The fight and flight responses of crickets depleted of biogenic amines

Abstract

Aggressive and escape behaviors were analysed in crickets (Orthoptera) treated with either reserpine, a nonspecific depleter of biogenic amines, or the synthesis inhibitors ␣-methyltryptophan (AMTP) and ␣-methyl-p-tyrosine (AMT) to specifically deplete serotonin, respectively dopamine and octopamine. Standard immunocytochemical techniques were used to verify depletion from central nervous tissue, and determine the effective dosages. Reserpinized crickets became exceedingly lethargic and had severely depressed escape responses. However, they were still able to express all the major elements of the escalating sequences of stereotype motor performances that typifies normal aggressive behavior in the cricket. AMT and AMTP treatment had opposing influences on escape behavior, being enhanced by serotonin depletion, but depressed by dopamine/octopamine depletion. AMTP-induced serotonin depletion had no influence on aggressive or submissive behaviors.AMT-treated crickets could normally only be brought to fight by coaxing. Though capable of expressing aggressive behavior per se, agonistic encounters between AMT-treated crickets were shorter, and rarely involved actual physical interactions. Hence, although amines seem to have similar actions on escape behavior in insects and crustaceans, the aminergic control of aggression seems to be fundamentally different in these arthropods groups. We conclude that amines are not in principle required for the initiation and operation of the motor circuits underlying aggression in the cricket. However, octopamine and/or dopamine seem necessary for establishing a level of excitability sufficient for aggressive behavior to become overt in response to appropriate natural releasing stimuli.

Rapid behavioural gregarization in the desert locust, Schistocerca gregaria entails synchronous changes in both activity and attraction to conspecifics

“…In this experiment locusts were pre-treated by repeated 40 μl injections of 0.1 mM AMTP or a locust saline control 5 days, 3 days and 1 day before the experiment, and on the day of the experiment itself, when locusts also were subjected to 2 h of tactile stimulation on a hind femur before being observed in the arena. Like 5HTP, AMTP injected systemically has a behavioural effect in Orthoptera (Stevenson et al, 2000). AMTP-treated locusts failed to gregarize, whereas the saline treated controls underwent considerable behavioural change (Fig.…”

A Circuit Node that Integrates Convergent Input from Neuromodulatory and Social Behavior-Promoting Neurons to Control Aggression in Drosophila

“…Consistent with such a function, OAergic fibers are broadly distributed across the entire Drosophila CNS (Monastirioti et al , 1995), as are NE fibers in vertebrates (Schwarz et al , 2015; Espana et al , 2016). Thus OARNs could enhance aggression by increasing arousal, and there is evidence for such a function in crickets (Stevenson et al , 2000). However, manipulations of R47A04 aSP2 neurons that increased or decreased aggression did not affect locomotion, circadian activity or sleep.…”

Assessing segmental versus non-segmental features in the ventral nervous system of onychophorans (velvet worms)

“…Its specificity has been tested by Steinbusch and Tilders [93] and Steinbusch et al [94]. The staining protocol is based on that of Stevenson et al [95], developed for insects. The nerve cords were dissected in ice-cold sodium cacodylate buffer (pH 6.2) and fixed in 6% glutaraldehyde in 0.1 M sodium cacodylate buffer containing 0.5% glacial acetic acid with 1% sodium metabisulphite (SMB) for 3 h at room temperature.…”

“…This antiserum was shown to recognise serotonergic neurons in molluscs [96], insects [95] and rats [97]. The dissected nerve cords were fixed in 3% PFA in PBS and treated as described above for the anti-GABA immunohistochemistry, except for the following modifications: The nerve cords were not incubated in sodium borohydride, which is only required for the glutaraldehyde fixation, and the primary antibody was diluted 1:1500.…”