This study examined stimulus-response properties of somatosensory receptors on the head of rainbow trout, Oncorhynchus mykiss, using extracellular recording from single cells in the trigeminal ganglion. Of 121 receptors recorded from 39 fish, 17 were polymodal nociceptors, 22 were mechanothermal nociceptors, 18 were mechanochemical receptors, 33 were fast adapting mechanical receptors and 31 were slowly adapting mechanical receptors. Mechanical thresholds were higher in polymodal nociceptors than in either slowly adapting or fast adapting mechanical receptors, whereas thermal thresholds of mechanothermal nociceptors were higher than those of polymodal nociceptors. Polymodal nociceptors and mechanochemical receptors gave similar responses to topical applications of acid. All receptor types except mechanothermal nociceptors showed an increase in peak firing frequency with increased strength of mechanical stimulation, with evidence of response saturation at higher intensities. Mechanothermal, but not polymodal, nociceptors showed an increase in firing response to increased temperature. None out of 120 receptors tested gave any response to the temperature range +4 degrees C to -7 degrees C, indicating an absence of cold nociceptors. Attempts to evoke sensitization of receptors using chemical or heat stimuli were unsuccessful, with receptors showing either a return to control responses or irreversible damage. Comparisons are made between somatosensory receptors characterized here in a fish and those of higher vertebrates.

A potentially painful experience may modify normal behavioural responses. To gauge the importance of pain relative to predation or social status, we presented competing stimuli, a predator cue or an unfamiliar social group, to two groups of noxiously treated rainbow trout, Oncorhynchus mykiss. In the predator cue experiment, fish were classified as bold or shy. Noxiously stimulated fish did not show antipredator responses, suggesting that pain is the imperative. In the social status experiment, noxiously stimulated fish held individually and undisturbed showed an increase in respiration rate and plasma cortisol. As a comparison, we used the dominant or subordinate fish in a group as the noxiously stimulated fish. After the noxious treatment, we returned this test fish to a familiar or unfamiliar social group. Neither dominants nor subordinates showed a negative change in physiology compared to their controls. However, in a familiar group the dominant was much less aggressive, suggesting a behavioural impairment in response to noxious stimulation. In an unfamiliar group, no reduction of aggression was seen, suggesting that maintaining dominance status took priority over showing signs of pain. These findings may reflect an ability to prioritize motivational drivers in fish, and as such provides evidence for central processing of pain rather than merely showing a nociceptive reflex. In animal models of pain, exposure to a new circumstance or a potentially fear-inducing or stressful situation reduces pain reactivity (e.g.

Recent research has shown the possibility of pain perception in fish; therefore, the use of analgesia or "painkillers" should be considered for invasive procedures. However, there is relatively little information on the effectiveness of analgesic drugs nor on the appropriate dose for fish. This study assessed the efficacy of three types of drug: an opioid, buprenorphine, a non-steroidal anti-inflammatory drug (NSAID), carprofen and a local anaesthetic, lidocaine. Each drug was tested at three doses on rainbow trout that were noxiously stimulated and the most effective dose was also given to fish experiencing no pain to investigate side-effects. Ventilation rate and time to resume feeding were used as pain indicators, together with the amount of activity and plasma cortisol concentrations to gauge any detrimental side effects. Buprenorphine at all three doses had limited impact on the fish's response to a painful stimulus. Carprofen ameliorated effects of noxious stimulation on time to resume feeding but activity was reduced more than by noxious treatment alone. Lidocaine reduced all of the pain indicators measured with the lowest, most effective dose being 1 mg per fish. None of the analgesics led to raised plasma cortisol compared to control groups. This study demonstrates that lidocaine could be recommended for use in rainbow trout to ameliorate possible pain-related responses.

Urotensin II (UII) is a potent vasoconstrictor in mammals, but the source of circulating UII remains unclear. Investigations of the caudal neurosecretory system (CNSS), considered the major source of UII in fish, alongside target tissue expression of UII receptor (UT), can provide valuable insights into this highly conserved regulatory system. We report UII gene characterization, expression of the first fish UT, and responses to salinity challenge in flounder. The 12-aa UII peptide shares 73% sequence identity with pig and human UII. Flounder UT receptor shares 56.7% identity with rat. Although the CNSS is the major site of UII expression, RT-PCR revealed expression of UII and UT in all tissues tested. Around 30-40% of large CNSS Dahlgren cells expressed UII, alone or in combination with urotensin I and/or corticotrophin releasing hormone. Immunolocalization of UT in osmoregulatory tissues (gill, kidney) was associated with vascular elements. There were no consistent differences in CNSS UII expression or plasma UII between seawater (SW)- and freshwater (FW)-adapted fish, although gill and kidney UT expression was lower in FW animals. After acute transfer from SW to FW, plasma UII and kidney and gill UT expression were reduced, whereas UT expression in kidney was increased after reverse transfer. UII appears to be more important to combat dehydration and salt-loading in SW than the hemodilution faced in FW. Potentially, altered target tissue sensitivity through changes in UT expression, is an important physiological controlling mechanism, not only relevant for migratory fish but also likely conserved in mammals.

CRH and urotensin I (UI) are neuroendocrine peptides that belong to the superfamily of corticotropin-releasing factors. In mammals, these peptides regulate the stress response and other central nervous system functions, whereas in fish an involvement for UI in osmoregulation has also been suggested. We have identified, characterized, and localized the genes encoding these peptides in a unique fish neuroendocrine organ, the caudal neurosecretory system (CNSS). The CRH and UI precursors, isolated from a European flounder CNSS library, consist of 168 and 147 amino acid residues, respectively, with an overall homology of approximately 50%. Both precursors contain a signal peptide, a divergent cryptic region and a 41-amino acid mature peptide with cleavage and amidation sites. Genomic organization showed that whole CRH and UI coding sequences are contained in a single exon. Northern blot analysis and quantitative PCR of a range of tissues confirmed the CNSS as a major site of expression of both CRH and UI and thus serves as a likely source of circulating peptides. In situ hybridization demonstrated that CRH and UI colocalize to the same cells of the CNSS. Our findings suggest that, in euryhaline fish, the CNSS is a major site of production of CRH and probably contributes to the high circulating levels observed in response to specific environmental challenges. Furthermore, the localization of CRH and UI within the same cell population suggests an early, possibly shared role for these peptides in controlling stress-mediated adaptive plasticity.

The exact nature of the olfactory signals that arrive in the brain from the periphery, and their reproducibility, remain essentially unknown. In most organisms, the sheer number of olfactory sensory neurons (OSNs) makes it impossible to measure the individual responses of the entire population. We measured the individual in situ electrophysiological activity of OSNs in Drosophila larvae, in response to stimulation with 10 aliphatic odors (alcohols and esters). We studied control larvae (a total of 296 OSNs) and larvae with a single functional OSN, created using the Gal4-upstream activator sequence system. Most OSNs showed consistent, precise responses (either excitation or inhibition) in response to a given odor. Some OSNs also showed qualitatively variable responses ("fuzzy coding"). This robust variability was an intrinsic property of these neurons: it was not attributable to odor type, concentration, stimulus duration, genotype, or interindividual differences, and was seen in control larvae and in larvae with one and two functional OSNs. We conclude that in Drosophila larvae the peripheral code combines precise coding with fuzzy, stochastic responses in which neurons show qualitative variability in their responses to a given odor. We hypothesize that fuzzy coding occurs in other organisms, is translated into differing degrees of activation of the glomeruli, and forms a key component of response variability in the first stages of olfactory processing.

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The effects of a variety of neuromodulator substances on rhythmic motor output and activity in neurons in the feeding circuitry of Lymnaea stagnalis were examined. Each neuromodulator produced a unique combination of effects at different levels in the network: i.e., pattern-generating interneurons (N1, N2, and N3), an identified higher-order interneuron (cerebral giant cell, CGC), and buccal motoneurons. 5-Hydroxytryptamine, acetylcholine, and FMRFamide all inhibited rhythmic motor activity. However, this was achieved in different ways. Dopamine changed the nature of rhythmic activity from one in which N2 interneuronal activity was predominant ("N2 rhythm") to a feeding rhythm. Dopamine was the only substance capable of activating the feeding rhythm. Activity in the CGC was increased by 5-hydroxytryptamine, dopamine, and acetylcholine and reduced by FMRFamide. Differential responses in buccal motoneurons were also observed. The results are discussed in relation to previous work on other species and also in terms of the selection of different patterns of motor output by neuromodulators.