Behavior of upper cervical inspiratory propriospinal neurons during fictive vomiting

1991 ◽  
Vol 65 (6) ◽  
pp. 1492-1500 ◽  
Author(s):  
S. Nonaka ◽  
A. D. Miller
Keyword(s):  
Firing Pattern ◽  
Impulse Activity ◽  
Abdominal Muscle ◽  
Lateral Funiculus ◽  
Upper Cervical ◽  
Spinal Segments ◽  
Propriospinal Neurons ◽  
Lumbar Cord ◽  
Stimulation Of

1. The role of upper cervical inspiratory (UCI)-modulated neurons in respiratory muscle control during vomiting was examined by recording the impulse activity of these neurons during fictive vomiting in decerebrate, paralyzed cats. Fictive vomiting was identified by a characteristic series of bursts of coactivation of phrenic and abdominal muscle nerves, elicited either by electrical stimulation of supradiaphragmatic vagal nerve afferents or by emetic drugs, which would be expected to produce expulsion of gastric contents in nonparalyzed animals. 2. Data were recorded from 43 propriospinal UCI neurons, located in the C1-C3 spinal segments near the border of the intermediate gray matter and lateral funiculus, which were antidromically activated with floating pin electrodes placed in the ipsilateral lateral funiculus, usually at T1-T3. Some cells (9/21 tested) were also activated from the upper lumbar cord (L1). During respiration, most neurons (n = 40) had an augmenting discharge pattern during inspiration. In addition, more than one-half (55%) fired tonically during the remainder of the respiratory cycle. About 40% of UCI neurons showed variations in their firing pattern during the noninspiratory portion of respiration. These latter two properties of UCI neurons were not observed in dorsal and ventral respiratory group (DRG and VRG-, respectively) bulbospinal inspiratory (I) neurons previously recorded under similar conditions. 3. During fictive vomiting, the firing pattern of most UCI neurons fell into one of three main categories. More than one-half (53%) were active in phase with bursts of phrenic discharge and were thus classified as Active-type cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragmatic and external intercostal muscle control during vomiting: behavior of inspiratory bulbospinal neurons

1990 ◽  
Vol 63 (1) ◽  
pp. 31-36 ◽  
Author(s):  
A. D. Miller ◽  
S. Nonaka ◽  
S. F. Lakos ◽  
L. K. Tan
Keyword(s):  
Abdominal Muscle ◽  
Neuronal Firing ◽  
Vagal Afferents ◽  
Response Patterns ◽  
Spinal Segment ◽  
Initial Activation ◽  
Different Response ◽  
Onset Rate ◽  
Stimulation Of

1. The role of dorsal and ventral respiratory group (DRG and VRG) bulbospinal inspiratory (I) neurons in the control of diaphragmatic and external intercostal (inspiratory) muscle activity during vomiting was examined by recording from these neurons during fictive vomiting in decerebrate, paralyzed cats. Fictive vomiting was defined by a characteristic series of bursts of coactivation of phrenic and abdominal muscle nerves, elicited either by electrical stimulation of abdominal vagal afferents or by emetic drugs, which would be expected to produce vomiting if the animals were not paralyzed. 2. Data were recorded from 22 DRG and 29 VRG I neurons that were antidromically activated from the fourth cervical spinal segment (C4). Only 10% (5/51) of these neurons started to fire near the beginning of phrenic discharge during fictive vomiting and thus had the appropriate discharge pattern to contribute to the initial activation of the diaphragm and coactive external intercostal muscles during vomiting. The frequency of occurrence of these Active neurons was not significantly different in the DRG (3/22) and VRG (2/29) (chi 2 test). Most remaining neurons were either totally silent (n = 7) or had only sporadic, infrequent firing (n = 16) (Silent neurons, 23/51 = 45%), or else fired near the end of phrenic discharge during fictive vomiting (End neurons, 21/51 = 41%). Two neurons were categorized as having miscellaneous (Misc) behavior. 3. No differences were found among neurons having different response patterns during fictive vomiting in regard to the following: the manner in which fictive vomiting was elicited: cell location: conduction velocity; and neuronal firing onset, rate, and pattern during respiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Signal transduction in activation of ischemically sensitive abdominal visceral afferents: role of PKC

1998 ◽  
Vol 275 (3) ◽  
pp. H1024-H1031 ◽  
Author(s):  
Zhi-Ling Guo ◽  
Liang-Wu Fu ◽  
J. David Symons ◽  
John C. Longhurst
Keyword(s):  
Signal Transduction ◽  
Impulse Activity ◽  
Visceral Afferents ◽  
C Fibers ◽  
Kinase C ◽  
C Fiber ◽  
Afferent Nerve Endings ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia reflexly activates the cardiovascular system by stimulating abdominal visceral afferent nerve endings. Whereas many ischemic metabolites responsible for activating these nerves have been identified (e.g., bradykinin), their precise mechanism of action is unclear. Protein kinase C (PKC) is an important part of the signal transduction process underlying the action of metabolites such as bradykinin and is a regulator of neuronal activity. Therefore, we hypothesized that PKC contributes to stimulation of ischemically sensitive abdominal visceral afferents. Single-unit activity was recorded from the right thoracic sympathetic chain of anesthetized cats. Exogenous activation of PKC using phorbol 12,13-dibutyrate (PDBu, 5 μg/kg ia) increased the impulse activity of ischemically sensitve C-fiber afferents from 0.04 ± 0.01 to 0.67 ± 0.23 impulses/s ( n = 11; P < 0.05). The influence of endogenous activation of PKC also was evaluated during 10 min of mesenteric ischemia. Inhibition of PKC using PKC-(19—36) (20 μg/kg iv) reduced ischemia-induced increases in afferent activity from 0.46 ± 0.11 to 0.19 ± 0.08 impulses/s ( n = 7, P < 0.05). Moreover, PKC-(19—36) (20 μg/kg iv) reduced the response of ischemically sensitive C fibers to bradykinin (0.5–1.0 μg/kg ia) from 1.18 ± 0.20 to 0.66 ± 0.14 impulses/s ( n = 13, P < 0.05). These results indicate that PKC contributes to activation of abdominal visceral afferents during ischemia and specifically to part of the bradykinin-induced activation of these afferents.

Tonic neck reflex of the decerebrate cat: a role for propriospinal neurons

1985 ◽  
Vol 54 (4) ◽  
pp. 978-987 ◽  
Author(s):  
E. E. Brink ◽  
I. Suzuki ◽  
S. J. Timerick ◽  
V. J. Wilson
Keyword(s):  
Decerebrate Cat ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Upper Cervical ◽  
Dorsal Columns ◽  
Qualitative Effect ◽  
Neck Rotation ◽  
Propriospinal Neurons ◽  
Tonic Neck Reflex

In decerebrate, acutely labyrinthectomized cats we used neck rotation to study the role of direct upper cervical afferents to the cervical enlargement and of cervical and lumbar propriospinal neurons in the tonic neck reflex. Interruption of the dorsal columns between C4 and C5 had no qualitative effect on the dynamics of the reflex although gain usually increased. Direct upper cervical afferents to the cervical enlargement therefore have no unique role in producing the reflex. Many medially located propriospinal neurons in C4 were modulated by neck rotation. About 40% had axons, mostly crossed, that terminated in the cervical enlargement. The others projected more caudally, some as far as L3-L4 or even the lumbar enlargement. For a population of C4 neurons, including propriospinal neurons, we measured the response vector with combinations of roll and pitch stimuli. These vectors ranged from pitch to roll. Many propriospinal neurons in L3-L4, projecting to the lumbosacral enlargement, were also modulated by neck rotation with a variety of response vectors. Some of these neurons had an ascending projection. As in previous experiments, C4 neurons were modulated by neck rotation after spinal transection rostral to the C1 dorsal root entry zone; a wide variety of response vectors was observed. In contrast, almost no modulated L3-L4 neurons were found in the same experiments. The results suggest a role for propriospinal neurons in the tonic neck reflex. They also demonstrate that responses of lumbar neurons to neck rotation are much more dependent on supraspinal pathways than are those of cervical neurons.

Salivary responses to cortical and sciatic stimulation

1961 ◽  
Vol 200 (1) ◽  
pp. 46-50 ◽  
Author(s):  
A. G. Velo ◽  
E. C. Hoff
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Sciatic Nerve ◽  
Cortical Area ◽  
Dorsal Part ◽  
Parasympathetic Innervation ◽  
Lateral Funiculus ◽  
Upper Cervical ◽  
Cervical Level ◽  
Stimulation Of

In cats under ether and Flaxedil, submandibular salivation in response to electrical stimulation of the central cut end of the sciatic nerve and cortical loci on sigmoid gyrus and gyrus proreus has been evoked. These responses were obtained in animals with solely sympathetic or parasympathetic innervation of the gland intact. The ascending path in the cord (for parasympathetic and sympathetic effects) runs in the dorsal part of the lateral funiculus. In acute animals, the relay for both effects takes place somewhere between the upper cervical level of the spinal cord and the midcollicular level of the brainstem. A segmental activation of sympathetic salivary responses may have been masked by autonomic spinal shock. The excitable cortical area overlaps those yielding vasomotor responses, adrenal medullary activity and bladder contractions. The descending pathway for sympathetic effects runs in the spinal cord (at the cervical level) at the junction of the dorsal and ventral parts of the lateral funiculus, a region also containing descending vasomotor fibers.

The Role of the Lateral-Line Efferent System in Xenopus Laevis

1971 ◽  
Vol 54 (3) ◽  
pp. 621-641 ◽  
Author(s):  
I. J. RUSSELL
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Lateral Line ◽  
Impulse Activity ◽  
Close Correlation ◽  
Active Movement ◽  
Nerve Fibres ◽  
Efferent Nerve ◽  
Stimulation Of

1. Efferent impulses have been recorded from branches of lateral-line nerves. The functional significance of the efferent innervation and its action on afferent impulse activity has been examined. 2. Neither mechanical stimulation of the lateral-line receptors nor electrical stimulation of afferent nerves excites lateral-line efferent activity. 3. Trains of efferent impulses accompany all active movements for their duration. In immobilized animals a close correlation exists between impulses in lateral-line efferent nerve fibres and motor impulses in ‘large’ nerves innervating ‘twitch’ muscles, but not with impulses in nerves innervating ‘slow’ muscles. A close similarity also exists between impulse activity in different lateral-line efferent fibres. 4. Whereas electrical stimulation of ascending tracts in the spinal cord fails to excite lateral-line efferent fibres, stimulation of the spinal cord in the region of descending reticular motor axons causes efferent impulses to follow each pulse after brief, constant, latencies. It is suggested that the efferent neurones may be innervated by axon collaterals from reticular cells. 5. Electrical stimulation of efferent fibres innervating a lateral-line receptor produces transitory inhibition of impulse activity in the afferent nerve fibres. The inhibition has a long variable latency (11-30 ms) and persists for 40-60 ms. Upon cessation of inhibition, caused by a train of efferent impulses, afferent impulses reappear at an accelerated frequency (after-discharge), and quickly return to resting frequency. 6. A role of the lateral-line efferent neurones during active movement is discussed.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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