scholarly journals Serotonergic modulation of swimming speed in the pteropod mollusc Clione limacina. III. Cerebral neurons.

1995 ◽  
Vol 198 (4) ◽  
pp. 917-930 ◽  
Author(s):  
R A Satterlie ◽  
T P Norekian
Keyword(s):  
Motor Neurons ◽  
Time Course ◽  
Neuron Activity ◽  
Target Cells ◽  
Cellular Mechanisms ◽  
Cycle Frequency ◽  
Course Of Action ◽  
Cell Groups ◽  
Cerebral Neurons ◽  
Clione Limacina

Swim acceleration in Clione limacina can occur via central inputs to pattern generator interneurons and motor neurons and through peripheral inputs to the swim musculature. In the previous paper, peripheral modulation of the swim muscles was shown to increase wing contractility. In the present paper, central inputs are described that trigger an increase in swim frequency and an increase in motor neuron activity. In dissected preparations, spontaneous acceleration from slow to fast swimming included an increase in the cycle frequency, a baseline depolarization in the swim interneurons and an increase in the intensity of motoneuron firing. Similar effects could be elicited by bath application of 10(-5) mol l-1 serotonin. Two clusters of cerebral serotonin-immunoreactive interneurons were found to produce acceleration of swimming accompanied by changes in neuronal activity. Posterior cluster neurons triggered an increase in swim frequency, depolarization of the swim interneurons, an increase in general excitor motoneuron activity and activation of type 12 interneurons and pedal peripheral modulatory neurons. Cells from the anterior cerebral cluster also increased swim frequency, increased activity in the swim motoneurons and activated type 12 interneurons, pedal peripheral modulatory neurons and the heart excitor neuron. The time course of action of the anterior cluster neurons did not greatly outlast the duration of spike activity, while that of the posterior cluster neurons typically outlasted burst duration. It appears that the two discrete clusters of serotonin-immunoreactive neurons have similar, but not identical, effects on swim neurons, raising the possibility that the two serotonergic cell groups modulate the same target cells through different cellular mechanisms.

Whole body withdrawal circuit and its involvement in the behavioral hierarchy of the mollusk Clione limacina

1996 ◽  
Vol 75 (2) ◽  
pp. 529-537 ◽  
Author(s):  
T. P. Norekian ◽  
R. A. Satterlie
Keyword(s):  
Feeding Behavior ◽  
Motor Neurons ◽  
Prey Capture ◽  
The Body ◽  
Whole Body ◽  
High Threshold ◽  
Behavioral Repertoire ◽  
Withdrawal Behavior ◽  
Cerebral Neurons ◽  
Clione Limacina

1. The behavioral repertoire of the holoplanktonic pteropod mollusk Clione limacina includes a few well-defined behaviors organized in a priority sequence. Whole body withdrawal takes precedence over slow swimming behavior, whereas feeding behavior is dominant over withdrawal. In this study a group of neurons is described in the pleural ganglia, which controls whole body withdrawal behavior in Clione. Each pleural withdrawal (Pl-W) neuron has a high threshold for spike generation and is capable of inducing whole body withdrawal in a semi-intact preparation: retraction of the body-tail, wings, and head. Each Pl-W neuron projects axons into the main central nerves and innervates all major regions of the body. 2. Stimulation of Pl-W neurons produces inhibitory inputs to swim motor neurons that terminate swimming activity in the preparation. In turn, Pl-W neurons receive inhibitory inputs from the cerebral neurons involved in the control of feeding behavior in Clione, neurons underlying extrusion of specialized prey capture appendages. Thus it appears that specific inhibitory connections between motor centers can explain the dominance of withdrawal behavior over slow swimming and feeding over withdrawal in Clione.

A mechanism for production of phase shifts in a pattern generator

1984 ◽  
Vol 51 (6) ◽  
pp. 1375-1393 ◽  
Author(s):  
J. S. Eisen ◽  
E. Marder
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Phase Relations ◽  
Significant Advance ◽  
Neuron Activity ◽  
Cycle Frequency ◽  
Bath Application ◽  
Pyloric Dilator ◽  
Wide Range ◽  
Post Synaptic Potential

During motor activity of the pyloric system of the lobster stomatogastric ganglion, there are rhythmic alternations between activity in the pyloric dilator (PD) and pyloric (PY) motor neurons. We studied the phase relations between PD motor neuron activity and PY motor neuron activity in preparations cycling at a wide range of frequencies and after altering the activity of the PD neurons. The PY neurons fall into two classes, early (PE) and late (PL) (21), distinguished by the different phases in the pyloric cycle at which they fire. The phase at which PE neurons fired and the phase at which PL neurons fired was independent of pyloric cycle frequency over a range of frequencies from 0.5 to 2.25 Hz. The anterior burster (AB) interneuron is electrically coupled to the PD motor neurons. Together the AB and PD neurons form the pacemaker for the pyloric system. Synchronous depolarization of the AB and PD neurons evokes a complex inhibitory post-synaptic potential (IPSP) in PY neurons. This IPSP has two components: an early, AB neuron-derived component and a late, PD neuron-derived component. Deletion of the PD neurons from the pyloric circuit by photoinactivation removed the PD-evoked component of the pacemaker-evoked IPSP. This resulted in a decrease in the duration of the IPSP evoked by pacemaker depolarization and a significant advance in the firing phase of PY neurons. Bath application of dopamine was used to hyperpolarize and inhibit the PD neurons (30), causing them to release less neurotransmitter. As a consequence, the duration of the IPSP evoked by pacemaker depolarization was decreased and the firing phase of the PY neurons was significantly advanced. Stimulation of the inferior ventricular nerve (IVN) produces a slow excitation of the PD neurons (30), causing them to release more neurotransmitter. Consequently, the duration of the IPSP evoked by pacemaker depolarization was increased and the firing phase of the PY neurons was significantly retarded for several cycles of pyloric activity following IVN stimulation. Thus, modulation of the strength of PD-evoked inhibition in PY neurons is responsible for altering the firing phase of the PY neurons with respect to the pyloric pacemaker. We suggest that frequency of the pyloric output and the phase relations of the elements within the pyloric cycle can be regulated independently. The potential implications of these data for modulation of synaptic efficacy in other preparations are discussed.

Cerebral serotonergic neurons reciprocally modulate swim and withdrawal neural networks in the mollusk Clione limacina

1996 ◽  
Vol 75 (2) ◽  
pp. 538-546 ◽  
Author(s):  
T. P. Norekian ◽  
R. A. Satterlie
Keyword(s):  
Neural Networks ◽  
Motor Neurons ◽  
Swimming Behavior ◽  
Whole Body ◽  
Inhibitory Effects ◽  
Serotonergic Neurons ◽  
Serotonin Antagonist ◽  
Cerebral Ganglia ◽  
Cerebral Neurons ◽  
Clione Limacina

1. A pair of serotonin-immunoreactive neurons has been identified in the cerebral ganglia of the pteropod mollusk Clione limacina, which produce coordinated, excitatory/inhibitory effects on neurons controlling two incompatible behaviors, swimming and whole body withdrawal. These cells were designated cerebral serotonergic ventral (Cr-SV) neurons. 2. Activation of Cr-SV neurons produces a prominent inhibition of the pleural withdrawal neurons, which have been previously shown to induce whole body withdrawal in Clione. In addition, the cerebral neurons produce weak excitatory inputs to swim motor neurons, pedal serotonergic neurons involved in the peripheral modulation of swimming, and to the serotonergic heart excitor neuron. 3. Inhibitory and excitatory effects appear to be produced by serotonin because they are mimicked by exogenous serotonin and are blocked by the serotonin antagonist mianserin. 4. All serotonergic neurons identified thus far in the CNS of Clione appear to function in a coordinated manner, altering a variety of neural centers all directed toward the activation of swimming behavior.

Plasma clearance in the rat of the LH bioactivity of two human LH standards of differing molecular composition

1988 ◽  
Vol 119 (2) ◽  
pp. 327-334 ◽  
Author(s):  
P. L. Storring ◽  
S. A. Khan ◽  
Y. G. Mistry ◽  
E. Diczfalusy
Keyword(s):  
Plasma Clearance ◽  
Time Course ◽  
Intrinsic Activity ◽  
Plasma Testosterone ◽  
Target Cells ◽  
Human Pituitary ◽  
Course Of Action ◽  
Seminal Vesicle Weight

ABSTRACT The LH biological potency of the International Reference Preparation (IRP) of Human Pituitary LH for Immunoassay (IRP 68/40) relative to that of the 2nd IRP of Human Pituitary FSH and LH for Bioassay (IRP 78/549) is markedly greater when estimated by in-vitro interstitial cell testosterone production (TICT) bioassay than by in-vivo bioassay, and by the 4-h ovarian ascorbate depletion (OAAD) assay than by the 4-day seminal vesicle weight gain assay. Other preparations of human LH which, like IRP 68/40, were highly purified, showed a similar spectrum of bioactivity in these assay systems and also contained a higher proportion of more basic LH isoforms than are found in crude pituitary extracts such as IRP 78/549. In an attempt to explain these differences, a comparison was made of the plasma survival in rats of the LH bioactivity (by TICT assay) of these two preparations. Contrary to expectation, their relative plasma clearance rates over a 4-h period did not account for their differing bioactivities. The plasma half-life of the LH bioactivity (with 95% confidence limits) was estimated to be 42·4 (35·3–49·5) min for IRP 68/40 and 41·3 (31·5–51·0) min for IRP 78/549. Furthermore the time-course of action in vivo of IRP 78/549 did not appear to be more prolonged than that of IRP 68/40. Thus their plasma testosterone responses during the course of these 4-h plasma clearance studies were similar, and estimates of the LH potency of IRP 68/40 relative to that of IRP 78/549 were no greater by 2-h than by 4-h OAAD assay. The more basic isoforms of LH present in IRP 68/40 and in other purified human LH preparations may therefore differ from those in crude pituitary extracts, such as IRP 78/549, in their intrinsic activity to stimulate the different target cells in these assay systems rather than in their bioavailability in vivo. J. Endocr. (1988) 119, 327–334

In progressive nephropathies, overload of tubular cells with filtered proteins translates glomerular permeability dysfunction into cellular signals of interstitial inflammation.

1998 ◽  
Vol 9 (7) ◽  
pp. 1213-1224 ◽  
Author(s):  
M Abbate ◽  
C Zoja ◽  
D Corna ◽  
M Capitanio ◽  
T Bertani ◽  
...  
Keyword(s):  
Time Course ◽  
Early Stage ◽  
Protein Accumulation ◽  
Glomerular Injury ◽  
Cellular Mechanisms ◽  
Proinflammatory Response ◽  
Glomerular Permeability ◽  
Tubular Cells ◽  
Interstitial Inflammation ◽  
Tubulointerstitial Lesions

Progression to end-stage renal failure is the final common pathway of many forms of glomerular disease, independent of the type of initial insult. Progressive glomerulopathies have in common persistently high levels of urinary protein excretion and tubulointerstitial lesions at biopsy. Among the cellular mechanisms that may determine progression regardless of etiology, the traffic of excess proteins filtered from glomerulus in renal tubule may have functional importance by initiating interstitial inflammation in the early phase of parenchymal injury. This study analyzes the time course and sites of protein accumulation and interstitial cellular infiltration in two different models of proteinuric nephropathies. In remnant kidneys after 5/6 renal mass ablation, albumin and IgG accumulation by proximal tubular cells was visualized in the early stage, preceding interstitial infiltration of MHC-II-positive cells and macrophages. By double-staining, infiltrates developed at or near tubules containing intracellular IgG or luminal casts. This relationship persisted thereafter despite more irregular distribution of infiltrate. Similar patterns were found in an immune model (passive Heymann nephritis), indicating that the interstitial inflammatory reaction develops at the sites of protein overload, regardless of the type of glomerular injury. Osteopontin was detectable in cells of proximal tubules congested with protein in both models at sites of interstitial infiltration, and by virtue of its chemoattractive action this is likely mediator of a proximal tubule-dependent inflammatory pathway in response to protein load. Protein overload of tubules is a key candidate process translating glomerular protein leakage into cellular signals of interstitial inflammation. Mechanisms underlying the proinflammatory response of tubular cells to protein challenge in diseased kidney should be explored, as well as ways of limiting protein reabsorption/deposition to prevent consequent inflammation and progressive disease.

scholarly journals The intellectual disability gene Kirrel3 regulates target-specific mossy fiber synapse development in the hippocampus

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
E Anne Martin ◽  
Shruti Muralidhar ◽  
Zhirong Wang ◽  
Diégo Cordero Cervantes ◽  
Raunak Basu ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Mossy Fiber ◽  
Neuron Activity ◽  
Target Cells ◽  
Synaptic Changes ◽  
Mossy Fiber Synapse ◽  
Ca3 Neurons ◽  
Circuit Function ◽  
Feed Forward Inhibition

Synaptic target specificity, whereby neurons make distinct types of synapses with different target cells, is critical for brain function, yet the mechanisms driving it are poorly understood. In this study, we demonstrate Kirrel3 regulates target-specific synapse formation at hippocampal mossy fiber (MF) synapses, which connect dentate granule (DG) neurons to both CA3 and GABAergic neurons. Here, we show Kirrel3 is required for formation of MF filopodia; the structures that give rise to DG-GABA synapses and that regulate feed-forward inhibition of CA3 neurons. Consequently, loss of Kirrel3 robustly increases CA3 neuron activity in developing mice. Alterations in the Kirrel3 gene are repeatedly associated with intellectual disabilities, but the role of Kirrel3 at synapses remained largely unknown. Our findings demonstrate that subtle synaptic changes during development impact circuit function and provide the first insight toward understanding the cellular basis of Kirrel3-dependent neurodevelopmental disorders.

Aplysia ink release: central locus for selective sensitivity to long-duration stimuli

1979 ◽  
Vol 42 (5) ◽  
pp. 1223-1232 ◽  
Author(s):  
E. Shapiro ◽  
J. Koester ◽  
J. H. Byrne
Keyword(s):  
Motor Neuron ◽  
Spike Train ◽  
Motor Neurons ◽  
Neural Circuit ◽  
Reversal Potential ◽  
Secretory Process ◽  
Neuron Activity ◽  
Long Duration ◽  
Noxious Stimuli ◽  
Selective Sensitivity

1. A behavioral and electrophysiological analysis of defensive ink release in Aplysia californica was performed to examine the response of this behavior and its underlying neural circuit to various-duration noxious stimuli. 2. Three separate behavioral protocols were employed using electrical shocks to the head as noxious stimuli to elicit ink release. Ink release was found to be selectively responsive to longer duration stimuli, and to increase in a steeply graded fashion as duration is increased. 3. Intracellular stimulation of ink motor neurons revealed that ink release is a linear function of motor neuron spike train duration, indicating that the selective sensitivity of the behavior to long-duration stimuli is not due to a nonlinearity in the glandular secretory process. 4. In contrast, electrophysiological examination of ink motor neuron activity in response to sustained head shock revealed an accelerating spike train. During the later part of the spike train, compound excitatory synaptic potentials show a positive shift in reversal potential. 5. Our results suggest a central locus for the mechanisms that determine sensitivity of inking behavior to stimulus duration. 6. In contrast to ink release, defensive gill withdrawal was found to be extremely sensitive to short-duration stimuli.

Time Course of Action of Calcitonin on Resorbing Mouse Bones in vitro

Nature ◽  
1968 ◽  
Vol 218 (5147) ◽  
pp. 1178-1179 ◽  
Author(s):  
J. J. REYNOLDS ◽  
J. T. DINGLE
Keyword(s):  
Time Course ◽  
Course Of Action
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