Modulatory role for the serotonergic cerebral giant cells in the feeding system of the snail, Lymnaea. II. Photoinactivation

1994 ◽  
Vol 72 (3) ◽  
pp. 1372-1382 ◽  
Author(s):  
M. S. Yeoman ◽  
G. Kemenes ◽  
P. R. Benjamin ◽  
C. J. Elliott

1. Photoinactivation of dye-filled neurons was used to examine the modulatory role of the paired cerebral giant cells (CGCs) in the Lymnaea feeding system. 2. Both CGCs were filled with fluorescent dyes. Lucifer yellow was used for "soma" kills and injected via intracellular microelectrodes. CGC axons were retrogradely filled with 5 (6)-carboxyfluorescein (5-CF), through the cut ends of the ventro- and lateral buccal nerves, for "axonal" kills. 3. Irradiation of the CGC soma with a blue laser light (0.5 MW/m2) led to a loss of their recorded membrane potentials and the synaptic responses with their postsynaptic cells (feeding motor neurons). CGC coupling and axonal fluorescence were lost after axonal irradiation. 4. The tonic firing rate of CGC axon spikes in peripheral nerve roots following bilateral soma kills was reduced to approximately 15% of preirradiation levels (n = 2; from 52.5 +/- 3.75 spikes/min to 8.2 +/- 0.95 spikes/min; mean +/- SE) but spike activity was not completely eliminated. 5. The fictive feeding rhythm was evoked by depolarizing a modulatory neuron, the slow oscillator (SO), before and after laser irradiation. Thirty minutes after both the CGCs were irradiated (n = 8), the frequency of the SO-driven feeding rhythm was reduced. Mean fictive feeding rates were reduced from 8.3 to 4.5 cycles/min for soma kills (n = 3) and from 16.2 to 9.6 cycles/min for axonal kills (n = 5; P < 0.05). 6. The results suggest that the CGCs play a modulatory role in controlling the frequency of oscillation of the feeding central pattern generator (CPG) in Lymnaea. The SO could still drive a full fictive feeding rhythm after irradiation but at a reduced rate. At least in the soma kills, the residual spike activity retained in the distal branches of the CGCs appeared sufficient to allow the SO to drive this slow rhythm.

1996 ◽  
Vol 75 (1) ◽  
pp. 11-25 ◽  
Author(s):  
M. S. Yeoman ◽  
M. J. Brierley ◽  
P. R. Benjamin

1. The objective of the experiments was to explore the modulatory functions of the serotonergic cerebral giant cells (CGCs) of the Lymnaea feeding system by examining their synaptic connections with the central pattern generator (CPG) interneurons and the modulatory slow oscillator (SO) interneuron. 2. One type of modulatory function, "gating," requires that the CGCs fire tonically at a minimum of 7 spikes/min. Above this minimum level the CGCs control the frequency of CPG interneuron oscillation-- "frequency control," a second type of modulation. In an SO-driven fictive feeding rhythm, an increase in the frequency of the rhythm, with increased CGC firing rate, resulted from a reduction in the duration of the N1 (protraction) and N2 (rasp) phases of the feeding cycle with little effect on the N3 (swallow) phase. 3. The CGCs excited the N1 phase interneurons SO and N1M (N1 medial) cells but had no consistent effects on the N1 lateral cells. The CGC-->SO postsynaptic response was probably monosynaptic (< or = 200 ms in duration) with unitary 1:1 excitatory postsynaptic potentials (EPSPs) following each CGC spike. The CGC-->N1M excitatory response was slow and nonunitary, and a burst of CGC spikes evoked a depolarization of the N1M cells that lasted up to 10 s and triggered N1M cell bursts. Both CGC-->SO and CGC-->N1M excitatory responses could be mimicked by the focal application of serotonin (5-HT). 4. Both CGC-->SO and CGC-->N1M excitatory connections systematically increased the N1M cell firing rate within the CGCs' physiological firing range (0-40 spikes/min). This was due to both the direct (CGC-->N1M) and indirect (CGC-->SO-->N1M) excitatory synaptic pathways. The CGC-induced increase in N1M cell firing rate probably accounted for the reduced duration of the N1M cell feeding burst by causing a more rapid reversal of the feeding cycle from the N1 phase to the N2 phase. This phase reversal was due to the previously described recurrent inhibitory pathway (N1-->N2 excitation followed by N2-->N1 inhibition). 5. The CGCs' ability to provide a depolarizing drive to the N1M cells meant that this excitatory connection was also likely to be important for gating. 6. Activity in the CGCs produced nonunitary, long-lasting, excitatory postsynaptic responses on the N2 ventral (N2v) CPG interneurons, and these were likely to be involved in both the gating and the frequency control by the CGCs on the N2 phase of the feeding rhythm. Suppressing CGC tonic firing initially increased the duration of the N2v plateau (which determines the duration of the N2 phase of the feeding cycle, frequency function) but eventually led to a loss of N2v plateauing (gating function). 7. Nonunitary, weakly inhibitory CGC-->N2 dorsal responses were recorded that could be mimicked by the application of 5-HT. 8. Spikes in the CGCs evoked 1:1 monosynaptic EPSPs in the N3 tonic (N3t) CPG interneurons. This excitatory effect could be mimicked by the application of 5-HT. Within the physiological range of CGC firing, this excitation did not appear to influence the firing rate of the N3t cells. 9. N3 phasic (N3p) CPG interneurons showed biphasic (hyperpolarizing followed by depolarizing) unitary responses to spikes evoked in the CGCs. The inhibitory synaptic response was maintained in a high-Ca2+/high-Mg2+ (Hi-Di) saline and was mimicked by the focal application of 5-HT, indicating that it was probably monosynaptic. The excitatory component was, however, reduced in a Hi-Di saline, indicating that it was probably polysynaptic. Suppressing the CGCs during an SO-driven feeding rhythm caused the N3p cells to fire less, suggesting that the removal of the excitatory component of the response might be significant. 10. We conclude that the general depolarizing effects of the CGCs on a number of the CP


1982 ◽  
Vol 30 (2) ◽  
pp. 189-191 ◽  
Author(s):  
R L Michaels

Lucifer Yellow CH may be injected into pancreatic islet cells and visualized in Epon sections of the embedded tissue both before and after plastic removal and immunocyto-chemical staining. The dye retains its fluorescence, clearly marking the injected cell and adjacent dye-coupled cells, but does not interfere with the indirect immunofluorescent staining patterns that are characteristic of the islet cells


2021 ◽  
pp. 1-10
Author(s):  
H. Knaggs ◽  
G. Tabor ◽  
J.M. Williams

The equine transeva technique (ETT), is a novel electrotherapy, which utilises pulsating current electrotherapy to target sensory and motor neurons. The technique may facilitate increased circulation and correction of musculoskeletal issues and injuries, such as tendon and ligament tears and muscle atrophy. Despite the importance of understanding the impact of ETT on horses, no current scientific research exists in this area. This preliminary study investigated the effects of ETT on the musculoskeletal system of the horse, specifically within the Gluteus superficialis (GS). Using surface electromyography, muscle workload was measured in 11 sound and healthy horses of varying breeds and disciplines within the inclusion criteria. Integrated electromyography (iEMG) calculated the percentage change in maximal contractions before and after ETT treatment during one minute trials at 30 s intervals. An ANCOVA determined if these constituted significant changes (Bonferroni adjusted alpha: P≤0.02). Significant differences in muscle workload were found on the left side between pre- and post-treatment readings across trials (P≤0.02), however no significant changes occurred for the right side. The majority of horses (82%; n=9) experienced bilateral changes, with 78% of these (n=7) exhibiting a negative change in muscle workload recorded from the pretreatment condition, which may indicate muscular relaxation. The results suggest ETT may have some effect on muscle workload in the athletic horse, however further research is needed to confirm the effects observed. Future studies should include randomising the side which is treated first, a larger sample size, expansion of temporal variables and consideration of a longitudinal study to determine if these trends accrue over multiple maintenance-purposed treatments.


1984 ◽  
Vol 51 (6) ◽  
pp. 1362-1374 ◽  
Author(s):  
E. Marder ◽  
J. S. Eisen

The two pyloric dilator (PD) motor neurons and the single anterior burster (AB) interneuron are electrically coupled and together comprise the pacemaker for the pyloric central pattern generator of the stomatogastric ganglion of the lobster, Panulirus interruptus. Previous work (31) has shown that the AB neuron is an endogenously bursting neuron, while the PD neuron is a conditional burster. In this paper the effects of physiological inputs and neurotransmitters on isolated PD neurons and AB neurons were studied using the lucifer yellow photoinactivation technique (33). Stimulation of the inferior ventricular nerve (IVN) fibers at high frequencies elicits a triphasic response in AB and PD neurons: a rapid excitatory postsynaptic potential (EPSP) followed by a slow inhibitory postsynaptic potential (IPSP), followed by an enhancement of the pacemaker slow-wave depolarizations. Photoinactivation experiments indicate that the enhancement of the slow wave is due primarily to actions of the IVN fibers on the PD neurons but not on the AB neuron. Bath-applied dopamine dramatically alters the motor output of the pyloric system. Photoinactivation experiments show that 10(-4) M dopamine increases the amplitude and frequency of the slow-wave depolarizations recorded in the AB neurons but hyperpolarizes and inhibits the PD neurons. Bath-applied serotonin increases the frequency and amplitude of the slow-wave depolarizations in the AB neuron but has no effect on PD neurons. Pilocarpine, a muscarinic cholinergic agonist, stimulates slow-wave depolarization production in both PD neurons and the AB neuron, but the waveform and frequency of the slow waves elicited are quite different. These results show that although the electrically coupled PD and AB neurons always depolarize synchronously and act together as the pacemaker for the pyloric system, they respond differently to a neuronal input and to several putative neuromodulators. Thus, despite electrical coupling sufficient to ensure synchronous activity, the PD and AB neurons can be modulated independently.


1992 ◽  
Vol 336 (1277) ◽  
pp. 157-166 ◽  

All the identified feeding motoneurons of Lymnaea respond to bath or iontophoretically applied acetylcholine (ACh). Three kinds of receptors (one excitatory, one fast inhibitory and one slow inhibitory) were distinguished pharmacologically. The agonist TMA (tetram ethylam m onium ) activates all three receptors, being weakest at the slow inhibitory receptor. PTMA (phenyltrim ethylam monium ) is less potent than TMA and is ineffective at the slow inhibitory receptor, which is the only receptor sensitive to arecoline. At 0.5 mM the antagonists HMT (hexamethonium) and ATR (atropine) selectively block the excitatory response, while PTMA reduces the response to ACh at all three receptors. d-TC (curare) antagonizes only the fast excitatory and the fast inhibitory responses, but MeXCh (methylxylocholine) blocks the fast excitatory and slow inhibitory responses solely. For each of the feeding motoneurons, the sign of the cholinergic response (excitation or inhibition) is the same as the synaptic input received in the N1 phase of the feeding rhythm .


2006 ◽  
Vol 27 (12) ◽  
pp. 1892-1901 ◽  
Author(s):  
B.A. Patel ◽  
M. Arundell ◽  
M.C. Allen ◽  
P. Gard ◽  
D. O’Hare ◽  
...  
Keyword(s):  

2003 ◽  
Vol 15 (10) ◽  
pp. 2359-2377 ◽  
Author(s):  
Liqiang Zhu ◽  
Ying-Cheng Lai ◽  
Frank C. Hoppensteadt ◽  
Jiping He

A procedure is developed to probe the changes in the functional interactions among neurons in primary motor cortex of the monkey brain during adaptation. A monkey is trained to learn a new skill, moving its arm to reach a target under the influence of external perturbations. The spike trains of multiple neurons in the primary motor cortex are recorded simultaneously. We utilize the methodology of directed transfer function, derived from a class of linear stochastic models, to quantify the causal interactions between the neurons. We find that the coupling between the motor neurons tends to increase during the adaptation but return to the original level after the adaptation. Furthermore, there is evidence that adaptation tends to affect the topology of the neural network, despite the approximate conservation of the average coupling strength in the network before and after the adaptation.


2000 ◽  
Vol 42 (5) ◽  
pp. 239-243 ◽  
Author(s):  
Suzana MADEIRA ◽  
Diltor Vladimir Araújo OPROMOLLA ◽  
Andréa de Faria Fernandes BELONE

In a previous study, the authors inoculated Swiss mice with Lacazia loboi (L. loboi) and succeeded in maintaining a granulomatous infiltrate and viable fungal cells up to one year and six months after inoculation. Considering the experimental work on paracoccidioidomycosis, 0.03 ml of a fungal suspension obtained from a biopsy of a Jorge Lobo's Disease patient were inoculated into both hind foot pads of 32 six week-old BALB/c mice of both sexes. The animals were sacrificed 1, 4, 7 and 10 months post inoculation. The suspension contained 1.3 x 10(6) fungi/ml and presented 38% viability. Seven months after inoculation, most of the animals presented profuse infiltrates consisting of isolated histiocytes, foreign body and Langhans' giant cells and a large number of fungi, most of them viable. Emergence of macroscopic lesions was observed during the 8th month. Based on fungal count, viability index before and after inoculation, presence of macroscopic lesions and histopathological findings similar to the findings in humans, the authors believe that BALB/c mice may be a good experimental model to study Jorge Lobo's Disease, mainly regarding therapeutic evaluation.


1995 ◽  
Vol 73 (1) ◽  
pp. 112-124 ◽  
Author(s):  
M. S. Yeoman ◽  
A. Vehovszky ◽  
G. Kemenes ◽  
C. J. Elliott ◽  
P. R. Benjamin

1. We used intracellular recording techniques to examine the role of a novel type of protraction phase interneuron, the lateral N1 (N1L) in the feeding system of the snail Lymnaea stagnalis. 2. The N1Ls are a bilaterally symmetrical pair of electrotonically coupled interneurons located in the buccal ganglia. Each N1L sends a single axon to the contralateral buccal ganglia. Their neurite processes are confined to the buccal neuropile. 3. In the isolated CNS, depolarization of an N1L is capable of driving a full (N1-->N2-->N3), fast (1 cycle every 5 s) fictive feeding rhythm. This was unlike the previously described N1 medial (N1M) central pattern generator (CPG) interneurons that were only capable of driving a slow, irregular rhythm. Attempts to control the frequency of the fictive feeding rhythm by injecting varying amounts of steady current into the N1Ls were unsuccessful. This contrasts with a modulatory neuron, the slow oscillator (SO), that has very similar firing patterns to the N1Ls, but where the frequency of the rhythm depends on the level of injected current. 4. The N1Ls' ability to drive a fictive feeding rhythm in the isolated preparation was due to their strong, monosynaptic excitatory chemical connection with the N1M CPG interneurons. Bursts of spikes in the N1Ls generated summating excitatory postsynaptic potentials (EPSPs) in the N1Ms to drive them to firing. The SO excited the N1M cells in a similar way, but the EPSPs are strongly facilitatory, unlike the N1L-->N1M connection. 5. Fast (1 cycle every 5 s) fictive feeding rhythms driven by the N1L occurred in the absence of spike activity in the SO modulatory neuron. In contrast, the N1L was usually active in SO-driven rhythms. 6. The ability of the SO to drive the N1L was due to strong electrotonic coupling, SO-->N1L. The weaker coupling in the opposite direction, N1L-->SO, did not allow the N1L to drive the SO. 7. Experiments on semintact lip-brain preparations allowed fictive feeding to be evoked by application of 0.1 M sucrose to the lips (mimicking the normal sensory input) rather than by injection of depolarizing current. Rhythmic bursting, characteristic of fictive feeding, began in both the SO and N1L at exactly the same time, indicating that these two cell types are activated in "parallel" to drive the feeding rhythm. 8. The N1L is also part of the CPG network. It Excited the N2s and inhibited the N3 phasic (N3p) and N3 tonic (N3t) CPG interneurons like the N1Ms.(ABSTRACT TRUNCATED AT 400 WORDS)


2009 ◽  
Vol 296 (2) ◽  
pp. H396-H403 ◽  
Author(s):  
Kazuyuki Naitoh ◽  
Toshiyuki Yano ◽  
Tetsuji Miura ◽  
Takahito Itoh ◽  
Takayuki Miki ◽  
...  

Ischemic preconditioning (PC) suppresses chemical coupling of cardiomyocytes via gap junctions (GJs) during ischemia, which is an adjunct mechanism of protection. The aim of this study was to characterize roles of protein kinases in PC-induced GJ modulation. In isolated rat hearts, ventricular tissues were sampled before and after ischemia with or without PC, and intercalated disc-rich fractions were separated for immunoprecipitation and immunoblotting. Levels of protein kinase C (PKC)-ε, p38mitogen-activated protein kinase (MAPK)-α, and Src coimmunoprecipitated with connexin-43 (Cx43) were increased after ischemia, whereas p38MAPKβ was not detected in the Cx43 immunoprecipitates. PC did not modify the level of Cx43-Src complex after ischemia. However, PC enhanced Cx43-PKCε complex formation, which was abolished by PKCε translocation inhibitory peptide (TIP). In contrast, PC reduced Cx43-p38MAPKα complex level and p38MAPK activity in the Cx43 immunoprecipitates after ischemia. The effect of PC on Cx43-p38MAPKα interaction was mimicked by SB-203580, a p38MAPK inhibitor. PC reduced permeability of GJs to Lucifer yellow in the myocardium at 25 min after ischemia, and this effect was abolished by PKCε-TIP. SB-203580 increased the GJ permeability at 15 min after ischemia compared with that in untreated controls, but the difference became insignificant 25 min after ischemia. In conclusion, PC has distinct effects on interaction of GJ Cx43 with PKCε, p38MAPKα, and Src during ischemia. Suppression of GJ permeability during ischemia by PC is primarily achieved by enhanced interaction of Cx43 with PKCε, which overwhelms the counterbalancing effect of reduced Cx43-p38MAPKα interaction.


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