Norbornan, a new irreversible ligand of the GABAA-receptor chloride channels

1996 ◽  
Vol 121 (4) ◽  
pp. 404-406 ◽  
Author(s):  
A. I. Golovko ◽  
G. A. Sofronov ◽  
T. V. Klyuntina
2007 ◽  
Vol 564 (1-3) ◽  
pp. 112-115 ◽  
Author(s):  
Glaucia Reis ◽  
Daniela Pacheco ◽  
Janetti Francischi ◽  
Maria Castro ◽  
Andréa Perez ◽  
...  

Synapse ◽  
1995 ◽  
Vol 19 (3) ◽  
pp. 188-196 ◽  
Author(s):  
Yoshihisa Ito ◽  
Katsuya Segawa ◽  
Hideomi Fukuda

1998 ◽  
Vol 779 (1-2) ◽  
pp. 9-16 ◽  
Author(s):  
Jeong-Seop Rhee ◽  
Young-Ho Jin ◽  
Norio Akaike

Author(s):  
Jodi T Thomas ◽  
Blake L Spady ◽  
Philip L Munday ◽  
Sue-Ann Watson

Projected future carbon dioxide (CO2) levels in the ocean can alter marine animal behaviours. Disrupted functioning of γ-aminobutyric acid type A (GABAA) receptors (ligand-gated chloride channels) is suggested to underlie CO2-induced behavioural changes in fish. However, the mechanisms underlying behavioural changes in marine invertebrates are poorly understood. We pharmacologically tested the role of GABA-, glutamate-, acetylcholine- and dopamine-gated chloride channels in CO2-induced behavioural changes in a cephalopod, the two-toned pygmy squid (Idiosepius pygmaeus). We exposed squid to ambient (∼450 µatm) or elevated (∼1,000 µatm) CO2 for seven days. Squid were treated with sham, the GABAA receptor antagonist gabazine, or the non-specific GABAA receptor antagonist picrotoxin, before measurement of conspecific-directed behaviours and activity levels upon mirror exposure. Elevated CO2 increased conspecific-directed attraction and aggression, as well as activity levels. For some CO2-affected behaviours, both gabazine and picrotoxin had a different effect at elevated compared to ambient CO2, providing robust support for the GABA hypothesis within cephalopods. In another behavioural trait, picrotoxin but not gabazine had a different effect in elevated compared to ambient CO2, providing the first pharmacological evidence, in fish and marine invertebrates, for altered functioning of ligand-gated chloride channels, other than the GABAA R, underlying CO2-induced behavioural changes. For some other behaviours, both gabazine and picrotoxin had a similar effect in elevated and ambient CO2, suggesting altered function of ligand-gated chloride channels was not responsible for these CO2-induced changes. Multiple mechanisms may be involved, which could explain the variability in the CO2 and drug treatment effects across behaviours.


Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4366-4375 ◽  
Author(s):  
Shannon D. Sullivan ◽  
Suzanne M. Moenter

Pulsatile GnRH release is required for fertility and is regulated by steroid feedback. Whether or not steroids or their metabolites act directly on GnRH neurons is not well established. In some neurons, steroid metabolites known as neurosteroids modulate the function of the GABAA receptor. Specifically, the progesterone derivative allopregnanolone is an allosteric agonist at this receptor, whereas the androgen dehydroepiandrosterone sulfate (DHEAS) is an allosteric antagonist. We hypothesized these metabolites act similarly on GnRH neurons to modify the response to GABA. Whole-cell voltage-clamp recordings of GABAergic miniature postsynaptic currents (mPSCs) were made from green fluorescent protein-identified GnRH neurons in brain slices from diestrous mice. Glutamatergic currents were blocked with antagonists and action potentials blocked with tetrodotoxin, minimizing presynaptic effects of treatments. Allopregnanolone (5 μm) increased mPSC rate of rise, amplitude and decay time by 15.9 ± 6.1%, 16.5 ± 6.3%, and 58.3 ± 18.6%, respectively (n = 7 cells). DHEAS (5 μm) reduced mPSC rate of rise (32.1 ± 5.7%) and amplitude (27.6 ± 4.3%) but did not alter decay time (n = 8). Effects of both neurosteroids were dose dependent between 0.1 and 10 μm. In addition to independent actions, DHEAS also reversed effects of allopregnanolone on rate of rise and amplitude so that these parameters were returned to pretreatment baseline values (n = 6). These data indicate allopregnanolone increases and DHEAS decreases responsiveness of GnRH neurons to activation of GABAA receptors by differentially modulating current flow through GABAA receptor chloride channels. This provides one mechanism for direct steroid feedback to GnRH neurons.


1992 ◽  
Vol 12 (1-3) ◽  
pp. 1-6 ◽  
Author(s):  
E. Louiset ◽  
J.A. Valentijn ◽  
H. Vaudry ◽  
L. Cazin

2013 ◽  
Vol 1533 ◽  
pp. 141-151 ◽  
Author(s):  
Irene L. Llorente ◽  
Diego Perez-Rodriguez ◽  
Beatriz Martínez-Villayandre ◽  
Severiano Dos-Anjos ◽  
Mark G. Darlison ◽  
...  

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