| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T731 |
0-297 |
Sentence |
denotes |
Fig. 2 Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. |
| T732 |
298-650 |
Sentence |
denotes |
Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p < 0.05 vs. control, #p < 0.05 vs. Tat 50 nM, §p < 0.05 vs. TM, TM: |
| T733 |
651-779 |
Sentence |
denotes |
Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. |
| T734 |
780-1225 |
Sentence |
denotes |
Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. |
| T735 |
1226-1657 |
Sentence |
denotes |
Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a) |
