Increase In Discharge Frequency Research Articles

Effects of voltage distribution along an induction coil and discharge frequency in inductively coupled plasmas

Recent etching processes often use low to middle plasma density in order to increase etching controllability or to reduce charging damages. In inductively coupled plasmas (ICPs) in low to middle plasma density, effects of a capacitively coupled discharge (E discharge) on the total plasma characteristic cannot be neglected. It is thus more difficult to understand the ICPs in low to middle density than to understand high-density ICPs which can be regarded as being generated by an inductively coupled discharge (H discharge) only. In this research, we changed the voltage distribution of the induction coil of an ICP-modified gaseous electronics conference reference cell by inserting a termination capacitor between the coil and the ground. We also changed the discharge frequencies (6.28 MHz, 13.56 MHz, and 20 MHz), and investigated their effects on Ar plasmas. As a result, it was observed that the structure of the E discharge was changed by the voltage distribution of the coil and, therefore, E-to-H mode transitions were dramatically altered. Although no difference between the electron energy distribution functions (EEDFs) was observed in a pure H discharge with an electrostatic shield for the experimental conditions studied (1.33 Pa and 150 W), it was observed that EEDFs were affected by the discharge frequency without an electrostatic shield, probably due to a decrease of electron density by the effect of an E discharge and an increase of the ratio of the E to H discharge with increasing discharge frequency.

Kv1.2-containing K+ channels regulate subthreshold excitability of striatal medium spiny neurons.

A slowly inactivating, low-threshold K(+) current has been implicated in the regulation of state transitions and repetitive activity in striatal medium spiny neurons. However, the molecular identity of the channels underlying this current and their biophysical properties remain to be clearly determined. Because previous work had suggested this current arose from Kv1 family channels, high-affinity toxins for this family were tested for their ability to block whole cell K(+) currents activated by depolarization of acutely isolated neurons. alpha-Dendrotoxin, which blocks channels containing Kv1.1, Kv1.2, or Kv1.6 subunits, decreased currents evoked by depolarization. Three other Kv1 family toxins that lack a high affinity for Kv1.2 subunits, r-agitoxin-2, dendrotoxin-K, and r-margatoxin, failed to significantly reduce currents, implicating channels with Kv1.2 subunits. RT-PCR results confirmed the expression of Kv1.2 mRNA in identified medium spiny neurons. Currents attributable to Kv1.2 channels activated rapidly, inactivated slowly, and recovered from inactivation slowly. In the subthreshold range (ca. -60 mV), these currents accounted for as much as 50% of the depolarization-activated K(+) current. Moreover, their rapid activation and relatively slow deactivation suggested that they contribute to spike afterpotentials regulating repetitive discharge. This inference was confirmed in current-clamp recordings from medium spiny neurons in the slice preparation where Kv1.2 blockade reduced first-spike latency and increased discharge frequency evoked from hyperpolarized membrane potentials resembling the "down-state" found in vivo. These studies establish a clear functional role for somato-dendritic Kv1.2 channels in the regulation of state transitions and repetitive discharge in striatal medium spiny neurons.

Neuron activity in the prefrontal cortex of the brain in rats with different typological characteristics in conditions of emotional stimulation.

Male Wistar rats were separated according to the "emotional resonance" method (groups of animals avoiding ("altruists") and not avoiding ("egotists") the pain cries of partner rats) and neuron activity in the prefrontal areas of the cortex was studied in the right and left hemispheres. Assessments were made of changes in the frequency of nerve cell spike activity (in relation to the baseline activity of neurons in sated animals) in rats subjected to one day of food deprivation and after electrical stimulation of emotionally positive (lateral hypothalamus) and negative (tegmentum of the midbrain) brain structures and after exposure to the pain cries of partner rats. The results of these experiments revealed a series of differences in the cell activities of the two groups of rats. In conditions of hunger, the discharge frequency in the "altruists" was higher than that in "egotists." Cortical neuron responses to positive stimulation were greater than those to negative stimulation in rats of both groups. Intracerebral stimulation produced significantly greater increases in discharge frequency in neurons of both prefrontal areas of the cortex in "altruists" than in "egotists." In both groups of rats, neurons in the right hemisphere responded to emotionally negative stimulation with significantly greater activation than cells in the left hemisphere, while activity in the left hemisphere was greater in conditions of emotionally positive stimulation. "Altruists" showed significantly greater neuron responses during exposure to pain cries from "victim" rats in both the right and left hemispheres. The responses of "egotists" to "victim" cries were not significantly different from baseline activity levels.

Vestibulospinal and reticulospinal neuronal activity during locomotion in the intact cat. II. Walking on an inclined plane.

The experiments described in this report were designed to determine the contribution of vestibulospinal neurons (VSNs) in Deiters' nucleus and of reticulospinal neurons (RSNs) in the medullary reticular formation to the modifications of the walking pattern that are associated with locomotion on an inclined plane. Neuronal discharge patterns were recorded from 44 VSNs and 63 RSNs in cats trained to walk on a treadmill whose orientation was varied from +20 degrees (uphill) to -10 degrees (downhill), referred to as pitch tilt, and from 20 degrees roll tilt left to 20 degrees roll tilt right. During uphill locomotion, a majority of VSNs (25/44) and rhythmically active RSNs (24/39) showed an increase in peak discharge frequency, above that observed during locomotion on a level surface. VSNs, unlike some of the RSNs, exhibited no major deviations from the overall pattern of the activity recorded during level walking. The relative increase in discharge frequency of the RSNs (on average, 31.8%) was slightly more than twice that observed in the VSNs (on average, 14.4%), although the average absolute change in discharge frequency was similar (18.2 Hz in VSNs and 21.6 Hz in RSNs). Changes in discharge frequency during roll tilt were generally more modest and were more variable, than those observed during uphill locomotion as were the relative changes in the different limb muscle electromyograms that we recorded. In general, discharge frequency in VSNs was more frequently increased when the treadmill was rolled to the right (ear down contralateral to the recording site) than when it was rolled to the left. Most VSNs that showed significant linear relationships with treadmill orientation in the roll plane increased their activity during right roll and decreased activity during left roll. Discharge activity in phasically modulated RSNs was also modified by roll tilt of the treadmill. Modulation of activity in RSNs that discharged twice in each step cycle was frequently reciprocal in that one burst of activity would increase during left roll and the other during right roll. The overall results indicate that each system contributes to the changes in postural tone that are required to adapt the gait for modification on an inclined surface. The characteristics of the discharge activity of the VSNs suggest a role primarily in the overall control of the level of electromyographic activity, while the characteristics of the RSNs suggest an additional role in determining the relative level of different muscles, particularly when the pattern is asymmetric.

Comparison of electron cyclotron resonance plasma characteristics discharged by 7.0, 8.0, and 9.4 GHz

Argon electron cyclotron resonance plasma characteristics discharged by 7.0, 8.0, and 9.4 GHz microwaves are measured at 0.013 and 0.080 Pa in a cylindrical chamber. The plasma densities and electron temperatures were found to be almost independent of the microwave frequency at 0.013 Pa, whereas clear differences were seen at 0.080 Pa. At 0.080 Pa, the plasma densities were observed to increase with the increase in the discharge frequency. Electron temperatures at 0.080 Pa also appeared to become higher with the increase in discharge frequency.

Chemoreceptor discharges and cytochrome redox changes of the rat carotid body: role of heme ligands.

In superfused in vitro rat carotid body, we recorded chemoreceptor discharges and the redox state of cytochromes simultaneously to identify the primary oxygen-sensing protein controlling transmitter release and electrical activity of the carotid sinus nerve. These parameters were tested under the influence of heme ligands such as oxygen, cyanide, 4-(2-aminoethyl)-benzenesulfonyl fluoride, and CO. During stimulation, there was an initial increase in discharge frequency followed by a decline or suppression of activity. Photometric changes lagged and were maintained as nerve activity decreased. Reducing mitochondrial cytochromes by cyanide or prolonged severe hypoxia, suppressed the chemoreceptor discharge. 4-(2-Aminoethyl)-benzenesulfonyl fluoride, a specific inhibitor of the phagocytic cytochrome b(558), also silenced the chemoreceptors after an initial excitation. CO increased the chemoreceptor discharge under normoxia, an effect inhibited by light, when the cytochromes were not reduced. When the discharges were depressed by severe hypoxia, exposure to light excited the chemoreceptors and the cytochromes were reduced. The rapidity of the chemosensory responses to light and lack of effect on dopamine release from type I cells led us to hypothesize that carotid body type I cells and the apposed nerve endings use different mechanisms for oxygen sensing: the nerve endings generate action potentials in association with membrane heme proteins whereas cytosolic heme proteins signal the redox state, releasing modulators or transmitters from type I cells.

Respiration-modulated membrane potential and chemosensitivity of locus coeruleus neurones in the in vitro brainstem-spinal cord of the neonatal rat.

1. The activity of locus coeruleus (LC) neurones (n = 126) was examined in whole-cell (conventional and amphotericin B-perforated patch) recordings, and the relationship of this activity to the respiratory discharge recorded on the C4 or C5 phrenic nerve roots was determined at different CO2 concentrations (2 and 8 %; bath pH 7. 8 and 7.2) in the in vitro brainstem-spinal cord preparation of the neonatal rat (1-5 days old). 2. In most neurones (n = 105) ongoing activity was modulated at respiratory frequency. Typically, this consisted of a phase of depolarization and increased discharge frequency synchronous with the phrenic burst, followed by a phase of hyperpolarization and inhibition of discharge (n = 94 of 105). The incidence of respiratory modulation decreased from 91 % on P1 to 57 % on P5. 3. Bath application of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5 microM) or the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV; 100 microM) abolished both phases of respiratory modulation. The hyperpolarizing phase alone was abolished by the adrenoceptor antagonists idazoxan (5 microM) or phentolamine (0.8 microM). These results indicate that excitatory amino acid pathways are involved in the transmission of both the excitatory and inhibitory components and that the latter involves in addition an alpha2-adrenoceptor-mediated pathway. 4. Increasing the CO2 concentration from 2 to 8 % resulted in a shortening of expiratory duration and weakening or loss of respiratory-phased inhibition; this was accompanied by depolarization, increased discharge frequency and, in those neurones where they were initially present (60 %), an increase in the frequency of subthreshold membrane potential oscillations. The depolarizing response was retained in the presence of tetrodotoxin (TTX, 0.2-1.0 microM). 5. These results indicate that in this neonatal preparation LC neurones form part of the synaptically connected brainstem respiratory network, and that the LC constitutes a site of CO2- or pH-dependent chemoreception.

Effects of biliary tract pressure on dynamics of the Oddi's sphincter and its nerve mechanism.

In order to explore the effect of biliary tract pressure on Oddi's sphincter and the mechanism of development of high pressure of biliary tract during acute obstructive and suppurative cholangitis (AOSC), house rabbits were used to establish model of high biliary pressure in acute biliary duct caecus. It was observed that when the pressure of the acute biliary tract was increased to 8 kPa, the electric activity of Oddi's sphincter was obviously enhanced, the pressure of Oddioes sphincter increased remarkably (P < 0.05), and even constant spasm appeared with accompanying increase of discharge frequency of the right greater splanchnic nerves (P < 0.05) and progressive decrease of mean arterial pressure. However, when lidocaine of 0.6% was used to block the right celiac plexus, no above-mentioned reaction happened when the biliary tract pressure was increased again. The results indicated that the acute biliary tract obstruction might induce the contraction or spasm of Oddi's sphincter and bring about a vicious cycle. Its mechanism is related to splanchnic nerves reflection and it is one of important factors in the development of AOSC course.

Suppression of drug-induced epileptiform discharges by cyclic AMP in rat hippocampus.

The effect of cyclic adenosine 3',5'-monophosphate (cAMP) on epileptiform activity in rat hippocampal slices was investigated. Bath-applied cAMP reversibly decreased the frequency of extracellularly recorded discharges in the CA3 subfield induced by bethanechol- or theophylline-containing solutions. Because cAMP was presumed to be relatively membrane impermeant, we developed and tested the hypothesis that this cAMP-mediated effect occurred extracellularly through the catabolic conversion of cAMP to 5'-AMP and, in turn, to adenosine, a known inhibitory neuromodulator. Three predictions derived from this catabolic hypothesis were tested. First, blockers of the enzymes involved were predicted to antagonize this effect of cAMP. In contrast, the coapplication of a cAMP-phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), or a 5'-nucleotidase inhibitor, adenosine 5'-[alpha, beta-methylene] diphosphate (AMP-CP), enhanced the cAMP-induced suppressive effect. Second, the nonhydrolyzable cAMP analogs, dibutyryl- and 8-bromo-cAMP, were predicted to be ineffective. Low concentrations (5-40 microM) of these two derivatives, however, also suppressed bethanechol-induced discharges, while, at a higher concentration (100 microM), both analogs increased discharge frequencies. Third, enzymatic catabolism of adenosine was predicted to antagonize cAMP's effect, but coapplying adenosine deaminase (10 U/mL) did not diminish this action. Because these data did not support the catabolic hypothesis, other, as yet undefined, mechanisms must be responsible for the discharge-suppressant effect of cAMP.

Integrative role of medullary neurons of the cat during exercise.

The co-ordinated cardiovascular and respiratory responses observed during exercise are mediated by both afferent activation arising in contracting skeletal muscles and descending central drive originating in brain regions rostral to the medulla. Even though integration of these two mechanisms must occur in order to produce alterations in cardiorespiratory activity proportional to the intensity of the exercise, little is known about how this integration occurs. The purpose of the present study was to examine the role of medullary sites in the integration of exercise drives to the cardiovascular and respiratory systems. The responses of neurons in the ventrolateral medulla and the lateral tegmental fields to contraction of hindlimb muscles (elicited by stimulation of the L7 S1 ventral roots) and to activation of simulated central command (caudal hypothalamic stimulation) were examined in anaesthetized cats. Muscular contraction evoked an increase in discharge frequency in 59% (24/41) of the medullary neurons; 58% (14/24) of these neurons excited by muscular contraction displayed an immediate increase and 42% (10/24) had a more delayed increase in discharge frequency. Eighty-three per cent (10/12) of neurons rapidly excited by hindlimb muscle contraction were inhibited by hypothalamic stimulation. In contrast, most neurons which showed a delayed increase in discharge frequency during muscle contraction were either excited by hypothalamic stimulation (5/10) or unaffected (4/10). The majority of medullary neurons studied possessed a basal discharge related to the cardiovascular, respiratory and/or sympathetic cycles. These findings demonstrate that both feedback from contracting muscles and descending central command impinge upon individual medullary neurons. This is consistent with the idea that medullary neurons are important in integrating both the central drive and peripheral reflexes controlling the cardiorespiratory responses to exercise.

Identification of CO2Chemoreceptors inHelix pomatia

SYNOPSIS. Gas exchange in pulmonate snails of the family Helicidae occurs through a highly vascularized diffusion lung known as the mantle. The extent of ventilation of the mantle depends upon the duration and size of opening of an occlusible pore known as the pneumostome. In Helix aspersa and Helix pomatia , pneumostomal size and frequency of opening are exquisitely sensitive to CO2. Respiratory CO2 chemosensitivity resides in a discrete region of the subesophageal ganglia. The discharge pattern of many neurons in the chemoreceptor area changes during stimulation with CO2. However, the electrophysiological response to CO, stimulation alone does not discriminate between CO2 chemoreceptor cells and CO2-insensitive neurons active in the pneumostomal response to CO2. We identified a subset of CO2-sensitive neurons from the larger population of neurons active during CO2 stimulation. The action potential discharge frequency of CO2 chemosensory neurons increased in response to CO2 stimulation. An increased discharge frequency of CO2-sensitive neurons was associated with increased pneumostomal opening, and both the size and the frequency of pneumostomal opening increased during CO2 stimulation. Injecting depolarizing current into individual chemosensory neurons elicited opening of the pneumostome in the absence of CO2. Action potential generation in response to CO2 was independent of synaptic transmission. Removal of individual CO2-sensitive cells or inhibition of action potential generation in CO2-sensitive cells reduced or eliminated pneumostomal responses to CO2. CO2 sensitivity in chemoreceptor cells required extracellular calcium, but not sodium. Substituting barium for calcium supported chemoreceptor activity. In summary, we have identified respiratory related, chemosensory neurons that are CO2 sensitive in the absence of synaptic input.

Gastric and Brain Stem Effects of Substance P on Nucleus Tractus Solitarius Unitary Responses

Yuan, C.-S. and T. K. Lowell. Gastric and brain stem effects of substance P on nucleus tractus solitarius unitary responses. Peptides 18(8) 1169–1173, 1997.—Subdiaphragmatic vagally evoked unitary responses were recorded in the medial subnucleus of the nucleus tractus solitarius in an in vitro neonatal rat brain stem–gastric preparation. Substance P was applied to the gastric compartment and/or the brain stem compartment of the bath chamber to evaluate the peripheral gastric and central brain stem effects of the peptide on the nucleus tractus solitarius unitary activity. After substance P application to the gastric or brain stem compartment, a concentration-related change in the nucleus tractus solitarius unitary activity was observed. The gastric effects of substance P, at a concentration of 30 nM (minimum concentration for maximum effect), produced a 31 ± 6.5% (mean ± SD) increase in neuronal discharge frequency compared to the control recording. Both the proximal and the distal stomach were important in the gastric effect of the peptide on subdiaphragmatic vagally evoked nucleus tractus solitarius unitary responses. The brain stem effects of substance P, at a concentration of 10 nM (minimum concentration for maximum effect), induced a 52 ± 11.3% increase in discharge frequency. Application of the peptide into both the gastric and brain stem compartments resulted in a subadditive response of 73 ± 5.9%. This suggests that, peripherally and centrally, there are two different mechanisms of substance P activation. Our results suggest that substance P may play a role in regulating the ingestive process in neonates.

Phrenic motoneuron discharge during sustained inspiratory resistive loading.

I determined whether prolonged inspiratory resistive loading (IRL) affects phrenic motoneuron discharge, independent of changes in chemical drive. In seven decerebrate spontaneously breathing cats, the discharge patterns of eight phrenic motoneurons from filaments of one phrenic nerve were monitored, along with the global activity of the contralateral phrenic nerve, transdiaphragmatic pressure, and fractional end-tidal CO2 levels. Discharge patterns during hyperoxic CO2 rebreathing and breathing against an IRL (2,500-4,000 cmH2O.1-1.s) were compared. During IRL, transdiaphragmatic pressure increased and then either plateaued or decreased. At the highest fractional end-tidal CO2 common to both runs, instantaneous discharge frequencies in six motoneurons were greater during sustained IRL than during rebreathing, when compared at the same time after the onset of inspiration. These increased discharge frequencies suggest the presence of a load-induced nonchemical drive to phrenic motoneurons from unidentified source(s).

Effects of glutamate application on the rhythm of low magnesium-induced epileptiform activity in hippocampal slices of guinea-pigs.

The extracellular concentration of glutamate has previously been reported to increase to more than 10-fold the basal level during seizure activity. In the present study, we tested whether localized increases in extracellular glutamate concentration influence the rhythm of epileptiform discharges in the low-magnesium epilepsy model. In hippocampal slices of guinea-pigs, epileptiform activity was induced by omission of magnesium from the bath fluid. Glutamate and its subreceptor agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were ejected into different strata of the CA3 and CA1 regions using microiontophoretic and micropressure application. Glutamate, NMDA and AMPA applied to the CA3 region, but not to the CA1 region, induced a short-lasting increase in epileptiform discharge frequency, often followed by a transient reduction. The effect was most pronounced with application into the stratum lacunosum-moleculare of the CA3 region and could only be evoked in slices exceeding 400 microns in thickness. The effects on the rhythm of epileptiform discharges induced by NMDA and AMPA were blocked by their specific receptor antagonists. They were not influenced by application of GABAA and GABAB receptor antagonists. Changes in somatic membrane potential of CA3 pyramidal neurons did not correlate with changes in the rhythm of epileptiform discharges elicited in this region. The transient suppression of epileptiform discharges that followed the increase in discharge frequency was abolished by an adenosine A1 receptor antagonist. We propose that localized increases in extracellular glutamate concentration modify the rhythm of epileptiform discharges due to changes in neuronal network activity.

In vitro responses of VLM neurons to hypoxia after normobaric hypoxic acclimatization

Hypoxic acclimatization involves an initial rapid ventilatory response followed by a more gradual increase in ventilation over a period of 24 to 48 h in both humans and rats. In addition, the acute ventilatory response to hypoxia is accentuated following hypoxic acclimatization. The purpose of the present investigation was to determine if hypoxic acclimatization augments the acute hypoxic response of neurons in the ventrolateral medulla (VLM). Brain slices (400 μm) containing the ventrolateral medulla were prepared from Sprague-Dawley rats acclimatized to hypoxia (10% O 2) for 4–5 days ( n = 4) and 9–10 days ( n = 4) and from rats maintained in a normoxic environment ( n = 4). Extracellular recordings demonstrated that there were no significant differences in the basal pattern or discharge rate of VLM neurons from animals exposed to short (10.8 ± 0.9 Hz, n = 51), or long (10.1 ± 1.1 Hz, n = 59) periods of hypoxia compared to control neurons (10.8 ± 1.1 Hz, n = 52). The proportion of neurons stimulated (∼70%), inhibited (∼20%) and unaffected (∼10%) by an acute bout of hypoxia (10% O 2) was also similar among groups. However, acute hypoxia elicited a greater increase in discharge frequency in neurons from rats exposed to the short period of hypoxia compared to the responses from neurons in the control and longer acclimatization groups. Thus, the responsivity of VLM neurons during the early stages of hypoxic acclimatization is altered in a manner consistent with the respiratory responses associated with acclimatization.

ATP-sensitive K+ channels are functional in expiratory neurones of normoxic cats.

1. We analysed spontaneously active expiratory neurones (n = 48) of anaesthetized cats for the presence of ATP-sensitive K+ (KATP) channels. 2. Intracellular injection of ATP reversibly depolarized neurones during all phases of the respiratory cycle. During expiration, membrane potential depolarized by an average of 1.5 +/- 0.1 mV leading to a 25% increase of discharge frequency. During inspiration, ATP induced a 1.8 +/- 0.2 mV depolarization, which was accompanied by a maximum of 20% increase of input resistance (Rn). 3. Extracellular application of diazoxide, an agonist of KATP channels, resulted in reversible membrane hyperpolarization in 68% of neurones (n = 19). This hyperpolarization (2.5 mV during expiration and 3.1 mV during inspiration) was accompanied by a 22% decrease in Rn. 4. Extracellular application of tolbutamide and glibenclamide, two antagonists of KATP channels, evoked reversible depolarizations in 76% of neurones (n = 21). The depolarization was relatively constant throughout the respiratory cycle (1.4 mV during expiration and 2.3 mV during inspiration). Rn increased by 22%. 5. The same sulphonylureas also changed the steepness of membrane depolarization when neurones escaped spontaneous synaptic inhibition during postinspiration. Extracellularly applied tolbutamide and glibenclamide increased the steepness of depolarization by 21%, while diazoxide reduced it by 20%. 6. Antagonism of drugs was verified by simultaneous extra- and intracellular application of diazoxide and glibenclamide, respectively. 7. During voltage clamp at holding potential at -60 to -67 mV, intracellular or extracellular application of tolbutamide and glibenclamide blocked a persistent outward current. 8. We conclude that KATP channels are functional in expiratory neurones of adult cats and contribute to the control of excitability even during normoxia.

Role of the motor cortex in the control of visually triggered gait modifications

One important aspect of locomotor control is the ability of an animal to make anticipatory gait modifications to avoid obstacles, by stepping either around them or over them. This paper reviews some of the evidence that suggests that the motor cortex is one of the principal structures involved in the control of such anticipatory gait modifications in cats, in particular when they are triggered by a visual signal. Evidence for this statement is provided both from experiments in which the motor cortex has been lesioned or inactivated and from studies in which the activity of motor cortical neurones has been recorded during locomotor tasks in which visual information is required to ensure the correct positioning of the paw or an appropriate modification of the limb trajectory. Inactivation of small regions of the motor cortex with the GABA agonist muscimol results in changes in the limb trajectory so that cats hit an obstacle instead of stepping over it as they do normally. A similar disruption of the hindlimb trajectory is seen following lesions of the spinal cord at T13 that interrupt the corticospinal tract. The results from cell recording studies are complementary in that they show that the activity of many identified pyramidal tract neurones increases when the cat is required to modify the forelimb or hindlimb trajectory to step over obstacles. We suggest that the major function of this increased discharge frequency is to regulate the amplitude, duration, and temporal pattern of muscle activity during the gait modification to ensure an appropriate modification of limb trajectory. We further suggest that different groups of pyramidal tract neurones are involved in regulating the activity of groups of synergistic muscles active at different times in the gait modification. For example, some groups of pyramidal tract neurones would be involved in ensuring the appropriate and sequential activation of the muscle groups involved in the initial flexion of the elbow, while others would be active prior to the repositioning of the paw on the support surface. We discuss the possibility that the motor cortical activity seen during locomotion is the sum result of a feedforward signal, which provides visuospatial information about the environment, and feedback activity, which signals, in part, the state of the interneuronal pattern generating networks in the spinal cord. The way in which the resulting descending command may interact with the basic locomotor rhythm to produce the gait modifications is discussed.

Inhibitions mediated by glycine and GABA A receptors shape the discharge pattern of bulbar respiratory neurons

Experiments were performed to identify the glycinergic or GABAergic nature, and the timing of discharge, of the neurons which produce chloride-dependent inhibitions on other bulbar respiratory neurons (RNs) during their silent and active phases. RNs recorded extracellularly in pentobarbital-anesthetized or decerebrate cats, were subjected to iontophoretic applications of glutamate, of the glycine antagonist strychnine, and of the GABA A receptor antagonist bicuculline. Both antagonists induced discharge or increased discharge frequency in restricted parts of the respiratory cycle without affecting the discharge frequency in other parts of the cycle. Strychnine most often elicited activity in late-inspiration and early-expiration, but also in early inspiration and in late expiration. Bicuculline was most often effective throughout the entire discharge period of each neuron with no effect during the silent period, although it also acted selectively during late-inspiration in inspiratory neurons, an effect attributed to GABA A receptor blockade. The convergence of glycinergic afferent inputs during late inspiration and early expiration suggests that glycinergic neurons may play an important role in the inspiratory to expiratory phase transition.

Ventrolateral medullary neurons show age-dependent depolarizations to hypoxia in vitro

Central mechanisms are likely responsible for the larger respiratory activation in response to hypoxia in the adult compared to the neonatal animal. One possible site for this effect is in the ventrolateral medulla, an area known to be involved in the cardiorespiratory responses to hypoxia. Neurons in this area are stimulated by hypoxia both in vivo and in vitro. The purpose of the present study was to determine if changes in the magnitude of this excitatory response occur during early postnatal development. Whole-cell patch recordings were made from neurons in the ventrolateral medulla (VLM) in a 400-μm brain slice preparation. The basal properties and responses to a brief (90 s) hypoxic stimulus (5% CO 2/95% N 2) were compared between neurons from neonatal ( P < 16) and juvenile (P16–38) rats. An excitation consisting of a depolarization, increase in spike frequency and decrease in input resistance was observed during hypoxia in eighty-three percent of juvenile but in only 58% of the neonatal VLM neurons. Moreover, the magnitude of this response was greater in the juvenile (8.2 ± 1.3 mV) than in the neonatal (4.8 ± 0.5 mV) neurons. A second type of depolarizing response, consisting of a more pronounced depolarization interrupted by a brief hyperpolarization that returned to a depolarized state and not associated with an increased discharge frequency, occurred in only 3% of the neurons from the juvenile animals compared to 18% of those from neonatal rats. The remaining proportion of the VLM neurons studied were hyperpolarized or were unaffected by hypoxia. Measurements of tissue pO 2 indicate that none of the above differences are due to variations in the hypoxic stimulus between neonatal and adult slices. The results of this study suggest that the hypoxic-induced depolarizations observed in VLM neurons change during development. These developmental changes may contribute to the changes that occur in cardiorespiratory responses to acute systemic hypoxia during early development.

Functional properties of single neurons in the primate face primary somatosensory cortex. II. Relations with different directions of trained tongue protrusion

1. In previous papers we have presented evidence suggesting an important role for the face primary somatosensory cortex (SI) in the fine control of tongue movements. These findings, plus our earlier evidence that many neurons in face motor cortex (MI) may exhibit firing rates related to the direction of tongue protrusion, led us to test the hypothesis that variations in the direction of a tongue-protrusion movement would be associated with variations in the activity of different face SI neurons. 2. Two monkeys were trained to perform a tongue-protrusion task in each of three directions: the task transducer was positioned at 0 degrees, 30 degrees to the left, or 30 degrees to the right from the midsagittal plane. The latter two positions were termed asymmetrical tongue-protrusion task positions. Single-neuron activity was recorded from face SI during trials of the tongue-protrusion task at each of two or three of the above positions. In addition, the mechanoreceptive field (RF) was delineated for each neuron. 3. Directional relations were found in 25 (58%) of the 43 neurons studied; this included 20 neurons showing a significant direction-by-time interaction in firing rate, i.e., the change of firing rate from the pretrial period to the task period was significantly different between different directions, and 5 showing no direction-by-time interaction but a significant difference in firing rate between different directions of the tongue-protrusion task. 4. Of the 43 neurons investigated, 21 and 20 had a RF on the tongue and lips, respectively ("tongue RF" and "lip RF" neurons), and the remaining 2 received mechanosensitive afferent inputs from other orofacial regions. There was no significant difference in the incidence of directional sensitivity between the neurons with a tongue RF and those with a lip RF (12/21 and 11/20, respectively). 5. Eight of the 25 "directional" neurons were located in area 3b and 17 in area 1. There was no significant difference in the proportion of directional neurons between areas 3b and 1. 6. The increase in discharge frequency at the preferred direction was, on the average for the 25 directional neurons, 39% over the mean discharge frequency observed during the task period for all directions of the tongue-protrusion task. Eight directional neurons showed a significant increase in firing rate during the tongue-protrusion task up to 130 ms before the onset of genioglossus electromyographic activity.(ABSTRACT TRUNCATED AT 400 WORDS)