Agonistic behaviour and electric signalling in a mormyrid fish, Gnathonemus petersii

1. Agonistic motor behaviour and concurrent electric signalling were studied in individually held, residential Gnathonemus petersii. Aggressive behaviour was elicited by presenting a specimen of a closely related species, Mormyrus rume, for 3 min a day. 2. The principal agonistic motor patterns are described (Fig. 2). Among them head butt, approach and lateral display were further analysed. 3. The electrical activity displayed during agonistic behaviour was found to differ fundamentally both from isolated resting and swimming conditions. The mean discharge rate recorded during aggressive behaviour (31 Hz, Fig. 3 c) is approximately twice the rate observed in an isolated swimming fish (Fig. 3b) and three times the rate displayed by a resting animal (Fig. 3a). An attacking G. petersii exhibits a much greater range of electric organ discharge (EOD) intervals than isolated swimming or resting individuals. EOD-interval histograms recorded from attacking fish show two sharp modes at high discharge rate; there are no intermediate intervals. 4. During the course of an attack, the initially low and variable discharge rate increases fairly linearly as the distance from the attacked fish diminishes (Fig. 9). The EOD rate associated with physical contact (head butt) comprises between 60 and 80 Hz in 24 of 28 attacks analysed; the dominant mode of the distribution is 61 Hz (Fig. 8). 5. During subsequent lateral display, G. petersii emits a high discharge rate pattern consisting of two types of ldquosteady-staterdquo activities which may last up to a few seconds: the first is a fairly regular alternation of approx. 16 and 8 ms intervals (paired pulses); this pattern gives rise to the two peaks of high discharge rate in the interval histogram (Fig. 3c). The second is a regular sequence of either 16 or 8 ms intervals (Fig. 4A). The only female among the animals used in our study showed the same display but did not exhibit the highest possible discharge rate (i.e. a regular sequence or 8 ms intervals; Fig. 4B). The high discharge rate is terminated by a sudden discharge break (Figs. 4A and 6). 6. It is suggested that the attack-associated EOD rate increase is a remnant of an ordinary locomotory pattern which has changed its function to a ritualised aggressive signal that occurs in a socially significant and well-defined context. The high discharge rate might serve three functions: (i) behavioural isolation of closely related, sympatrically living mormyrids (perhaps by character displacement); (ii) recognition of sexes; (iii)_synchronisation of mates during courtship

Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats

In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces status epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in postnatal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stag