Activity-Dependent Enhancement of Presynaptic Inhibition in
            <i>Aplysia</i>
            Sensory Neurons

Small, SA; Kandel, ER; Hawkins, RD

doi:10.1126/science.2538924

Cited by 33 publications

(16 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On average, LPL16 stimulation produced a decrease in spike duration in the sensory neuron, which was maximal immediately after the stimulation and had not fully recovered 1 min later. Small et al -Identified FMRFamide-immunoreactive Inhibitory Neuron similar in amplitude and duration to the inhibition produced by tail shock (Mackey et al, 1987) or by brief exposure to FMRFamide (Small et al, 1989). The inhibition produced by LPL16 stimulation has a presynaptic component.…”

Section: Distributionmentioning

confidence: 99%

“…This synaptic inhibition can be mimicked by application of the peptide FMRFamide, which acts through the intracellular second messenger arachidonic acid and its lipoxygenase metabolites to open S-type K+ channels, narrow action potentials, and decrease transmitter release from the sensory neurons (Abrams et al, 1984;Belardetti et al, 1987;Mackey et al, 1987;Piomelli et al, 1987). Like the facilitation produced by S-HT, the inhibition produced by FMRFamide undergoes activity-dependent enhancement (Eliot et al, 1989;Small et al, 1989).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Identified FMRFamide-immunoreactive neuron LPL16 in the left pleural ganglion of Aplysia produces presynaptic inhibition of siphon sensory neurons

et al. 1992

View full text Add to dashboard Cite

The gill- and siphon-withdrawal reflex of Aplysia undergoes transient inhibition following noxious stimuli such as tail shock. This behavioral inhibition appears to be due in part to transient presynaptic inhibition of the siphon sensory cells, which can be mimicked by application of the peptide FMRFamide. Although FMRFamide is widespread in the Aplysia nervous system, an FMRFamide-containing inhibitory neuron has not previously been identified. We have searched for such a neuron by combining FMRFamide immunofluorescence with fluorescent dye backfilling from the abdominal ganglion, the location of the siphon sensory cells. These methods localized a neuron in the left pleural ganglion, which we have named LPL16. LPL16 is FMRFamide immunoreactive; it is excited by tail shock; and stimulation of LPL16 produces inhibition of siphon sensory cell-to-motor cell postsynaptic potentials and narrowing of action potentials in the sensory cells in tetraethylammonium solution. These results indicate that LPL16 participates in the inhibitory effects of tail shock, and support the idea that FMRFamide plays a physiological role in the inhibition.

show abstract

Section: Distributionmentioning

confidence: 99%

mentioning

confidence: 99%

Identified FMRFamide-immunoreactive neuron LPL16 in the left pleural ganglion of Aplysia produces presynaptic inhibition of siphon sensory neurons

et al. 1992

View full text Add to dashboard Cite

show abstract

“…Inhibitory interactions within the ganglion play an important role in regulating the strength of the withdrawal reflex (Marcus et al, 1988;Small et al, 1989Small et al, , 1992Wright et al, 1991;Trudeau and Castellucci, 1992;Fischer and Carew, 1993). For example, recently Fischer and Carew (1993) found that an inhibitory feedback loop plays an important role in regulating the total synaptic input to the LFS motorneurons, and Trudeau and Castellucci (in press) found that cholinergic inhibition similarly influences the input to the motorneurons.…”

Section: Variability In Response Of Lfs Neurons To Fmrfamidementioning

confidence: 99%

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

Belkin

Abrams

1993

J. Neurosci.

View full text Add to dashboard Cite

The molluscan neuropeptide FMRFamide has an inhibitory effect on transmitter release from the presynaptic sensory neurons in the neural circuit for the siphon withdrawal reflex. We have explored whether FMRFamide also acts postsynaptically in motor neurons in this circuit, focusing on the LFS motor neurons. FMRFamide typically produces a biphasic response in LFS neurons: a fast excitatory response followed by a prolonged inhibitory response. We have analyzed these postsynaptic actions and compared them with the mechanism of FMRFamide's inhibition of the presynaptic sensory neurons. The transient excitatory effect of FMRFamide, which desensitizes rapidly, is due to activation of a TTX- insensitive, Na(+)-dependent inward current. The late hyperpolarizing phase of the FMRFamide response results from activation of at least two K+ currents. One component of the hyperpolarizing response is active at rest and at more hyperpolarized membrane potentials, and is blocked by 5 mM 4-aminopyridine, suggesting that it differs from the previously described FMRFamide-modulated K+ currents in the presynaptic sensory neurons. In addition, FMRFamide increases a 4-aminopyridine-insensitive K+ current. Presynaptically, FMRFamide increases K+ conductance, acting via release of arachidonic acid. In the LFS motor neurons, application of arachidonic acid mimicked the prolonged, hyperpolarizing phase of the FMRFamide response; 4-bromophenacyl bromide, an inhibitor of phospholipase A2, selectively blocked this component of the FMRFamide response. Thus, FMRFamide may act in parallel pre- and post- synaptically to inhibit the output of the siphon withdrawal reflex circuit, producing this inhibitory effect via the same second messenger in the sensory neurons and motor neurons, though a number of the K+ currents modulated in these two types of neurons are different.

show abstract

“…Other family members, such as Myosuppressins and Sulfakinins, affect spontaneous contractions of the visceral and oviduct muscles and thereby regulate feeding and egg-laying behaviors (Lange and Orchard, 1998;Nachman et al, 1986;Wang et al, 1994;Wang et al, 1995a;Wang et al, 1995b). In Aplysia, these peptides can influence learning and memory (Guan et al, 2002;Mackey et al, 1987;Small et al, 1989) while in vertebrates endogenous FaRPs regulate analgesic effects of opiate peptides and influence the electrical activity of some central brain synapses (Askwith et al, 2000;Gayton, 1982;Kavaliers, 1990;Kavaliers and Yang, 1991;Nishimura et al, 2000;Tang et al, 1984;Yang et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Retrograde Gbb signaling through the Bmp type 2 receptor Wishful Thinking regulates systemic FMRFa expression inDrosophila

et al. 2003

View full text Add to dashboard Cite

Amidated neuropeptides of the FMRFamide class regulate numerous physiological processes including synaptic efficacy at the Drosophilaneuromuscular junction (NMJ). We demonstrate here that mutations in wishful thinking (wit) a gene encoding a DrosophilaBmp type 2 receptor that is required for proper neurotransmitter release at the neuromuscular junction, also eliminates expression of FMRFa in that subset of neuroendocrine cells (Tv neurons) which provide the systemic supply of FMRFa peptides. We show that Gbb, a Bmp ligand expressed in the neurohemal organ provides a retrograde signal that helps specify the peptidergic phenotype of the Tv neurons. Finally, we show that supplying FMRFa in neurosecretory cells partially rescues the witlethal phenotype without rescuing the primary morphological or electrophysiological defects of wit mutants. We propose that Wit and Gbb globally regulate NMJ function by controlling both the growth and transmitter release properties of the synapse as well as the expression of systemic modulators of NMJ synaptic activity.

show abstract

Activity-Dependent Enhancement of Presynaptic Inhibition in Aplysia Sensory Neurons

Cited by 33 publications

References 29 publications

Identified FMRFamide-immunoreactive neuron LPL16 in the left pleural ganglion of Aplysia produces presynaptic inhibition of siphon sensory neurons

Identified FMRFamide-immunoreactive neuron LPL16 in the left pleural ganglion of Aplysia produces presynaptic inhibition of siphon sensory neurons

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

Retrograde Gbb signaling through the Bmp type 2 receptor Wishful Thinking regulates systemic FMRFa expression inDrosophila

Contact Info

Product

Resources

About