Aminergic Regulation of Anoxic Coma in Locusta migratoria

Abstract

Cortical spreading depression (CSD), a phenomenon underlying stroke and head trauma, involves the depolarization of neurons in one localized area that rapidly propagates to and depolarizes surrounding cells. CSD is characterized by a sudden increased concentration of extracellular potassium ions (K+), which is also generated by cellular stressors like anoxia. The purpose of this study is to examine the role of biogenic amines in the time to succumb and time to recover from anoxic coma in Locusta migratoria, a locust which is regularly exposed to anoxia in its natural environment and survive by entering a reversible coma (a spreading‐depression like event). Locusts were first immersed in water for 30 minutes and the time to succumb, ventilate, and stand upright were measured. There were 5 treatment groups with each one paired to a control group using saline injections: 1) octopamine (OA) and its antagonist epinastine (EP), 2) dopamine (DA) and its antagonist haloperidol, 3) serotonin (5‐HT) and its antagonist mianserin, 4) tyramine (TA) and its antagonist yohimbine, and 5) histamine (HA) and its antagonist pyrilamine maleate salt. Results indicated that EP‐injected locusts took significantly longer to succumb, ventilate, and stand upright compared to controls. Mianserin‐injected locusts also took significantly longer to succumb, ventilate, and stand upright.