scholarly journals Tonic excitation or inhibition is set by GABAA conductance in hippocampal interneurons

2011 ◽  
Vol 2 (1) ◽  
Author(s):  
Inseon Song ◽  
Leonid Savtchenko ◽  
Alexey Semyanov
Keyword(s):  
Tonic Excitation

Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats

1995 ◽  
Vol 269 (4) ◽  
pp. R807-R813 ◽  
Author(s):  
T. Hirai ◽  
T. I. Musch ◽  
D. A. Morgan ◽  
K. C. Kregel ◽  
D. E. Claassen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Important Means ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Tonic Excitation

Recent studies have suggested that the interaction between the sympathetic nervous system and nitric oxide (NO) or nitrosyl factors may be an important means by which arterial blood pressure is regulated. We investigated whether NO synthase (NOS) inhibition modulates basal sympathetic nerve discharge (SND) in baroreceptor-innervated and -denervated, chloralose-anesthetized Sprague-Dawley rats. We recorded mean arterial pressure (MAP), renal SND, and lumbar SND before and after administration of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg iv). Two minutes after L-NAME administration in baroreceptor-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decreased from control levels. These changes persisted for up to 20 min after L-NAME administration. In baroreceptor-denervated rats, L-NAME increased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10% from control at 20 min post-L-NAME). In contrast, renal SND progressively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These results demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nitrosyl factors provide tonic excitation to lumbar SND, whereas they provide a tonic restraint to renal SND.

Patterns of Phrenic Motor Output Evoked by Chemical Stimulation of Neurons Located in the Pre-Bötzinger Complex In Vivo

1999 ◽  
Vol 81 (3) ◽  
pp. 1150-1161 ◽  
Author(s):  
Irene C. Solomon ◽  
Norman H. Edelman ◽  
Judith A. Neubauer
Keyword(s):  
Short Duration ◽  
Respiratory Rhythm ◽  
High Amplitude ◽  
Chemical Stimulation ◽  
Arterial Blood ◽  
Bötzinger Complex ◽  
Tonic Excitation ◽  
Stimulation Of

Patterns of phrenic motor output evoked by chemical stimulation of neurons located in the pre-Bötzinger complex in vivo. The pre-Bötzinger complex (pre-BötC) has been proposed to be essential for respiratory rhythm generation from work in vitro. Much less, however, is known about its role in the generation and modulation of respiratory rhythm in vivo. Therefore we examined whether chemical stimulation of the in vivo pre-BötC manifests respiratory modulation consistent with a respiratory rhythm generator. In chloralose- or chloralose/urethan-anesthetized, vagotomized cats, we recorded phrenic nerve discharge and arterial blood pressure in response to chemical stimulation of neurons located in the pre-BötC with dl-homocysteic acid (DLH; 10 mM; 21 nl). In 115 of the 122 sites examined in the pre-BötC, unilateral microinjection of DLH produced an increase in phrenic nerve discharge that was characterized by one of the following changes in cycle timing and pattern: 1) a rapid series of high-amplitude, rapid rate of rise, short-duration bursts, 2) tonic excitation (with or without respiratory oscillations), 3) an integration of the first two types of responses (i.e., tonic excitation with high-amplitude, short-duration bursts superimposed), or 4) augmented bursts in the phrenic neurogram (i.e., eupneic breath ending with a high-amplitude, short-duration burst). In 107 of these sites, the phrenic neurogram response was accompanied by an increase or decrease (≥10 mmHg) in arterial blood pressure. Thus increases in respiratory burst frequency and production of tonic discharge of inspiratory output, both of which have been seen in vitro, as well as modulation of burst pattern can be produced by local perturbations of excitatory amino acid neurotransmission in the pre-BötC in vivo. These findings are consistent with the proposed role of this region as the locus for respiratory rhythm generation.

scholarly journals Analysis of Oscillations in a Reciprocally Inhibitory Network with Synaptic Depression

2002 ◽  
Vol 14 (3) ◽  
pp. 561-581 ◽  
Author(s):  
Adam L. Taylor ◽  
Garrison W. Cottrell ◽  
William B. Kristan
Keyword(s):  
Simple Model ◽  
Synaptic Depression ◽  
Spike Frequency Adaptation ◽  
Short Term ◽  
Principal Mechanism ◽  
Inhibitory Network ◽  
Postinhibitory Rebound ◽  
Analytical Expressions ◽  
Tonic Excitation ◽  
Good Agreement

We present and analyze a model of a two-cell reciprocally inhibitory network that oscillates. The principal mechanism of oscillation is short-term synaptic depression. Using a simple model of depression and analyzing the system in certain limits, we can derive analytical expressions for various features of the oscillation, including the parameter regime in which stable oscillations occur, as well as the period and amplitude of these oscillations. These expressions are functions of three parameters: the time constant of depression, the synaptic strengths, and the amount of tonic excitation the cells receive. We compare our analytical results with the output of numerical simulations and obtain good agreement between the two. Based on our analysis, we conclude that the oscillations in our network are qualitatively different from those in networks that oscillate due to postinhibitory rebound, spike-frequency adaptation, or other intrinsic (rather than synaptic) adaptational mechanisms. In particular, our network can oscillate only via the synaptic escape mode of Skinner, Kopell, and Marder (1994).

Influence of respiratory network drive on phrenic motor output evoked by activation of cat pre-Bötzinger complex

2003 ◽  
Vol 284 (2) ◽  
pp. R455-R466 ◽  
Author(s):  
Irene C. Solomon
Keyword(s):  
Phrenic Nerve ◽  
Chemical Stimulation ◽  
Motor Output ◽  
Peripheral Chemoreceptor ◽  
Homocysteic Acid ◽  
Respiratory Network ◽  
Bötzinger Complex ◽  
Tonic Excitation ◽  
Stimulation Of ◽  
Nerve Discharge

10.1152/ajpregu.00395.2002. We have previously demonstrated that microinjection of dl-homocysteic acid (DLH), a glutamate analog, into the pre-Bötzinger complex (pre-BötC) can produce either phasic or tonic excitation of phrenic nerve discharge during hyperoxic normocapnia. Breathing, however, is influenced by input from both central and peripheral chemoreceptor activation. This influence of increased respiratory network drive on pre-BötC-induced modulation of phrenic motor output is unclear. Therefore, these experiments were designed to examine the effects of chemical stimulation of neurons (DLH; 10 mM; 10–20 nl) in the pre-BötC during hyperoxic modulation of CO2 (i.e., hypercapnia and hypocapnia) and during normocapnic hypoxia in chloralose-anesthetized, vagotomized, mechanically ventilated cats. For these experiments, sites were selected in which unilateral microinjection of DLH into the pre-BötC during baseline conditions of hyperoxic normocapnia [arterial Pco 2 (PaCO2 ) = 37–43 mmHg; n = 22] produced a tonic (nonphasic) excitation of phrenic nerve discharge. During hypercapnia (PaCO2 = 59.7 ± 2.8 mmHg; n= 17), similar microinjection produced excitation in which phasic respiratory bursts were superimposed on varying levels of tonic discharge. These DLH-induced phasic respiratory bursts had an increased frequency compared with the preinjection baseline frequency ( P < 0.01). In contrast, during hypocapnia (PaCO2 = 29.4 ± 1.5 mmHg; n= 11), microinjection of DLH produced nonphasic tonic excitation of phrenic nerve discharge that was less robust than the initial (normocapnic) response (i.e., decreased amplitude). During normocapnic hypoxia (PaCO2 = 38.5 ± 3.7; arterial Po 2 = 38.4 ± 4.4; n= 8) microinjection of DLH produced phrenic excitation similar to that seen during hypercapnia (i.e., increased frequency of phasic respiratory bursts superimposed on tonic discharge). These findings demonstrate that phrenic motor activity evoked by chemical stimulation of the pre-BötC is influenced by and integrates with modulation of respiratory network drive mediated by input from central and peripheral chemoreceptors.

scholarly journals The Effects of Digital Anesthesia on Force Control Using a Precision Grip

2003 ◽  
Vol 89 (2) ◽  
pp. 672-683 ◽  
Author(s):  
Joël Monzée ◽  
Yves Lamarre ◽  
Allan M. Smith
Keyword(s):  
Internal Model ◽  
Grip Force ◽  
Index Finger ◽  
Precision Grip ◽  
Initial Study ◽  
Cutaneous Sensation ◽  
Surface Textures ◽  
Cutaneous Feedback ◽  
Resistive Forces ◽  
Tonic Excitation

A total of 20 right-handed subjects were asked to perform a grasp-lift-and-hold task using a precision grip. The grasped object was a one-degree-of-freedom manipuladum consisting of a vertically mounted linear motor capable of generating resistive forces to simulate a range of object weights. In the initial study, seven subjects (6 women, 1 man; ages 24–56 yr) were first asked to lift and hold the object stationary for 4 s. The object presented a metal tab with two different surface textures and offered one of four resistive forces (0.5, 1.0, 1.5, and 2.0 N). The lifts were performed both with and without visual feedback. Next, the subjects were asked to perform the same grasping sequence again after ring block anesthesia of the thumb and index finger with mepivacaine. The objective was to determine the degree to which an internal model obtained through prior familiarity might compensate for the loss of cutaneous sensation. In agreement with previous studies, it was found that all subjects applied significantly greater grip force after digital anesthesia, and the coordination between grip and load forces was disrupted. It appears from these data, that the internal model alone is insufficient to completely compensate for the loss of cutaneous sensation. Moreover, the results suggest that the internal model must have either continuous tonic excitation from cutaneous receptors or at least frequent intermittent reiteration to function optimally. A subsequent study performed with 10 additional subjects (9 women, 1 man; ages 24–49 yr) indicated that with unimpaired cutaneous feedback, the grasping and lifting forces were applied together with negligible forces and torques in other directions. In contrast, after digital anesthesia, significant additional linear and torsional forces appeared, particularly in the horizontal and frontal planes. These torques were thought to arise partially from the application of excessive grip force and partially from a misalignment of the two grasping fingers. These torques were further increased by an imbalance in the pressure exerted by the two opposing fingers. Vision of the grasping hand did not significantly correct the finger misalignment after digital anesthesia. Taken together, these results suggest that mechanoreceptors in the fingertips signal the source and direction of pressure applied to the skin. The nervous system uses this information to adjust the fingers and direct the pinch forces optimally for grasping and object manipulation.

Pontine reticular neurons provide tonic excitation to neurons in rostral ventrolateral medulla in rats

1994 ◽  
Vol 266 (1) ◽  
pp. R237-R244 ◽  
Author(s):  
K. Hayes ◽  
F. R. Calaresu ◽  
L. C. Weaver
Keyword(s):  
Cardiac Cycle ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Cardiovascular Neurons ◽  
Reticular Neurons ◽  
Baroreceptor Activation ◽  
Tonic Excitation ◽  
Excitatory Drive

To determine whether the pontine reticular formation (PRF) is a source of tonic activity for cardiovascular neurons in the rostral ventrolateral medulla (RVLM), the discharge of PRF neurons was inhibited by unilateral microinjections of glycine (1.0 M; 60 nl) while recording the discharge of single neurons in the RVLM in 14 Saffan-anesthetized rats. RVLM units were characterized as cardiovascular if their spontaneous activity was changed by baroreceptor activation and was synchronized to the cardiac cycle. Glycine injection into the ipsilateral PRF eliminated the ongoing activity of six cardiovascular units and reduced the activity of four (mean decrease -91 +/- 4%). Inhibition of these units lasted 20-115 s (mean 59 +/- 9 s). Glycine injection into the PRF had no effect on the discharge of five cardiovascular units. Activity of six noncardiovascular units did not respond to PRF blockade. Glycine injection into the PRF caused decreases in arterial pressure (-28 +/- 5 mmHg), heart rate (-23 +/- 3 beats/min), and renal nerve activity (-42 +/- 7%) that also returned to control values between 25 and 120 s (mean 55 +/- 5 s). These results indicate that PRF neurons provide tonic excitatory drive to some cardiovascular neurons located in the RVLM.

scholarly journals Multiple receptors mediate the modulatory effects of serotonergic neurons in a small neural network.

1994 ◽  
Vol 190 (1) ◽  
pp. 55-77 ◽  
Author(s):  
B Zhang ◽  
R M Harris-Warrick
Keyword(s):  
Neural Network ◽  
Neural Networks ◽  
Tonic Inhibition ◽  
Receptor Subtypes ◽  
Muscarinic Cholinergic Receptors ◽  
Multiple Receptors ◽  
Pyloric Dilator ◽  
Muscarinic Cholinergic ◽  
Tonic Excitation ◽  
Stimulation Of

The gastropyloric receptor (GPR) cells are a set of cholinergic/serotonergic mechanosensory neurons that modulate the activity of neural networks in the crab stomatogastric ganglion (STG). Stimulation of these cells evokes a variety of slow modulatory responses in different STG neurons that are mimicked by exogenously applied serotonin (5-HT); these responses include tonic inhibition, tonic excitation and induction of rhythmic bursting. We used pharmacological agonists and antagonists to show that these three classes of modulatory response in the STG neurons are mediated by distinct 5-HT receptor subtypes. GPR stimulation or application of 5-HT or 2-me-5HT (a vertebrate 5-HT3 agonist) inhibited the pyloric constrictor (PY) neurons; these actions were selectively antagonized by gramine. GPR stimulation or application of 5-HT induced rhythmic bursting in the electrically coupled anterior burster (AB) and pyloric dilator (PD) neurons; these effects were antagonized by the 5-HT1c/2 antagonist cinanserin and by atropine at concentrations that do not block muscarinic cholinergic receptors in the crab STG. The 5-HT agonists 5-CT (5-HT1) and alpha-me-5HT (5-HT2) also induced AB/PD bursting, which was blocked by cinanserin, but not by atropine. GPR stimulation or application of 5-HT and 5-CT evoked tonic excitation of the lateral pyloric (LP) neuron. These effects were blocked by cinanserin. Several other 5-HT agonists and nearly all the vertebrate 5-HT antagonists we tested had little or no effect on the crab pyloric 5-HT receptors. These results provide further evidence that the modulatory sensory GPR neuron uses serotonin to evoke multiple modulatory responses via multiple 5-HT receptors. However, the 5-HT receptors in the crab STG neurons are not pharmacologically similar to vertebrate 5-HT receptors.

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