Excitatory actions of synaptically released catecholamines in the rat lateral geniculate nucleus.
The gating properties of thalamic relay neurons are influenced by the actions of a variety of neuromodulators in concert with the intrinsic properties of these relay neurons. In this study, we have investigated the consequences of synaptically released catecholamines on the excitability of neurons in the rat dorsal lateral geniculate nucleus. Tetanic stimulation of the optic tract, in which catecholamine fibers also course near or through, produced a strong depolarization that consisted of a fast and slow component. The fast excitatory postsynaptic potential was attenuated by ionotropic glutamate receptor antagonists and further unmasked the slow excitatory postsynaptic potential. The amplitude of the slow excitatory postsynaptic potential was dependent on the frequency and intensity of the tetanic stimulation. The alpha1-adrenergic receptor antagonist, prazosin, and the D1-like dopamine receptor antagonist, SCH23390, attenuated the slow excitatory postsynaptic potential; however, the slow excitatory postsynaptic potential was unaltered by metabotropic glutamate, cholinergic, alpha2-adrenergic, and beta-adrenergic receptor antagonists. On the other hand, tetanic stimulation of the optic radiations (corticothalamic axons) evoked a slow excitatory postsynaptic potential that was completely attenuated by metabotropic glutamate receptor antagonists. Our results suggest that tetanic stimulation of catecholamine fibers within the optic tract produces synaptic release of norepinephrine and dopamine that in turn activates both alpha(1)-adrenergic and D1-like dopamine receptors leading to a robust membrane depolarization. By altering the excitability of relay neurons, ascending activating systems may modulate the efficacy of information transfer through the thalamus.
Govindaiah
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Department of Molecular and Integrative Physiology, University of Illinois, 524 Burrill Hall, 407 South Goodwin Avenue, Urbana, 61801, USA.
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D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000344:Afferent Pathways / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D018492:Dopamine Antagonists / Q000494:pharmacology; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D005829:Geniculate Bodies / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D009924:Organ Culture Techniques; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014795:Visual Pathways / Q000502:physiology
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D002395:Catecholamines; D018492:Dopamine Antagonists; D018691:Excitatory Amino Acid Antagonists; D018340:Receptors, Adrenergic, alpha-1; D017447:Receptors, Dopamine D1; D004298:Dopamine; D009638:Norepinephrine