No abstract

Neuroinflammation is a host defense mechanism associated with neutralization of an insult and restoration of normal structure and function of brain. Neuroinflammation is a hallmark of all major CNS diseases. The main mediators of neuroinflammation are microglial cells. These cells are activated during a CNS injury. Microglial cells initiate a rapid response that involves cell migration, proliferation, release of cytokines/chemokines and trophic and/or toxic effects. Cytokines/chemokines stimulate phospholipases A 2 and cyclooxygenases. This results in breakdown of membrane glycerophospholipids with the release of arachidonic acid (AA) and docosahexaenoic acid (DHA). Oxidation of AA produces pro-inflammatory prostaglandins, leukotrienes, and thromboxanes. One of the lyso-glycerophospholipids, the other products of reactions catalyzed by phospholipase A 2 , is used for the synthesis of pro-inflammatory platelet-activating factor. These pro-inflammatory mediators intensify neuroinflammation. Lipoxin, an oxidized product of AA through 5-lipoxygenase, is involved in the resolution of inflammation and is anti-inflammatory. Docosahexaenoic acid is metabolized to resolvins and neuroprotectins. These lipid mediators inhibit the generation of prostaglandins, leukotrienes, and thromboxanes. Levels of prostaglandins, leukotrienes, and thromboxanes are markedly increased in acute neural trauma and neurodegenerative diseases. Docosahexaenoic acid and its lipid mediators prevent neuroinflammation by inhibiting transcription factor NFjB, preventing cytokine secretion, blocking the synthesis of prostaglandins, leukotrienes, and thromboxanes, and modulating leukocyte trafficking. Depending on its timing and magnitude in brain tissue, inflammation serves multiple purposes. It is involved in the protection of uninjured neurons and removal of degenerating neuronal debris and also in assisting repair and recovery processes. The dietary ratio of AA to DHA may affect neurodegeneration associated with acute neural trauma and neurodegenerative diseases. The dietary intake of docosahexaenoic acid offers the possibility of counter-balancing the harmful effects of high levels of AA-derived pro-inflammatory lipid mediators.

Processing of olfactory information in the antennal lobes of insects and olfactory bulbs of vertebrates is modulated by centrifugal inputs that represent reinforcing events. Octopamine release by one such pathway in the honeybee antennal lobe modulates olfactory processing in relation to nectar (sucrose) reinforcement. To test more specifically what role octopamine plays in the antennal lobe, we used two treatments to disrupt an octopamine receptor from Apis mellifera brain (AmOAR) function: (1) an OAR antagonist, mianserin, was used to block receptor function, and (2) AmOAR double-stranded RNA was used to silence receptor expression. Both treatments inhibited olfactory acquisition and recall, but they did not disrupt odor discrimination. These results suggest that octopamine mediates consolidation of a component of olfactory memory at this early processing stage in the antennal lobe. Furthermore, after consolidation, octopamine release becomes essential for recall, which suggests that the modulatory circuits become incorporated as essential components of neural representations that activate odor memory.

Octopamine (OCT) belongs to a group of compounds known as biogenic amines. OCT, a monohydroxylic analog of norepinephrine, is found in both vertebrate and invertebrate nervous systems. OCT is present in relatively high concentrations in the neuronal and nonneuronal tissues of most invertebrate species studied. However, OCT occurs as a trace amine in vertebrates where its physiological significance remains uncertain. OCT acts as a neurotransmitter, neuromodulator, and neurohormone in insect nervous systems where it prominently influences multiple physiological events. In the peripheral nervous system, OCT modulates the activity of flight muscles, peripheral organs, and most sense organs. In the central nervous system, OCT is essential for the regulation of motivation, desensitization of sensory inputs, arousal, initiation, and maintenance of various rhythmic behaviors, hygiene behavior, and complex social behaviors, including establishment of labor, as well as learning and memory. As a neurotransmitter, OCT regulates endocrine gland activity and controls the emission of light in the firefly lantern. As a neurohormone, OCT is released into hemolymph, transported to target tissues, and induces mobilization of lipids and carbohydrates, preparing insects for a period of extended activity or assisting recovery from a period of increased energy demand. OCT modulates hemocytic nodulation in nonimmune larvae and enhances phagocytosis as a neurohormone. OCT exerts its effects by binding to specific receptors belonging to the superfamily of G protein-coupled receptors and shares the structural motif of seven transmembrane domains. Activation of octopaminergic receptor types is coupled with different second messenger pathways depending on the species, tissue source, receptor type, and cell line used for expression of the cloned receptor. OCT-mediated generation of second messengers is associated with changes in cellular response, affecting insect behaviors. This review describes the roles of OCT in insect nervous systems at the behavioral and molecular levels.

No abstract