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Articles 1 - 12 of 12
Full-Text Articles in Molecular and Cellular Neuroscience
Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine
Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine
fouad Lemtiri-Chlieh
In layer 2/3 of neocortex, brief trains of action potentials in pyramidal neurons (PNs) induce the mobilization of endogenous cannabinoids (eCBs), resulting in a depression of GABA release from the terminals of inhibitory interneurons (INs). This depolarization-induced suppression of inhibition (DSI) is mediated by activation of the type 1 cannabinoid receptor (CB1) on presynaptic terminals of a subset of INs. However, it is not clear whether CB1 receptors are also expressed at synapses between INs, and whether INs can release eCBs in response to depolarization. In the present studies, brain slices containing somatosensory cortex were prepared from 14- to 21-day-old …
A Role For The Forebrain In Mediating Time-Of-Day Differences In Glucocorticoid Counterregulatory Responses To Hypoglycemia In Rats, Lori M. Gorton, Arshad M. Khan, Maryann Bohland, Graciela Sanchez-Watts, Casey M. Donovan, Alan G. Watts
A Role For The Forebrain In Mediating Time-Of-Day Differences In Glucocorticoid Counterregulatory Responses To Hypoglycemia In Rats, Lori M. Gorton, Arshad M. Khan, Maryann Bohland, Graciela Sanchez-Watts, Casey M. Donovan, Alan G. Watts
Arshad M. Khan, Ph.D.
No abstract provided.
Nicotine Sensitization In Β-Arrestin 2 Knockout Adolescent Mice., Jennifer A. Correll
Nicotine Sensitization In Β-Arrestin 2 Knockout Adolescent Mice., Jennifer A. Correll
Electronic Theses and Dissertations
ß arrestin-2 is a protein involved in signaling of D2 receptors and plays a mediating role in sensitization to psychostimulants and the opiate morphine. In this study, 3-4 week old BA-2 KO and wild type C57/B6 mice received nicotine tartarate (s.c, 0.5 mg/kg free base) for 7 or 14 consecutive days followed by a drug-free period. An acute nicotine challenge followed the drugfree period. Results indicated that the absence of ß-arrestin-2 reduced sensitization to nicotine in Experiment 1. BA-2 KOs eventually demonstrated sensitization in Experiment 2. However, absence of ß-arrestin-2 blocked expression of sensitization on the challenge. After the challenge, …
Catecholaminergic Control Of Mitogen-Activated Protein Kinase Signaling In Paraventricular Neuroendocrine Neurons In Vivo And In Vitro: A Proposed Role During Glycemic Challenges, Arshad M. Khan, Todd A. Ponzio, Graciela Sanchez-Watts, B. Glenn Stanley, Glenn I. Hatton, Alan G. Watts
Catecholaminergic Control Of Mitogen-Activated Protein Kinase Signaling In Paraventricular Neuroendocrine Neurons In Vivo And In Vitro: A Proposed Role During Glycemic Challenges, Arshad M. Khan, Todd A. Ponzio, Graciela Sanchez-Watts, B. Glenn Stanley, Glenn I. Hatton, Alan G. Watts
Arshad M. Khan, Ph.D.
No abstract provided.
Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi
Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi
Christoph Lossin, Ph.D.
The inwardly rectifying K+ (Kir) channel Kir4.1 is responsible for astroglial K+ buffering. We recently found that tricyclic antidepressants (TCAs) inhibit Kir4.1 channel currents, which suggests that astroglial Kir currents might be involved in the pharmacological action of antidepressants. We therefore further examined the effects of the currently most popular antidepressants, selective serotonin reuptake inhibitors (SSRIs), and other related agents on Kir4.1 channels heterologously expressed in HEK293T cells. The whole-cell patch clamp technique was used. Fluoxetine, the typical SSRI, inhibited Kir4.1 channel currents in a concentration-dependent manner with an IC50 value of 15.2 microM. The inhibitory effect of fluoxetine was …
Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi
Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi
Christoph Lossin, Ph.D.
The inwardly rectifying K(+) (Kir) channel Kir4.1 is responsible for astroglial K(+) buffering. We examined the effects of nortriptyline, a tricyclic antidepressant (TCA), on Kir4.1 channel currents heterologously expressed in HEK293T cells, using a whole-cell patch-clamp technique. Nortriptyline (3-300 microM) reversibly inhibited Kir4.1 currents in a concentration-dependent manner, whereas it marginally affected neuronal Kir2.1 currents. The inhibition of Kir4.1 channels by nortriptyline depended on the voltage difference from the K(+) equilibrium potential (E(K)), with greater potency at more positive potentials. Blocking kinetics of the drug could be described by first-order kinetics, where dissociation of the drug slowed down and association …
Adolescent Nicotine Exposure Produces Less Affective Measures Of Withdrawal Relative To Adult Nicotine Exposure In Male Rats, Laura O'Dell
Adolescent Nicotine Exposure Produces Less Affective Measures Of Withdrawal Relative To Adult Nicotine Exposure In Male Rats, Laura O'Dell
Laura Elena O'Dell
No abstract provided.
“Nicotine Deprivation Effect” In Rats With Intermittent 23-Hour Access To Intravenous Nicotine Self-Administration, Laura O'Dell
“Nicotine Deprivation Effect” In Rats With Intermittent 23-Hour Access To Intravenous Nicotine Self-Administration, Laura O'Dell
Laura Elena O'Dell
No abstract provided.
Diminished Nicotine Withdrawal In Adolescent Rats: Implications For Vulnerability To Addiction, Laura O'Dell
Diminished Nicotine Withdrawal In Adolescent Rats: Implications For Vulnerability To Addiction, Laura O'Dell
Laura Elena O'Dell
No abstract provided.
Viral Vector-Induced Amygdala Npy Overexpression Reverses Increased Alcohol Intake Caused By Repeated Deprivations In Wistar Rats, Laura O'Dell
Laura Elena O'Dell
No abstract provided.
Crf–Crf1 System Activation Mediates Withdrawal-Induced Increases In Nicotine Self-Administration In Nicotine-Dependent Rats., Laura O'Dell
Crf–Crf1 System Activation Mediates Withdrawal-Induced Increases In Nicotine Self-Administration In Nicotine-Dependent Rats., Laura O'Dell
Laura Elena O'Dell
No abstract provided.
Glutamate Excitotoxicity In Epilepsy And Ischemia, Mangala Meenakshi Soundarapandian
Glutamate Excitotoxicity In Epilepsy And Ischemia, Mangala Meenakshi Soundarapandian
Electronic Theses and Dissertations
'Excitotoxicity' represents the excitatory amino acid mediated degeneration of neurons. Glutamate is the major excitatory neurotransmitter in the brain. Glutamate excitotoxicity has been implicated in a number of neurodegenerative disorders like Stroke, Epilepsy, Alzheimer's disease and traumatic brain injury. This neurotoxicity is summed up by the 'glutamate hypothesis' which describes the cause of neuronal cell death as an excessive release of glutamate causing over excitation of the glutamate receptors and subsequent increase in influx of calcium leading to cell death. An effort to counteract this neurotoxicity has lead to the development of glutamate receptor antagonists that can effectively serve as …