First published online August 9, 2007
Journal of Experimental Biology 210, 2873-2884 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.002949
Multiple modulators act on the cardiac ganglion of the crab, Cancer borealis
Nelson D. Cruz-Bermúdez* and
Eve Marder
Volen Center for Complex Systems and Department of Biology, Brandeis
University, MS-013, 415 South Street, Waltham, MA 02454, USA
View larger version (9K):
[in this window]
[in a new window]
|
Fig. 1. Anatomy and bursting activity of the Cancer borealis cardiac
ganglion (CG). (A) Schematic of the CG preparation. Large ovals, motor
neurons; small ovals, pacemaker cells; A-l.n., anterolateral nerve; P-l.n.,
posterolateral nerve. The black ring indicates the petroleum jelly well used
to record the activity of the CG. (B) Simultaneous recordings of the CG
bursting pattern from the trunk (top trace) and from a motor neuron axon
(bottom trace).
|
|
View larger version (14K):
[in this window]
[in a new window]
|
Fig. 2. Effects of red pigment concentrating hormone (RPCH) on the isolated cardiac
ganglion (CG). (A) Extracellular recording from the trunk during control (top
trace) and in the presence of 10–6 mol l–1
RPCH (bottom trace). RPCH increased the burst frequency as well as the number
of motor neuron spikes (large units). (B) Pooled data bar graphs showing
significant increases in burst frequency, duty cycle, number of spikes per
bursts and spike frequency in the burst induced by RPCH over control (C)
values (Student's t-test; N=12;
*P<0.05; **P<0.01).
|
|
View larger version (26K):
[in this window]
[in a new window]
|
Fig. 3. Effects of Cancer borealis tachykinin-related peptide Ia (CabTRP
Ia) on the isolated cardiac ganglion (CG). (A) Intra-axonal recording from a
motor neuron during control (top trace) and in the presence of
10–6 mol l–1 CabTRP Ia (bottom trace). (B)
Superimposed intra-axonal recordings from the same traces in A during control
(gray) and after the application of CabTRP Ia (black). CabTRP Ia induced a
 2 mV depolarization. (C) Scatter plots of the instantaneous burst
frequency (left plot) and number of spikes per burst (right plot)
versus time during control, CabTRP Ia (gray bar) and during wash. (D)
Bar plots of the pooled data comparing control (C) versus CabTRP Ia
for the different parameters measured (Student's t-test;
N=12; *P<0.05;
**P<0.01).
|
|
View larger version (14K):
[in this window]
[in a new window]
|
Fig. 4. Inhibitory effect of allatostatin III type A (AST-3) on the isolated
cardiac ganglion (CG). (A) Intra-axonal recording from a motor neuron during
control (top trace), in the presence of 10–6 mol
l–1 AST-3 (middle trace) and during wash (bottom trace). (B)
Pooled data bar graphs showing statistically significant changes on the CG
bursting activity with AST-3 (Student's t-test; N=6;
*P<0.05; **P<0.01).
|
|
View larger version (30K):
[in this window]
[in a new window]
|
Fig. 5. Excitatory actions of proctolin and crustacean cardioactive peptide (CCAP)
on the isolated cardiac ganglion (CG). (A) Intra-axonal recording from a motor
neuron in control (top trace) and during 10–6 mol
l–1 proctolin application (bottom trace). Note the increase
in the slow wave form depolarization of the burst. (B) Pooled data showing
significant effects of proctolin on burst frequency, duty cycle, number of
spikes per burst and spike frequency in the burst (Student's t-test;
N=8; *P<0.05;
**P<0.01). (C) Same preparation after proctolin was
washed out (top trace) and in 10–6 mol l–1
CCAP (bottom trace). CCAP increased the slow wave form depolarization of the
motor neurons. (D) Pooled data showing significant effects of CCAP on burst
frequency, duty cycle, number of spikes per burst and spike frequency in the
burst (Student's t-test; N=8;
*P<0.05; **P<0.01).
|
|
View larger version (28K):
[in this window]
[in a new window]
|
Fig. 6. Excitatory effects of biogenic amines on the isolated cardiac ganglion
(CG). (A) Extracellular recordings from the trunk during control and in the
presence of the 10–6 mol l–1 serotonin
(5HT). (B) Serotonin significantly increased the burst frequency, duty cycle,
number of spikes per burst and spike frequency in the burst (Student's
t-test; N=7; *P<0.05;
**P<0.01). (C) Extracellular recordings from the trunk
during control and in the presence of the 10–5 mol
l–1 dopamine (DA). (D) Dopamine also significantly increased
the burst frequency, duty cycle, number of spikes per burst and spike
frequency in the burst (Student's t-test; N=9;
*P<0.05; **P<0.01).
|
|
View larger version (27K):
[in this window]
[in a new window]
|
Fig. 7. Excitatory actions of cholinergic agonists on the isolated cardiac ganglion
(CG). (A) Extracellular recording from the trunk in control (top trace) and
during 10–5 mol l–1 pilocarpine perfusion
(bottom trace). (B) Pilocarpine (Pilocarp.) significantly increased the burst
frequency, duty cycle, number of spikes per burst and spike frequency in the
burst (Student's t-test; N=8;
*P<0.05; **P<0.01). (C) Same
preparation shown in A during wash (top trace) and in the presence of
10–5 mol l–1 nicotine (bottom trace). (D)
Nicotine significantly increased the duty cycle, number of spikes per burst
and spike frequency in the burst (Student's t-test; N=8;
*P<0.05; **P<0.01).
|
|
View larger version (12K):
[in this window]
[in a new window]
|
Fig. 8. Diagram of the C. borealis cardiac ganglion with neuromodulators
present in the pericardial organs. The excitatory actions (+) of peptides,
serotonin, dopamine and presumably acetylcholine on the cardiac ganglion [CG;
GAHKNYLRFa data were studied in Cruz-Bermudez et al.
(Cruz-Bermudez et al., 2006 )].
The peptide AST-3 and GABA are both potent inhibitors (–) of the CG
output. Other modulators such as histamine and octopamine did not induce
statistically significant changes on the CG motor pattern and were classified
as weak or ineffective modulators. Large ovals, motor neurons; small ovals,
pacemaker cells.
|
|
© The Company of Biologists Ltd 2007
