The octopus brain shows a robust hippocampal-like activity-dependent LTP, which is NMDA-independent, yet associative and presynaptically expressed and, as shown here, also independent of protein synthesis. Have the molecular mechanisms for mediating this LTP evolved independently or have they converged? Here we report on a distinctive adaptation of the nitric-oxide (NO) system for mediation of the octopus LTP. Unlike the suggested role of NO in LTP induction in the hippocampus, in octopus, inhibitors of NO-synthase (NOS) did not block LTP induction but either 1) reversibly 'erased' LTP expression, suggesting that a constitutive elevation in NO mediates the presynaptic LTP expression or 2) 'reversed' LTP induction and maintenance because a second LTP could be induced after inhibitor washout. We therefore propose a protein synthesis-independent 'molecular-switch', whereby NO-dependent NOS reactivation maintains NOS in its active state. Thus, while the octopus LTP shows marked evolutionary convergence with LTP in vertebrates, an extreme molecular novelty has evolved to mediate it.
Embryonic and early postembryonic development of the cuttlefish Sepia officinalis (a cephalopod mollusk) occurs in coastal waters, an environment subject to considerable pressure from xenobiotic pollutants such as pharmaceutical residues. Given the role of serotonin in brain development and its interaction with neurodevelopmental functions, this study focused on fluoxetine (FLX), a selective serotonin reuptake inhibitor (SSRI, antidepressant). The goal was to determine the effects of subchronic waterborne FLX exposure (1 and 10 μg L(-1)) during the last 15 days of embryonic development on neurochemical, neurodevelopmental, behavioral, and immunological endpoints at hatching. Our results showed for the first time that organic contaminants, such as FLX, could pass through the eggshell during embryonic development, leading to a substantial accumulation of this molecule in hatchlings. We also found that FLX embryonic exposure (1 and 10 μg L(-1)) (1) modulated dopaminergic but not serotonergic neurotransmission, (2) decreased cell proliferation in key brain structures for cognitive and visual processing, (3) did not induce a conspicuous change in camouflage quality, and (4) decreased lysozyme activity. In the long term, these alterations observed during a critical period of development may impair complex behaviors of the juvenile cuttlefish and thus lead to a decrease in their survival. Finally, we suggest a different mode of action by FLX between vertebrate and non-vertebrate species and raise questions regarding the vulnerability of early life stages of cuttlefish to the pharmaceutical contamination found in coastal waters.
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