The Amygdala Responds Rapidly to Flashes Linked to Direct Retinal Innervation: A Flash-evoked Potential Study Across Cortical and Subcortical Visual Pathways
10.1007/s12264-021-00699-4
- Author:
Yanmei CHEN
1
;
Yiling NI
1
;
Jianhong ZHOU
1
;
Hua ZHOU
1
;
Jichuan ZHANG
1
;
Qian ZHONG
2
;
Xinyue LI
2
;
Yuanye MA
2
;
Jingkuan WEI
2
Author Information
1. Department of Basic Medicine, Medical School, Kunming University of Science and Technology
2. State Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology
- Publication Type:Journal Article
- Keywords:
Amygdala;
Corticosterone;
Flash-evoked potential;
Subcortical visual pathway;
Superior colliculus
- From:
Neuroscience Bulletin
2021;37(8):1107-1118
- CountryChina
- Language:Chinese
-
Abstract:
Rapid detection and response to visual threats are critical for survival in animals. The amygdala (AMY) is hypothesized to be involved in this process, but how it interacts with the visual system to do this remains unclear. By recording flash-evoked potentials simultaneously from the superior colliculus (SC), lateral posterior nucleus of the thalamus, AMY, lateral geniculate nucleus (LGN) and visual cortex, which belong to the cortical and subcortical pathways for visual fear processing, we investigated the temporal relationship between these regions in visual processing in rats. A quick flash-evoked potential (FEP) component was identified in the AMY. This emerged as early as in the LGN and was approximately 25 ms prior to the earliest component recorded in the SC, which was assumed to be an important area in visual fear. This quick P1 component in the AMY was not affected by restraint stress or corticosterone injection, but was diminished by RU38486, a glucocorticoid receptor blocker. By injecting a monosynaptic retrograde AAV tracer into the AMY, we found that it received a direct projection from the retina. These results confirm the existence of a direct connection from the retina to the AMY, that the latency in the AMY to flashes is equivalent to that in the sensory thalamus, and that the response is modulated by glucocorticoids.
