Differential modulation of thalamic neurons by optokinetic nuclei in the pigeon.
The visual system in the pigeon is composed of the tectofugal, thalamofugal and accessory optic pathways. Though their anatomy and physiology have been extensively studied, the functional interactions between these pathways are largely unknown. The present study shows by using multiple electrophysiological techniques that firing activity in the nucleus opticus principalis thalami (OPT) of the thalamofugal pathway is differentially modulated by the pretectal nucleus lentiformis mesencephali (nLM) and the nucleus of the basal optic root (nBOR) of the accessory optic system, two optokinetic nuclei responsible for generating eye movements to stabilize the image on the retina. Reversible inactivation, electrical stimulation, microiontophoresis and receptive field mapping experiments all consistently indicate that the nBOR-OPT pathway is inhibitory and mediated by GABA as a transmitter and its GABAA receptors, whereas the nLM-OPT pathway is excitatory and mediated by glutamate as a transmitter and its NMDA receptors. They also differentially modulate the size and/or responsiveness of receptive fields in OPT cells as well. Numerous electrode tip sites were histologically confirmed in the neural structures under study. The results suggest that these optokinetic nuclei may dually modulate the transfer of visual information from the retina to the telencephalon at the thalamic level during eye movements.
Cao
Peng
P
Laboratory for Visual Information Processing, State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing 100101, PR China.
Yang
Yan
Y
Yang
Yang
Y
Wang
Shu-Rong
SR
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology / Q000528:radiation effects; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D001931:Brain Mapping; D010856:Columbidae; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D010775:Photic Stimulation / Q000379:methods; D010879:Piperazines / Q000494:pharmacology; D013788:Thalamus / Q000166:cytology*; D014795:Visual Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D000779:Anesthetics, Local; D018691:Excitatory Amino Acid Antagonists; D010879:Piperazines; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D008012:Lidocaine; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; D000109:Acetylcholine