MH, Vanderah TW, Porreca F, Lai J (2009) Neuropathic pain is maintained by brainstem neurons co-expressing opioid and cholecystokinin receptors. Brain 132:778-787. doi: 10.1093/brain/awn330 Summary: It has been hypothesized that a subset of rostral ventromedial medulla (RVM) neurons

Neuropathic pain is maintained by brainstem neurons co-expressing opioid and cholecystokinin receptors. Read More »

Lumbar intrathecal CCK-saporin: anatomic and nociceptive effects

Datta S, Chatterjee K, Kline IV RH, Wiley RG (2008) Lumbar intrathecal CCK-saporin: anatomic and nociceptive effects. Neuroscience 2008 Abstracts 773.4/MM32. Society for Neuroscience, Washington, DC. Summary: Lumbar intrathecal CCK (cholecystokinin) appears anti-opiate in nocifensive reflex testing and may be important in opiate-resistant neuropathic pain states suggesting a role for CCK receptor-expressing dorsal horn neurons

Lumbar intrathecal CCK-saporin: anatomic and nociceptive effects Read More »

Interactions between corticosterone and catecholaminergic afferents in the regulation of neuropeptide gene expression in neuroendocrine CRH neurons in the paraventricular nucleus of the hypothalamus

Rapp KL, Watts AG (2008) Interactions between corticosterone and catecholaminergic afferents in the regulation of neuropeptide gene expression in neuroendocrine CRH neurons in the paraventricular nucleus of the hypothalamus. Neuroscience 2008 Abstracts 782.2/RR7. Society for Neuroscience, Washington, DC. Summary: Neurons in the medial parvicellular part of the paraventricular nucleus of the hypothalamus (PVH) are responsible

Interactions between corticosterone and catecholaminergic afferents in the regulation of neuropeptide gene expression in neuroendocrine CRH neurons in the paraventricular nucleus of the hypothalamus Read More »

The retroabducens region is necessary for rapid eye movement (REM) during REM sleep in the rat

Pedersen NP, Anaclet C, Vetrivelan R, Saper CB, Lu J (2008) The retroabducens region is necessary for rapid eye movement (REM) during REM sleep in the rat. Neuroscience 2008 Abstracts 784.15/RR66. Society for Neuroscience, Washington, DC. Summary: REM sleep is characterized by REMs, atonia of the non-respiratory musculature, and active dreaming during which the electroencephalogram

The retroabducens region is necessary for rapid eye movement (REM) during REM sleep in the rat Read More »

Medullary circuitry regulating trigeminal motor nucleus phasic activity during rapid eye movement sleep in the rat

Anaclet C, Pedersen NP, Lu J (2008) Medullary circuitry regulating trigeminal motor nucleus phasic activity during rapid eye movement sleep in the rat. Neuroscience 2008 Abstracts 784.16/RR67. Society for Neuroscience, Washington, DC. Summary: Rapid Eye Movement (REM) sleep or paradoxical sleep is characterized by activation of the cortical and hippocampal EEG, atonia of postural muscles

Medullary circuitry regulating trigeminal motor nucleus phasic activity during rapid eye movement sleep in the rat Read More »

Contrasting effects of estrogen on memory tasks in young female rats

Saenz CM, Borowski T, De Lacalle S (2008) Contrasting effects of estrogen on memory tasks in young female rats. Neuroscience 2008 Abstracts 794.17/UU7. Society for Neuroscience, Washington, DC. Summary: Sleep deprivation may lead to behavioral alterations and it has been associated with a hyperalgesic state in human beings and animal models. The tricyclic antidepressant amitriptyline

Contrasting effects of estrogen on memory tasks in young female rats Read More »

Enhanced sensitivity to phencyclidine following cortical cholinergic denervation

Savage ST, Oberg J, Pernold K, Mattsson A (2008) Enhanced sensitivity to phencyclidine following cortical cholinergic denervation. Neuroscience 2008 Abstracts 842.7/X2. Society for Neuroscience, Washington, DC. Summary: Alterations in cholinergic signaling in the brain have been implicated as a contributing factor in the pathogenesis of schizophrenia. We have recently shown that cholinergic denervation of cortex

Enhanced sensitivity to phencyclidine following cortical cholinergic denervation Read More »

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