QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nagayama, T. Search for Related Content PubMed PubMed Citation Articles by Nagayama, T.

Serotonergic modulation of nonspiking local interneurones in the terminal abdominal ganglion of the crayfish

Toshiki Nagayama

Division of Biological Sciences, Graduate School of Science, Hokkaido University, 060 Sapporo, Japan

View larger version (30K): [in a new window]   Fig. 1. Serotonin-mediated inhibition of the exopodite reductor motor neurone. (A) The relative change in spike frequency of the reductor motor neurone during bath application of serotonin plotted every 1 min (mean ± S.E.M.). The number of tonically occurring spikes of the motor neurone is expressed as an average rate relative to the initial 3 min period prior to serotonin (5-HT) perfusion. The thick bar indicates the period of serotonin application. , 10 µmol l-1 (N=4); , 100 µmol l-1 (N=6); [UNK], 1 mmol l-1 (N=4) serotonin perfusion. (B) Input resistance of the reductor motor neurone (red mn) measured by a brief injection of 1 nA hyperpolarizing current was reduced during serotonin (5-HT; 1 mmol l-1)-mediated membrane hyperpolarization. The dashed line indicates the resting membrane potential level.

View larger version (42K): [in a new window]   Fig. 2. Serotonin-mediated membrane potential changes of nonspiking interneurones (ns int). (A) Serotonin-mediated hyperpolarization of a nonspiking interneurone. Bath application of serotonin (5-HT; 100 µmol l-1) for 3 min (indicated by thick bar) inhibited the motor neurone and elicited a hyperpolarization of the nonspiking interneurone. (B) Serotonin-mediated depolarization of a nonspiking interneurone. Bath application of 100 µmol l-1 serotonin for 3 min (indicated by thick bar) mediated a membrane depolarization of the nonspiking interneurone and suppressed the tonic discharge of the reductor motor neurone (red mn). (C) Brief application (100ms) of 0.1 µmol l-1 serotonin caused a long-lasting membrane hyperpolarization of the nonspiking interneurone. (D) Brief application (100ms) of 0.1 µmol l-1 serotonin caused a membrane depolarization. The dashed line indicates the resting membrane potential level.

View larger version (32K): [in a new window]   Fig. 3. Serotonin-mediated depolarization of a nonspiking interneurone (ns int). (A,B) Effect of current injected into a nonspiking interneurone upon the reductor motor neurone (red mn). The passage of a 2 nA depolarizing current into the interneurone decreased the tonic spike frequency of the motor neurone (A) while the injection of a 1 nA hyperpolarizing current had little effect upon the motor neurone (B). (C) Bath application of serotonin (5-HT; 100 µmol l-1) for 5 min (indicated by thick bar) decreased the number of tonically occurring spikes of the motor neurone (impulses s-1; ) and elicited a depolarization of the nonspiking interneurone ([UNK]). (D) Temporal relationship between the serotonin-mediated depolarization of the interneurone and the effect of hyperpolarizing current injected into the interneurone upon the motor neurone. The passage of a 1 nA hyperpolarizing current into the interneurone increased the tonic spike level of the motor neurones only during serotonin-mediated depolarization. The time indicated on each trace (Di—iii) shows the elapsed time after serotonin application. The dashed line indicates the resting membrane potential level.

View larger version (22K): [in a new window]   Fig. 4. Post-serotonin enhancement of the depolarizing response of a nonspiking interneurone (ns int) that showed a serotonin-mediated hyperpolarization during sensory stimulation. Bath application of 100 µmol l-1 serotonin for 3 min mediated a hyperpolarization of the membrane potential of the interneurone shown in Fig. 2A. The amplitude of the depolarizing postsynaptic potentials in the interneurone elicited by sensory stimulation at 20 Hz of 11 stimuli (indicated by arrows) increased after serotonin perfusion. The time indicated on each trace (A—D) shows the elapsed time after serotonin application. The dashed line indicates the resting membrane potential level; red mn, reductor motor neurone.

View larger version (24K): [in a new window]   Fig. 5. Post-serotonin enhancement of the depolarizing postsynaptic potentials of a nonspiking interneurone (ns int) that showed a serotonin-mediated depolarization during sensory stimulation. Bath application of 100 µmol l-1 serotonin for 3 min mediated a depolarization of the membrane potential of the nonspiking interneurone and decreased the tonic spike discharge of the reductor motor neurone (red mn). After serotonin perfusion, the amplitude of depolarizing postsynaptic potentials of the interneurone in response to the sensory stimulation at 20 Hz of 11 stimuli (indicated by arrows) initially decreased slightly in association with serotonin-mediated depolarization. The depolarizing postsynaptic potentials then increased in amplitude, although the membrane potential was still depolarized. The time indicated on each trace (A—D) shows the elapsed time after serotonin application. The dashed line indicates the resting membrane potential level.

View larger version (35K): [in a new window]   Fig. 6. Post-serotonin enhancement of the hyperpolarizing postsynaptic potentials of a nonspiking interneurone (ns int) during sensory stimulation. (A) Bath application of 100 µmol l-1 serotonin (5-HT) for 3 min mediated a hyperpolarization of the interneurone. After serotonin perfusion, the amplitude of hyperpolarizing postsynaptic potentials of the interneurone during sensory stimulation at 20 Hz of 11 stimuli (indicated by arrows) initially decreased in association with a serotonin-mediated hyperpolarization of the membrane. After approximately 10 min of washing, the amplitude of the evoked hyperpolarizing postsynaptic potentials increased, even though the membrane was still hyperpolarized. The time indicated on each trace (Ai—v) shows the elapsed time after serotonin application. The dashed line indicates the resting membrane potential level. (B) The amplitude of hyperpolarizing postsynaptic potentials of the interneurone during sensory stimulation at 20 Hz of 11 stimuli (indicated by arrows) increased after serotonin-mediated depolarization. red mn, reductor motor neurone.

View larger version (29K): [in a new window]   Fig. 7. Response of ascending interneurone (asc int) VE-1 to bath application of serotonin (5-HT). (A) Bath application of 1 mmol l-1 serotonin for 3 min (indicated by thick bar) elicited no significant changes in the membrane potential of VE-1, although the tonically occurring spikes of the reductor motor neurone (red mn) were completely suppressed for long periods. (B) The excitatory response of VE-1 to sensory stimulation at 20 Hz of 11 stimuli (indicated by arrows) was increased after serotonin perfusion, although the excitatory level of VE-1 returned to its initial level after approximately 20 min of washing. The time indicated on each trace (Bi-vi) shows the elapsed time after serotonin application. The dashed line indicates the resting membrane potential level.