GnRH suppresses excitability of visual processing neurons in the optic tectum.
Animals change their behavior in response to sensory cues in the environment as well as their physiological status. For example, it is generally accepted that their sexual behavior is modulated according to seasonal environmental changes or the individual's maturational/reproductive status, and neuropeptides have been suggested to play important roles in this process. Some behavioral modulation arises from neuropeptide modulation of sensory information processing in the central nervous system, but the neural mechanisms still remain unknown. Here we focused on the neural basis of neuropeptide modulation of visual processing in vertebrates. The terminal nerve neurons that contain gonadotropin-releasing hormone 3 (TN-GnRH3 neurons) are suggested to modulate reproductive behavior and have massive projections to the optic tectum (OT), which plays an important role in visual processing. In the present study, to examine whether GnRH3 modulates retino-tectal neurotransmission in the OT, we analyzed the effect of GnRH3 electrophysiologically and morphologically. We found that field potentials evoked by optic tract fiber stimulation, which represent retino-tectal neurotransmission, were modulated postsynaptically by GnRH3. Whole cell recording from postsynaptic neurons in the retino-tectal pathway suggested that GnRH3 activates large-conductance Ca(2+)-activated K(+) (BK) channels and thereby suppresses membrane excitability. Furthermore, our improved morphological analysis using fluorescently labeled GnRH peptides showed that GnRH receptors are localized mainly around the cell bodies of postsynaptic neurons. Our results indicate that TN-GnRH3 neurons modulate retino-tectal neurotransmission by suppressing the excitability of projection neurons in the OT, which underlies the neuromodulation of behaviorally relevant visual information processing by the neuropeptide GnRH3.
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan;
Chie
C
Umatani
Laboratory of Bioorganic Medical Chemistry and Chemogenomics, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan;
Ryosuke
R
Misu
Laboratory of Bioorganic Medical Chemistry and Chemogenomics, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan;
Shinya
S
Oishi
Laboratory for Behavioral Genetics, RIKEN Brain Science Institute (BSI), Saitama, Japan; and.
Kazuhiko
K
Yamaguchi
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan; Laboratory of Fish Biology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi, Japan.
Hideki
H
Abe
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan; okay@bs.s.u-tokyo.ac.jp.
Yoshitaka
Y
Oka
D000818:Animals; D004558:Electric Stimulation; D029941:Fish Proteins / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000008:administration & dosage / Q000502:physiology*; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D065866:Optic Tract / Q000502:physiology*; D011761:Pyrrolidonecarboxylic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives*; D011966:Receptors, LHRH / Q000378:metabolism; D013477:Superior Colliculi / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D055366:Synaptic Potentials / Q000187:drug effects; D014795:Visual Pathways / Q000187:drug effects / Q000502:physiology
D029941:Fish Proteins; D051036:Large-Conductance Calcium-Activated Potassium Channels; D011966:Receptors, LHRH; C448022:gonadotropin-releasing hormone-III; D007987:Gonadotropin-Releasing Hormone; D011761:Pyrrolidonecarboxylic Acid
GnRH; excitability; neuromodulation; neuropeptide; retino-tectal neurotransmission