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 F.-Tsukamoto, Y. Articles by Kuwasawa, K. Search for Related Content PubMed PubMed Citation Articles by F.-Tsukamoto, Y. Articles by Kuwasawa, K.

Neurohormonal and glutamatergic neuronal control of the cardioarterial valves in the isopod crustacean Bathynomus doederleini

Yoko F.-Tsukamoto and Kiyoaki Kuwasawa^*

Department of Biological Sciences, Tokyo Metropolitan University, 1-1 Minami-ohsawa, Hachioji 192-0397, Japan

View larger version (34K): [in a new window]   Fig. 1. Schematic drawing of the cardiovascular system and central nervous system (CNS). The right and left sides of the CNS are reversed for the sake of illustrating convenience. Cardiac nerves are shown by bold lines. The cardioarterial valves are located at the junctions between the heart and each artery. ACN, anterior cardiac nerve; AG1-5, first—fifth abdominal ganglion; ALA, anterior lateral artery; AMA, anterior median artery; CA, cardioacceleratory nerve; CI&VI, combined nerve of cardioinhibitory nerve and valve inhibitory nerve; CG, cerebral ganglion; VE, valve excitatory nerve; LA1-5, first—fifth lateral artery; LCN1-5, first—fifth lateral cardiac nerve; SEG, suboesophageal ganglion; TG1-8, first—eighth thoracic ganglion. Modified from Tanaka et al. (1996).

View larger version (80K): [in a new window]   Fig. 9. Micrographs (left) and schematic drawings (right) of cross sections of the anterior cardiac nerve (ACN) treated with (A) anti-GABA (-aminobutyric acid) antibody or (B) anti-Glu (glutamate) antibody. A and B are neighbouring sections. In A, one GABA-like immunoreactive axon profile is seen. In B, one strong and one weak (the hatched axon in the schematic drawing indicates the weak profile) Glu-like immunoreactive axon profile is seen. Scale bar, 5 µm. CI, cardioinhibitory nerve; VE, valve excitatory nerve.

View larger version (33K): [in a new window]   Fig. 11. Schematic drawing of anterior cardiac nerves (ACN) and valve nerves in the anterior part of the heart of Bathynomus. An ACN contains five axons; glutamatergic valve excitatory (VE; green), cholinergic valve inhibitory (VI) and cardioacceleratory (CA1 and CA2) (red), and GABAergic cardioinhibitory (CI; blue). The first lateral cardiac nerve (LCN1) contains two cholinergic axons, and LCN2 contains one cholinergic axon. The cell bodies and axons (green) in the heart are the cell bodies and axons of glutamatergic cardiac ganglionic neurons (CG). AMA, anterior median artery; lALA, left anterior lateral artery; rALA, right anterior lateral artery; LA, lateral artery; ACh, acetylcholine; GABA, -aminobutyric acid; Glu, glutamate.

View larger version (13K): [in a new window]   Fig. 2. Effects of (A) acetylcholine (ACh) and (B) dopamine (DA) on arterial pressure in each of the anterior median artery (AMA), anterior lateral artery (ALA) and fifth lateral artery (LA5) preparations without heartbeat (see Materials and methods). Arterial pressure of LA5 was decreased by perfusion with serotonin (5-HT) to accentuate the effects of ACh on pressure of the artery. Bars represent periods of agent application. It was confirmed that an agent solution reached the preparation in approximately 30 s after the start of perfusion.

View larger version (30K): [in a new window]   Fig. 3. Effects of (A) serotonin (5-HT), (B) octopamine (OA), (C) norepinephrine (NE), (D) glutamate (Glu) and (E) proctolin (Proc) on arterial pressure of the anterior median artery (AMA), anterior lateral artery (ALA) and fifth lateral artery (LA5). In B, C and E, the first (top) and second traces show simultaneous recordings of pressure pulses of AMA and mechanograms of heartbeat, respectively. Other traces show arterial pressure alone recorded from preparations without heartbeat. Scale bars, 30 s.

View larger version (76K): [in a new window]   Fig. 4. Simultaneously recorded mechanograms showing effects of (A) acetylcholine (ACh), (B) serotonin (5-HT), (C) octopamine (OA), (D) glutamate (Glu) and (E) proctolin (Proc) on pressure pulses of the fifth lateral artery (LA5) and heartbeat. Bars on each trace indicate the period of agent application.

View larger version (26K): [in a new window]   Fig. 5. Dose-response curves showing the relationship between cardioexcitatory substances — (A) acetylcholine (ACh), (B) serotonin (5-HT), (C) octopamine (OA), (D) glutamate (Glu) and (E) proctolin (Proc) — and amplitude of pressure pulses of the fifth lateral artery (LA5; filled circle), heart rate (open square) and contraction force of the heart (open triangle). All data (mean ± S.D., N=3) were obtained from one preparation for three times applications per one dose. Each of the five graphs was obtained from a different specimen. The values plotted for pressure pulses, heart rate and contraction force were obtained at the maximum change of the amplitude of pressure pulses.

View larger version (25K): [in a new window]   Fig. 6. Effects of stimulation of the fifth lateral cardiac nerve (LCN5) on pressure pulses recorded from the fifth lateral artery (LA5) during perfusion of SW (control), serotonin (5-HT) and octopamine (OA). These data were obtained from one preparation. Bars show the periods of stimulation. Frequencies of stimulation are shown at the beginning of the traces in the left column.

View larger version (19K): [in a new window]   Fig. 7. (A) Effects of glutamate (Glu) on the membrane potential of valve muscle cells in the anterior median artery (AMA). All data were obtained from the same muscle cell. Bars on each trace indicate the period of Glu application. Concentrations of Glu are indicated under the bars. Numerals at the beginning of traces represent membrane potential (mV) in this and following figures. (B) The dose—response relationship between Glu concentrations and depolarization of valve muscle cells of AMA (filled circle). Membrane potentials were obtained from four animals. Resting membrane potentials (r.m.p.; open circle) were measured before doses. Values represent mean ± S.D. (N=4-6). (C) Effects of glutamatergic agonists kainate and quisqualate on the membrane potential of valve muscle cells in AMA. Bars indicate the periods of agonist perfusion.

View larger version (14K): [in a new window]   Fig. 8. Effects of the glutamatergic antagonists MK-801 and Joro spider toxin (JSTX) on excitatory junctional potentials (EJPs) evoked on valve muscle cells of the anterior median artery (AMA) by stimuli applied to the valve excitatory nerve (VE). Three (A) and five (B) sweeps triggered by stimulus pulses were superimposed. (A) 3 min after the onset of perfusion with MK-801 (1 mmol l-1), EJPs were almost abolished. After washing with saline, EJPs recovered. (B) 25 min after bath application of JSTX (concentration was calculated to be 5 µmol l-1), the amplitude of each of five EJPs was diminished by more than half. The effect of JSTX did not reverse within one hour.

View larger version (62K): [in a new window]   Fig. 10. Micrographs of immunoreactive fibres and varicosity-like structures, which were revealed with anti-Glu (glutamate) antibody in the valve of the anterior median artery (AMA). The location of micrographs A and B is indicated in the schematic drawing. Scale bar, 10 µm. VE, valve excitatory nerve; rALA, right anterior lateral artery; lALA, left anterior lateral artery.