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Local cholinergic interneurons modulate GABA ergic inhibition in the chicken optic tectum
Author(s) -
Weigel Stefan,
Luksch Harald
Publication year - 2014
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12438
Subject(s) - neuroscience , tectum , superior colliculus , inhibitory postsynaptic potential , cholinergic , disinhibition , midbrain , bicuculline , muscarinic acetylcholine receptor , nicotinic agonist , chemistry , acetylcholine , stimulation , gabaa receptor , biology , receptor , central nervous system , endocrinology , biochemistry
Abstract The chicken optic tectum (TeO) and its mammalian counterpart, the superior colliculus, are important sensory integration centers. Multimodal information is represented in a topographic map, which plays a role in spatial attention and orientation movements. The TeO is organised in 15 layers with clear input and output regions, and further interconnected with the isthmic nuclei ( NI ), which modulate the response in a winner‐takes‐all fashion. While many studies have analysed tectal cell types and their modulation from the isthmic system physiologically, little is known about local network activity and its modulation in the tectum. We have recently shown with voltage‐sensitive dye imaging that electrical stimulation of the retinorecipient layers results in a stereotypic response, which is under inhibitory control [S. Weigel & H. Luksch ([Weigel, S., 2012]) J. Neurophysiol ., 107 , 640–648]. Here, we analysed the contribution of acetylcholine ( AC h) and the NI to evoked tectal responses using a pharmacological approach in a midbrain slice preparation. Application of the nicotinic AC h receptor ( AC hR) antagonist curarine increased the tectal response in amplitude, duration and lateral extent. This effect was similar but less pronounced when γ‐aminobutyric acid A receptors were blocked, indicating interaction of inhibitory and cholinergic neurons. The muscarinic AC hR antagonist atropine did not change the response pattern. Removal of the NI , which are thought to be the major source of cholinergic input to the TeO, reduced the response only slightly and did not result in a disinhibition. Based on the data presented here and the neuroanatomical literature of the avian TeO, we propose a model of the underlying local circuitry.