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Participation of the GABA-benzodiazepine system in the inhibition of defensive burying produced by ejaculation.

Behavioural pharmacology

Fernández-Guasti A, Saldívar A.
PMID: 11175427
Behav Pharmacol. 1990;1(5):429-436.

We recently reported a reduction in defensive burying behaviour after ejaculation. The present study analyzed whether this reduction was mediated via an increase in GABAergic transmission. Two experimental series were included: in the first series the reduction in burying...

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Fernández-Guasti A, Saldívar A. Participation of the GABA-benzodiazepine system in the inhibition of defensive burying produced by ejaculation. Behav Pharmacol. 1990;1(5):429-436
Fernández-Guasti, A., & Saldívar, A. (1990). Participation of the GABA-benzodiazepine system in the inhibition of defensive burying produced by ejaculation. Behavioural pharmacology, 1(5), 429-436.
Fernández-Guasti, A., and Saldívar, A.. "Participation of the GABA-benzodiazepine system in the inhibition of defensive burying produced by ejaculation." Behavioural pharmacology vol. 1,5 (1990): 429-436.
Fernández-Guasti A, Saldívar A. Participation of the GABA-benzodiazepine system in the inhibition of defensive burying produced by ejaculation. Behav Pharmacol. 1990;1(5):429-436. PMID: 11175427.
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Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells.

The European journal of neuroscience

Avoli M.
PMID: 12106438
Eur J Neurosci. 1992 Oct;4(1):16-26. doi: 10.1111/j.1460-9568.1992.tb00105.x.

Intracellular recordings with K-acetate-filled microelectrodes were performed in slices of the adult rat hippocampus maintained in vitro at 35 - 36 degrees C to analyse the potentials associated with the orthodromic inhibitory sequence generated by CA1 pyramidal cells. In...

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Avoli M. Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells. Eur J Neurosci. 1992;4(1):16-26doi: 10.1111/j.1460-9568.1992.tb00105.x.
Avoli, M. (1992). Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells. The European journal of neuroscience, 4(1), 16-26. https://doi.org/10.1111/j.1460-9568.1992.tb00105.x
Avoli, Massimo. "Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells." The European journal of neuroscience vol. 4,1 (1992): 16-26. doi: https://doi.org/10.1111/j.1460-9568.1992.tb00105.x
Avoli M. Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells. Eur J Neurosci. 1992 Oct;4(1):16-26. doi: 10.1111/j.1460-9568.1992.tb00105.x. PMID: 12106438.
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Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices.

The European journal of neuroscience

Berretta N, Berton F, Bianchi R, Brunelli M, Capogna M, Francesconi W.
PMID: 12106451
Eur J Neurosci. 1991;3(9):850-854. doi: 10.1111/j.1460-9568.1991.tb00096.x.

Hippocampal slices from guinea-pigs were used to examine the long-term potentiation (LTP) of the N-methyl-d-aspartate (NMDA)-mediated excitatory postsynaptic potential (EPSP). Intracellular recordings were performed from CA1 pyramidal neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5 - 10 microM) and...

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Berretta N, Berton F, Bianchi R, et al. Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices. Eur J Neurosci. 1991;3(9):850-854doi: 10.1111/j.1460-9568.1991.tb00096.x.
Berretta, N., Berton, F., Bianchi, R., Brunelli, M., Capogna, M., & Francesconi, W. (1991). Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices. The European journal of neuroscience, 3(9), 850-854. https://doi.org/10.1111/j.1460-9568.1991.tb00096.x
Berretta, N., et al. "Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices." The European journal of neuroscience vol. 3,9 (1991): 850-854. doi: https://doi.org/10.1111/j.1460-9568.1991.tb00096.x
Berretta N, Berton F, Bianchi R, Brunelli M, Capogna M, Francesconi W. Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices. Eur J Neurosci. 1991;3(9):850-854. doi: 10.1111/j.1460-9568.1991.tb00096.x. PMID: 12106451.
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Brain regional pharmacology of GABA(A) receptors in alcohol-preferring AA and alcohol-avoiding ANA rats.

Addiction biology

Wong G, Ovaska T, Korpi ER.
PMID: 12893465
Addict Biol. 1996;1(3):263-72. doi: 10.1080/1355621961000124876.

Compounds interacting with the GABA(A) receptor system modulate voluntary alcohol consumption in alcohol-preferring AA (Alko, Alcohol) rats. Therefore, we compared the central GABA(A) receptor pharmacology of the AA rats to that of their counterpart, alcohol-avoiding ANA (Alko, Non-Alcohol) rats...

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Wong G, Ovaska T, Korpi ER. Brain regional pharmacology of GABA(A) receptors in alcohol-preferring AA and alcohol-avoiding ANA rats. Addict Biol. 1996;1(3):263-72doi: 10.1080/1355621961000124876.
Wong, G., Ovaska, T., & Korpi, E. R. (1996). Brain regional pharmacology of GABA(A) receptors in alcohol-preferring AA and alcohol-avoiding ANA rats. Addiction biology, 1(3), 263-72. https://doi.org/10.1080/1355621961000124876
Wong, G, et al. "Brain regional pharmacology of GABA(A) receptors in alcohol-preferring AA and alcohol-avoiding ANA rats." Addiction biology vol. 1,3 (1996): 263-72. doi: https://doi.org/10.1080/1355621961000124876
Wong G, Ovaska T, Korpi ER. Brain regional pharmacology of GABA(A) receptors in alcohol-preferring AA and alcohol-avoiding ANA rats. Addict Biol. 1996;1(3):263-72. doi: 10.1080/1355621961000124876. PMID: 12893465.
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Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current.

Neuroscience bulletin

Wu YM, Wang R, He RR.
PMID: 17687407
Neurosci Bull. 2006 Mar;22(2):110-4.

Objective To examine the effects of urotensin II (UII) on the discharges of neurons in CA1 area of hippocampal slices by using extracellular recording technique. Results (1) In response to the application of UII (0.3, 3.0, 30.0, 300.0 nmol/L,...

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Wu YM, Wang R, He RR. Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current. Neurosci Bull. 2006;22(2):110-4
Wu, Y. M., Wang, R., & He, R. R. (2006). Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current. Neuroscience bulletin, 22(2), 110-4.
Wu, Yu-Ming, et al. "Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current." Neuroscience bulletin vol. 22,2 (2006): 110-4.
Wu YM, Wang R, He RR. Urotensin II inhibits electrical activity of hippoCampal CA1 neurons by potentiating the GABA(A) receptor-mediated Cl(-) current. Neurosci Bull. 2006 Mar;22(2):110-4. PMID: 17687407.
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Gamma-Aminobutyric Acid Modulation of Corticotrophin-Releasing Factor-41 Secretion from the Rat Hypothalamus in vitro.

Journal of neuroendocrinology

Tsagarakis S, Rees LH, Besser GM, Grossman A.
PMID: 19210387
J Neuroendocrinol. 1990 Apr 01;2(2):221-4. doi: 10.1111/j.1365-2826.1990.tb00854.x.

Abstract There is increasing evidence for a centrally mediated inhibitory effect of the amino-acid neurotransmitter y-aminobutyric acid (GABA) on the hypothalamo-pituitary-adrenal axis. In the present study, the direct effect of GABA in modulating the release of the 41-residue corticotrophin-releasing...

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Tsagarakis S, Rees LH, Besser GM, et al. Gamma-Aminobutyric Acid Modulation of Corticotrophin-Releasing Factor-41 Secretion from the Rat Hypothalamus in vitro. J Neuroendocrinol. 1990;2(2):221-4doi: 10.1111/j.1365-2826.1990.tb00854.x.
Tsagarakis, S., Rees, L. H., Besser, G. M., & Grossman, A. (1990). Gamma-Aminobutyric Acid Modulation of Corticotrophin-Releasing Factor-41 Secretion from the Rat Hypothalamus in vitro. Journal of neuroendocrinology, 2(2), 221-4. https://doi.org/10.1111/j.1365-2826.1990.tb00854.x
Tsagarakis, S, et al. "Gamma-Aminobutyric Acid Modulation of Corticotrophin-Releasing Factor-41 Secretion from the Rat Hypothalamus in vitro." Journal of neuroendocrinology vol. 2,2 (1990): 221-4. doi: https://doi.org/10.1111/j.1365-2826.1990.tb00854.x
Tsagarakis S, Rees LH, Besser GM, Grossman A. Gamma-Aminobutyric Acid Modulation of Corticotrophin-Releasing Factor-41 Secretion from the Rat Hypothalamus in vitro. J Neuroendocrinol. 1990 Apr 01;2(2):221-4. doi: 10.1111/j.1365-2826.1990.tb00854.x. PMID: 19210387.
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Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues.

Neurochemistry international

Yoneda Y, Ogita K, Nakamuta H, Koida M, Ohgaki T, Meguri H.
PMID: 20493157
Neurochem Int. 1986;9(4):521-31. doi: 10.1016/0197-0186(86)90145-2.

The effect of various ions on [(3)H]l-glutamic acid (Glu) binding was examined using crude synaptic membrane preparations from the rat brain. In vitro addition of sodium acetate (1-100 mM) exhibited a significant enhancement of the binding in a concentration...

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Yoneda Y, Ogita K, Nakamuta H, et al. Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues. Neurochem Int. 1986;9(4):521-31doi: 10.1016/0197-0186(86)90145-2.
Yoneda, Y., Ogita, K., Nakamuta, H., Koida, M., Ohgaki, T., & Meguri, H. (1986). Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues. Neurochemistry international, 9(4), 521-31. https://doi.org/10.1016/0197-0186(86)90145-2
Yoneda, Y, et al. "Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues." Neurochemistry international vol. 9,4 (1986): 521-31. doi: https://doi.org/10.1016/0197-0186(86)90145-2
Yoneda Y, Ogita K, Nakamuta H, Koida M, Ohgaki T, Meguri H. Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues. Neurochem Int. 1986;9(4):521-31. doi: 10.1016/0197-0186(86)90145-2. PMID: 20493157.
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The release of acetylcholine and amino acids from the rabbit retina in vivo.

Neurochemistry international

Neal MJ, Massey SC.
PMID: 20487736
Neurochem Int. 1980;1:191-208. doi: 10.1016/0197-0186(80)90061-3.

Rabbits were anaesthetised with urethane and an eye-cup was prepared by removing the cornea, iris, lens and vitreous. The retina was loaded with |(3)H|choline by filling the eye-cup with medium containing labelled choline and eserine. The retina was washed...

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Neal MJ, Massey SC. The release of acetylcholine and amino acids from the rabbit retina in vivo. Neurochem Int. 1980;1:191-208doi: 10.1016/0197-0186(80)90061-3.
Neal, M. J., & Massey, S. C. (1980). The release of acetylcholine and amino acids from the rabbit retina in vivo. Neurochemistry international, 1191-208. https://doi.org/10.1016/0197-0186(80)90061-3
Neal, M J, and Massey, S C. "The release of acetylcholine and amino acids from the rabbit retina in vivo." Neurochemistry international vol. 1 (1980): 191-208. doi: https://doi.org/10.1016/0197-0186(80)90061-3
Neal MJ, Massey SC. The release of acetylcholine and amino acids from the rabbit retina in vivo. Neurochem Int. 1980;1:191-208. doi: 10.1016/0197-0186(80)90061-3. PMID: 20487736.
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Inactivation of [(35)S]t-butylbicyclophosphorothionate binding sites by the arginine reagent, 2,3-butanedione.

Neurochemistry international

Martini C, Pacini R, Lucacchini A.
PMID: 20504675
Neurochem Int. 1991;18(1):51-4. doi: 10.1016/0197-0186(91)90035-c.

The "cage" convulsant [(35)S]t-butylbicyclophosphorothionate ([(35)S]TBPS) binds with high affinity to specific sites "at" or "near" a ?-amino-butyric acid (GABA)-gated chloride channel according to current hypothesis. We now report that pretreatment of membranes with 2,3-butanedione, an arginine-specific reagent, causes a...

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Martini C, Pacini R, Lucacchini A. Inactivation of [(35)S]t-butylbicyclophosphorothionate binding sites by the arginine reagent, 2,3-butanedione. Neurochem Int. 1991;18(1):51-4doi: 10.1016/0197-0186(91)90035-c.
Martini, C., Pacini, R., & Lucacchini, A. (1991). Inactivation of [(35)S]t-butylbicyclophosphorothionate binding sites by the arginine reagent, 2,3-butanedione. Neurochemistry international, 18(1), 51-4. https://doi.org/10.1016/0197-0186(91)90035-c
Martini, C, et al. "Inactivation of [(35)S]t-butylbicyclophosphorothionate binding sites by the arginine reagent, 2,3-butanedione." Neurochemistry international vol. 18,1 (1991): 51-4. doi: https://doi.org/10.1016/0197-0186(91)90035-c
Martini C, Pacini R, Lucacchini A. Inactivation of [(35)S]t-butylbicyclophosphorothionate binding sites by the arginine reagent, 2,3-butanedione. Neurochem Int. 1991;18(1):51-4. doi: 10.1016/0197-0186(91)90035-c. PMID: 20504675.
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The stimulation of GABA(B) receptors increases serotonin release in the rat suprachiasmatic area.

Neurochemistry international

François-Bellan AM, Hery M, Barrit MC, Faudon M, Hery F.
PMID: 20501142
Neurochem Int. 1987;11(1):55-62. doi: 10.1016/0197-0186(87)90148-3.

The action of ?-aminobutyric acid (GABA) and related compounds on the spontaneous release of newly synthesized [(3)H]5-hydroxytryptamine ([(3)H]5-HT) was studied in the suprachiasmatic area (SCA) using a superfusion system. GABA (10 ?M) increased [(3)H]5-HT release from SCA by up...

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François-Bellan AM, Hery M, Barrit MC, et al. The stimulation of GABA(B) receptors increases serotonin release in the rat suprachiasmatic area. Neurochem Int. 1987;11(1):55-62doi: 10.1016/0197-0186(87)90148-3.
François-Bellan, A. M., Hery, M., Barrit, M. C., Faudon, M., & Hery, F. (1987). The stimulation of GABA(B) receptors increases serotonin release in the rat suprachiasmatic area. Neurochemistry international, 11(1), 55-62. https://doi.org/10.1016/0197-0186(87)90148-3
François-Bellan, A M, et al. "The stimulation of GABA(B) receptors increases serotonin release in the rat suprachiasmatic area." Neurochemistry international vol. 11,1 (1987): 55-62. doi: https://doi.org/10.1016/0197-0186(87)90148-3
François-Bellan AM, Hery M, Barrit MC, Faudon M, Hery F. The stimulation of GABA(B) receptors increases serotonin release in the rat suprachiasmatic area. Neurochem Int. 1987;11(1):55-62. doi: 10.1016/0197-0186(87)90148-3. PMID: 20501142.
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Barbiturate (Soneryl) Poisoning. The Value of Picrotoxin in Treatment.

British medical journal

Slot GM.
PMID: 20783115
Br Med J. 1940 May 25;1(4142):849-50. doi: 10.1136/bmj.1.4142.849.

No abstract available.

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Slot GM. Barbiturate (Soneryl) Poisoning. The Value of Picrotoxin in Treatment. Br Med J. 1940;1(4142):849-50doi: 10.1136/bmj.1.4142.849.
Slot, G. M. (1940). Barbiturate (Soneryl) Poisoning. The Value of Picrotoxin in Treatment. British medical journal, 1(4142), 849-50. https://doi.org/10.1136/bmj.1.4142.849
Slot, G M. "Barbiturate (Soneryl) Poisoning. The Value of Picrotoxin in Treatment." British medical journal vol. 1,4142 (1940): 849-50. doi: https://doi.org/10.1136/bmj.1.4142.849
Slot GM. Barbiturate (Soneryl) Poisoning. The Value of Picrotoxin in Treatment. Br Med J. 1940 May 25;1(4142):849-50. doi: 10.1136/bmj.1.4142.849. PMID: 20783115; PMCID: PMC2177358.
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On the Actions of Picrotoxine, and the Antagonism between Picrotoxine and Chloral Hydrate.

British medical journal

Browne JC.
PMID: 20747837
Br Med J. 1875 Apr 24;1(747):540-2. doi: 10.1136/bmj.1.747.540.

No abstract available.

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Browne JC. On the Actions of Picrotoxine, and the Antagonism between Picrotoxine and Chloral Hydrate. Br Med J. 1875;1(747):540-2doi: 10.1136/bmj.1.747.540.
Browne, J. C. (1875). On the Actions of Picrotoxine, and the Antagonism between Picrotoxine and Chloral Hydrate. British medical journal, 1(747), 540-2. https://doi.org/10.1136/bmj.1.747.540
Browne, J C. "On the Actions of Picrotoxine, and the Antagonism between Picrotoxine and Chloral Hydrate." British medical journal vol. 1,747 (1875): 540-2. doi: https://doi.org/10.1136/bmj.1.747.540
Browne JC. On the Actions of Picrotoxine, and the Antagonism between Picrotoxine and Chloral Hydrate. Br Med J. 1875 Apr 24;1(747):540-2. doi: 10.1136/bmj.1.747.540. PMID: 20747837; PMCID: PMC2297492.
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