Journal of Neuroscience, Vol 13, 1862-1878, Copyright © 1993 by Society for Neuroscience
The jamming avoidance response in Eigenmannia is controlled by two separate motor pathways
W Metzner
University of California at San Diego, Neurobiology Unit, Scripps Institution of Oceanography, La Jolla 92093-0202.
The gymnotiform fish Eigenmannia generates weakly electric signals for
electrolocation and communication. The signals are produced by electric
organ discharges (EODs) that are driven by a medullary pacemaker nucleus.
To avoid jamming by neighboring conspecifics with similar frequencies, a
fish raises its own EOD frequency if the neighbor's frequency is lower, and
it lowers its EOD frequency if the neighbor's frequency is higher (Watanabe
and Takeda, 1963). Both the raising and lowering of EOD frequency of this
jamming avoidance response (JAR; Bullock et al., 1972) are thought to be
controlled by feature- extracting neurons in the diencephalic prepacemaker
nucleus (PPn-G) that discriminate the sign of the frequency difference
between the jamming signal and the fish's EOD (Kawasaki et al., 1988a; Rose
et al., 1988; for review, see Heiligenberg, 1991). These prepacemaker
neurons are excited in response to lower jamming frequencies, thereby
raising the frequency, and inhibited by higher jamming frequencies,
producing a discharge deceleration. The results of experiments presented
here, however, suggest a mechanism for the motor control of the JAR that is
different from the one described previously (see, e.g., Heiligenberg,
1991). Two prepacemaker nuclei, one PPn-G and one sublemniscal prepacemaker
nucleus (SPPn) (Keller et al., 1991 a,b), which provide the only known
inputs to the pacemaker, were lesioned selectively. This article explores
the effects of these lesions on the JAR. Pharmacological experiments were
used to elucidate the transmitter types involved. The results suggest that
the JAR is controlled by two separate motor pathways. One controls
frequency rises and originates in the dorsal substructure of the nucleus
electrosensorius (Keller, 1988). It sends excitatory connections to the
diencephalic prepacemaker and finally to the pacemaker nucleus, where
AMPA-type receptors mediate the synaptic transmission. The second pathway
controls frequency decreases and originates in the ventral substructure of
the nucleus electrosensorius. It provides GABAergic input to the SPPn. The
SPPn is tonically active and also controls the EOD frequency even in the
absence of jamming signals. Its projection to the pacemaker nucleus is
mediated by NMDA-type receptors. The results of this study suggest that
there is no single population of final, feature-extracting elements or
"recognition units" that controls JAR-related shifts of the pacemaker
frequency. Instead, the motor control of the JAR consists of an interaction
of two independent pathways according to a "push-pull" principle.
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