Potentiation of gamma-aminobutyric acid-mediated inhibition by isoproterenol in the cerebellar cortex: Receptor specificity

Parfitt, Karen D.; Hoffer, Barry J.; Bickford, Paula C.

doi:10.1016/0028-3908(90)90141-d

Cited by 70 publications

(10 citation statements)

References 36 publications

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“…28 for review). PKA or cAMP reduces GABAA receptor activity in spinal, hippocampal, and cortical neurons (15)(16)(17), but enhancement has been found in cerebellar Purkinje cells (18,19) and in bipolar and ganglion cells of the rat retina (20). PKA has no effect on GABA-induced currents in spinal trigeminal neurons (21).…”

Section: Discussionmentioning

confidence: 99%

“…These compounds also reduce the peak current evoked by GABA in mouse spinal neurons (16) and increase the rate of decay of the current in cultured cortical (15) and hippocampal neurons (17). Facilitation of GABAA receptor function by phosphorylation was observed in cerebellar Purkinje cells (18,19), where cAMP augments GABA-induced whole-cell currents and spontaneous miniature inhibitory synaptic currents (19). Vasoactive intestinal peptide (VIP) increases GABA-induced Cl-currents in bipolar and ganglion cells of the rat retina by activating the adenylate cyclase system (20).…”

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confidence: 95%

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Facilitation of GABAergic signaling in the retina by receptors stimulating adenylate cyclase.

Feigenspan

Bormann²

1994

Proc. Natl. Acad. Sci. U.S.A.

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The y-/aminobutyric acid type A (GABAA) receptor is the predominant Cl--channel protein mediating inhibition in the retina and elsewhere in the mammalian brain. We have observed a time-dependent increase ofGABA-induced whole-cell currents when dopamine was applied externally to rat retinal amacrine cells. After 20 min, the peak current was increased to 208% ± 10% of its initial value. A comparable effect was observed with the dopamine Di receptor agonist (+)-l-phenyl-2,3,4,5-tetrahydro(lH)-3-benzazepine-7, (21).In the present study we investigated the role of peptides and other transmitter substances such as dopamine, which are colocalized with GABA in the rat retina (22), as possible modulators of GABAA receptor function. Using patch-clamp techniques, we have identified a convergent pathway in amacrine cells that could facilitate GABA-mediated inhibition in the retina. This pathway involved stimulation of adenylate cyclase and phosphorylation of GABAA receptors by PKA. MATERIALS AND METHODSCel Culture. Organotypic retinal slices were prepared from 6-day-old Wistar rats as described (23). Briefly, vertical sections of 125-jum thickness were cut and embedded into a plasma clot made from chicken plasma (Sigma) and thrombin (Sigma). The coverslips were placed in culture tubes (Nunclon, Roskilde, Denmark) and 750 ,4 of culture medium was added. The medium contained 50%o basal medium Eagle (GIBCO), 25% Hanks' balanced salt solution (GIBCO), 25% horse serum (GIBCO), 6.5 mg of glucose per ml (Merck), 1 mM glutamine (Biochrom, Berlin), 3 mM taurine (Sigma), 1 ,.g of vitamin B12 per ml (Sigma), and 10 mM Hepes (Biochrom). After 2 and 3 weeks in culture, amacrine cells were visually identified in the inner nuclear layer of the retina (7,23).Electrophysiology. The preparation was viewed with Nomarski optics at 640x magnification using an inverted Zeiss microscope and continuously perfused (0.5 ml/min) at room temperature (21-250C). The extracellular bath solution contained (in mM) 137 NaCl, 5.4 KCl, 1.8 CaCl2, 1 MgCl2, and 5 Hepes (pH 7.4). Membrane currents were recorded with whole-cell and cell-attached patch-clamp methods (24), using an EPC-9 amplifier (HEKA Electronik, Lambrecht/ Pfalz, Germany). Pipettes were coated with silicone elastomer and then filled with a solution containing (in mM) 120 I-V, current-voltage.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

Facilitation of GABAergic signaling in the retina by receptors stimulating adenylate cyclase.

Feigenspan

Bormann²

1994

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition to serotoninergic neurons, noradrenalinergic neurons have been shown to interact The cocaine-withdrawal rats 1 week after chronic administration of cocaine showed a significant increase in [ 35 S]TBPS binding in layers II-III and IV of fronto-parietal cortex, and the CA1 region and dentate gyrus of hippocampus. closely with GABAergic systems in the cerebellum (Parfitt et al, 1990;Cheun and Yeh, 1996). These studies have indicated that both serotonin and noradrenaline modulate the GABA-mediated inhibition of the Purkinje cells.…”

Section: Changes In the Gaba A Receptor Subunit Mrna In The Hippocampmentioning

confidence: 96%

Effects of cocaine administration on receptor binding and subunits mRNA of GABAA-benzodiazepine receptor complexes

Suzuki

Abe

Yamaguchi

et al. 2000

Synapse

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“…Thus NE acts as a neuromodulator in the cerebellum by post-synaptically facilitating stellate and/or basket cell induced GABA inhibition of Purkinje cell firing. This facilitation of GABAergic inhibition of Purkinje cell firing is specific to the GABA A receptor but not the GABA B receptor (10,11).…”

Section: Introductionmentioning

confidence: 82%

A review of age-related changes in cerebellar β-adrenergic function and associated motor learning

Gould

1999

AGE

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The present review provides an overview of agerelated changes in cerebellar ~-adrenergic function, associated motor learning, causal agents and possible treatments. Norepinephrine acts as a neuromodulator of Purkinje cell activity. With aging, however, the ability of norepinephrine to modulate Purkinje cell activity and specifically GABAergic inhibition of Purkinje cell activity is decreased. This age-associated deficit in cerebellar noradrenergic function correlates with deficits in acquisition of a motor learning task. Aged rats are delayed in acquiring a motor learning task that requires rats to adjust footfalls in order to cross a runway. The degree of deficit in cerebellar I~-adrenergic activity correlated positively with the degree of impairment in task acquisition. One possible causal agent for the ~-adrenergic deficit is free radical damage. Hyperoxia, which may generate free radical damage, induces cerebellar 13-adrenergic deficits in young rats but diet restriction and treatment with antioxidants can delay or reverse age-related deficits in cerebellar 13-adrenergic function in old rats.

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Potentiation of gamma-aminobutyric acid-mediated inhibition by isoproterenol in the cerebellar cortex: Receptor specificity

Cited by 70 publications

References 36 publications

Facilitation of GABAergic signaling in the retina by receptors stimulating adenylate cyclase.

Facilitation of GABAergic signaling in the retina by receptors stimulating adenylate cyclase.

Effects of cocaine administration on receptor binding and subunits mRNA of GABAA-benzodiazepine receptor complexes

A review of age-related changes in cerebellar β-adrenergic function and associated motor learning

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