Diazepam potentiation of purinergie depression of central neurons

Intravenously or iontophoretically applied diazepam potentiated the depressant action of iontophoretically applied 5′-AMP on the spontaneous firing of rat cerebral cortical neurons. This potentiation of purinergic depression may be a result of the previously reported inhibition by diazepam of uptake of adenosine into brain tissues.

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The actions of motilin, luteinizing hormone releasing hormone, cholecystokinin, somatostatin, vasoactive intestinal peptide, and other peptides on rat cerebral cortical neurons

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y80-102 ◽

1980 ◽

Vol 58 (6) ◽

pp. 612-623 ◽

Cited By ~ 214

Author(s):

J. W. Phillis ◽

J. R. Kirkpatrick

Keyword(s):

Cerebral Cortex ◽

Luteinizing Hormone ◽

Vasoactive Intestinal Peptide ◽

Cortical Neurons ◽

Spontaneous Firing ◽

Luteinizing Hormone Releasing Hormone ◽

Releasing Hormone ◽

Depressant Action ◽

Cerebral Cortical Neurons ◽

Excitatory Action

The effects of a number of neuronally localized peptides have been ascertained on corticospinal and other unidentified neurons in the rat cerebral cortex. Motilin, somatostatin, and luteinizing hormone releasing hormone excited most of the corticospinal neurons on which they were tested. Cholecystokinin, Met-enkephalin, vasoactive intestinal peptide, and neurotensin also excited some corticospinal neurons. Many nonidentified neurons were excited by all of these peptides. Met-enkephalin had a depressant action on some (14%) corticospinal neurons. Leu-enkephalin depressed many identified and nonidentified neurons and had an excitatory action on a few neurons. Both excitatory and inhibitory actions of the enkephalins were antagonized by naloxone. Thyrotropin-releasing hormone had predominantly depressant actions on the spontaneous firing of corticospinal and nonidentified neurons but did excite some unidentified cortical neurons. Secretin had no effect on the firing of most of the neurons tested.

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Estradiol and progesterone potentiate adenosine's depressant action on rat cerebral cortical neurons

General Pharmacology The Vascular System ◽

10.1016/0306-3623(85)90151-x ◽

1985 ◽

Vol 16 (6) ◽

pp. 609-612 ◽

Cited By ~ 15

Author(s):

J.W. Phillis ◽

A.S. Bender ◽

W. Marszalec

Keyword(s):

Cortical Neurons ◽

Depressant Action ◽

Cerebral Cortical Neurons

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Theophylline antagonizes flurazepam-induced depression of cerebral cortical neurons

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y79-140 ◽

1979 ◽

Vol 57 (8) ◽

pp. 917-920 ◽

Cited By ~ 45

Author(s):

J. W. Phillis ◽

J. P. Edstrom ◽

S. W. Ellis ◽

J. R. Kirkpatrick

Keyword(s):

Brain Tissue ◽

Binding Sites ◽

Cortical Neurons ◽

Purinergic Receptor ◽

Central Neurons ◽

Cerebral Cortical Neurons

Intravenously administered theophylline (50–100 mg/kg) antagonized the depressant actions of adenosine and flurazepam on rat cerebral cortical neurons. When assessed in conjunction with recent reports that theophylline competes with diazepam for binding sites in brain tissue, this finding suggests that one action of the benzodiazepines may be exerted at a purinergic receptor associated with central neurons.

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Effects of adenosine and adenine nucleotides on synaptic transmission in the cerebral cortex

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y79-194 ◽

1979 ◽

Vol 57 (11) ◽

pp. 1289-1312 ◽

Cited By ~ 252

Author(s):

J. W. Phillis ◽

J. P. Edstrom ◽

G. K. Kostopoulos ◽

J. R. Kirkpatrick

Keyword(s):

Cortical Neurons ◽

Adenine Nucleotides ◽

Membrane Resistance ◽

Neuronal Firing ◽

Depressant Action ◽

Cerebral Cortical Neurons ◽

Adenosine Transport ◽

Evoked Activity ◽

Presynaptic Nerve Terminals ◽

Spontaneous Firing Rate

Adenosine and the adenine nucleotides have a potent depressant action on cerebral cortical neurons, including identified corticospinal cells. Other purine and pyrrolidine nucleotides were either weakly depressant (inosine and guanosine derivatives) or largely inactive (xanthine, cytidine, thymidine, uridine derivatives). The 5′-triphosphates and to a lesser extent the 5′-diphosphates of all the purine and pyrimidines tested had excitant actions on cortical neurons. Adenosine transport blockers and deaminase inhibitors depressed the firing of cortical neurons and potentiated the depressant actions of adenosine and the adenine nucleotides. Methyl-xanthines (theophylline, caffeine, and isobutylmethylxanthine) antagonized the depressant effects of adenosine and the adenine nucleotides and enhanced the spontaneous firing rate of cerebral cortical neurons. Intracellular recordings showed that adenosine 5′-monophosphate hyperpolarizes cerebral cortical neurons and suppresses spontaneous and evoked excitatory postsynaptic potentials in the absence of any pronounced alterations in membrane resistance or of the threshold for action potential generation. It is suggested that adenosine depresses spontaneous and evoked activity by inhibiting the release of transmitter from presynaptic nerve terminals. Furthermore, the depressant effects of potentiators and excitant effects of antagonists of adenosine on neuronal firing are consistent with the hypothesis that cortical neurons are subject to control by endogenously released purines.

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