Synaptic specificity in the first instar cockroach: patterns of monosynaptic input from filiform hair afferents to giant interneurons

1989 ◽  
Vol 166 (1) ◽  
Author(s):  
JonathanM. Blagburn
Keyword(s):  
Synaptic Specificity ◽  
Giant Interneurons ◽  
First Instar ◽  
Filiform Hair

Regeneration of cercal filiform hair sensory neurons in the first-instar cockroach restores escape behavior

1997 ◽  
Vol 33 (4) ◽  
pp. 439-458 ◽  
Author(s):  
Michael Stern ◽  
Vernita L. Ediger ◽  
Charles R. Gibbon ◽  
Jonathan M. Blagburn ◽  
Jonathan P. Bacon
Keyword(s):  
Sensory Neurons ◽  
Escape Behavior ◽  
First Instar ◽  
Filiform Hair

Ectopic sensory neurons in mutant cockroaches compete with normal cells for central targets

Development ◽  
1992 ◽  
Vol 115 (3) ◽  
pp. 773-784
Author(s):  
J.P. Bacon ◽  
J.M. Blagburn
Keyword(s):  
Sensory Neurons ◽  
Periplaneta Americana ◽  
Normal Development ◽  
Lateral Position ◽  
Competitive Interactions ◽  
Afferent Neuron ◽  
Synaptic Connections ◽  
First Instar ◽  
Terminal Ganglion ◽  
Filiform Hair

The cercus of the first instar cockroach, Periplaneta americana, bears two filiform hairs, lateral (L) and medial (M), each of which is innervated by a single sensory neuron. These project into the terminal ganglion of the CNS where they make synaptic connections with a number of ascending interneurons. We have discovered mutant animals that have more hairs on the cercus; the most typical phenotype, called “Space Invader” (SI), has an extra filiform hair in a proximo-lateral position on one of the cerci. The afferent neuron of this supernumerary hair (SIN) “invades the space” occupied by L in the CNS and makes similar synaptic connections to giant interneurons (GIs). SIN and L compete for these synaptic targets: the size of the L EPSP in a target interneuron GI3 is significantly reduced in the presence of SIN. Morphometric analysis of the L afferent in the presence or absence of SIN shows no anatomical concomitant of competition. Ablation of L afferent allows SIN to increase the size of its synaptic input to GI3. Less frequently in the mutant population, we find animals with a supernumerary medical (SuM) sensillum. Its afferent projects to the same neuropilar region as the M afferent, makes the same set of synaptic connections to GIs, and competes with M for these synaptic targets. The study of these competitive interactions between identified afferents and identified target interneurons reveals some of the dynamic processes that go on in normal development to shape the nervous system.

scholarly journals Presynaptic Depolarization Mediates Presynaptic Inhibition at a Synapse Between An Identified Mechanosensory Neurone and Giant Interneurone 3 in the First Instar Cockroach, Periplaneta Americana

1987 ◽  
Vol 127 (1) ◽  
pp. 135-157 ◽  
Author(s):  
JONATHAN M. BLAGBURN ◽  
DAVID B. SATTELLE
Keyword(s):  
Presynaptic Inhibition ◽  
Periplaneta Americana ◽  
Cholinergic Synapse ◽  
Sensory Neurone ◽  
First Instar ◽  
Delayed Rectification ◽  
Intracellular Microelectrodes ◽  
Spike Bursts ◽  
Giant Interneurone ◽  
Filiform Hair

Intracellular microelectrodes were used to study presynaptic inhibition at a cholinergic synapse between identified neurones: the lateral filiform hair sensory neurone (LFHSN) and giant interneurone 3 (GI3) in the terminal ganglion of the first instar cockroach Periplaneta americana. The LFHSN-GI3 synapse was shown to fulfil physiological criteria for monosynaptic transmission: the latency of the EPSPs was 1.4 ms and was constant during high-frequency firing of LFHSN; transmission was progressively and reversibly abolished by replacement of Ca2+ with Mg2+. Movement of the lateral filiform hair towards the cereal tip produced a burst of spikes in LFHSN and a burst of EPSPs in GI 3. Movement of the medial filiform hair towards the base of the cercus produced a burst of spikes in the medial filiform hair sensory neurone (MFHSN) and a burst of EPSPs in GI 2. EPSPs evoked in GI 3 by LFHSN spikes were inhibited during bursts of EPSPs in GI 2 which were evoked by MFHSN spikes. LFHSN was depolarized and its spikes were reduced in amplitude during spike bursts in MFHSN. Reduction in LFHSN spike amplitude reduced GI 3 EPSPs. This phenomenon was attributed, therefore, to presynaptic inhibition. The occurrence of presynaptic inhibition was dependent upon the degree of delayed rectification exhibited by the LFHSN axon. Hyperpolarization of LFHSN increased spike height, but did not increase the amplitude of GI 3 EPSPs. The delay between the onset of MFHSN-evoked EPSPs in GI 2 and MFHSNevoked depolarizations in LFHSN suggested that MFHSN does not synapse directly onto LFHSN. Neither depolarization nor hyperpolarization of GI 2 had any effect on MFHSN-mediated presynaptic inhibition of LFHSN-GI 3 transmission, therefore it was considered unlikely that GI 2 synapses onto LFHSN. Prolonged hyperpolarization lowered the LFHSN spike threshold and temporarily abolished presynaptic inhibition. Bursts of spikes in LFHSN mediated presynaptic inhibition of MFHSN-GI2 EPSPs. Mutual presynaptic inhibition by the FHSNs may have a functional significance in sharpening the boundaries of the GIs' directional sensitivities.

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