Biomedical subjects

E Garcia-Rill

Publications and source records attributed to E Garcia-Rill.

At least 19 recordsLinked to original sources

PubMed2006

Alpha-2 adrenergic regulation of pedunculopontine nucleus neurons during development.

Rapid eye movement sleep decreases between 10 and 30 days postnatally in the rat. The pedunculopontine nucleus is known to modulate waking and rapid eye movement sleep, and pedunculopontine nucleus neurons are thought to be hyperpolarized by noradrenergic input from the locus coeruleus. The goal of the study was to investigate the possibility that a change in alpha-2 adrenergic inhibition of pedunculopontine nucleus cells during this period could explain at least part of the developmental decrease in rapid eye movement sleep. We, therefore, recorded intracellularly in 12-21 day rat brainstem slices maintained in oxygenated artificial cerebrospinal fluid. Putative cholinergic vs. non-cholinergic pedunculopontine nucleus neurons were identified using nicotinamide adenine dinucleotide phosphate diaphorase histochemistry and intracellular injection of neurobiotin (Texas Red immunocytochemistry). Pedunculopontine nucleus neurons also were identified by intrinsic membrane properties, type I (low threshold spike), type II (A) and type III (A+low threshold spike), as previously described. Clonidine (20 microM) hyperpolarized most cholinergic and non-cholinergic pedunculopontine nucleus cells. This hyperpolarization decreased significantly in amplitude (mean+/-S.E.) from -6.8+/-1.0 mV at 12-13 days, to -3.0+/-0.7 mV at 20-21 days. However, much of these early effects (12-15 days) were indirect such that direct effects (tested following sodium channel blockade with tetrodotoxin (0.3 microM)) resulted in hyperpolarization averaging -3.4+/-0.5 mV, similar to that evident at 16-21 days. Non-cholinergic cells were less hyperpolarized than cholinergic cells at 12-13 days (-1.6+/-0.3 mV), but equally hyperpolarized at 20-21 days (-3.3+/-1.3 mV). In those cells tested, hyperpolarization was blocked by yohimbine, an alpha-2 adrenergic receptor antagonist (1.5 microM). These results suggest that the alpha-2 adrenergic receptor on cholinergic pedunculopontine nucleus neurons activated by clonidine may play only a modest role, if any, in the developmental decrease in rapid eye movement sleep. Clonidine blocked or reduced the hyperpolarization-activated inward cation conductance, so that its effects on the firing rate of a specific population of pedunculopontine nucleus neurons could be significant. In conclusion, the alpha-2 adrenergic input to pedunculopontine nucleus neurons appears to consistently modulate the firing rate of cholinergic and non-cholinergic pedunculopontine nucleus neurons, with important effects on the regulation of sleep-wake states.

Acetylcholine↗

PubMed2006

Prenatal exposure to cigarette smoke affects the physiology of pedunculopontine nucleus (PPN) neurons in development.

Prenatal exposure to cigarette smoke is known to produce lasting arousal, attentional and cognitive deficits in humans. The pedunculopontine nucleus (PPN), as the cholinergic arm of the reticular activating system (RAS), is known to modulate arousal, waking and rapid eye movement (REM) sleep. REM sleep decreases between 10 and 30 days postnatally in the rat, especially at 12-21 days. Pregnant dams were exposed to 350 ml of cigarette smoke for 15 min, 3 times per day, from day E14 until birth, and the pups allowed to mature. Intracellularly recorded PPN neurons in 12-21 day rat brainstem slices were tested for intrinsic membrane properties, including the hyperpolarization-activated cation current Ih, which is known to drive oscillatory activity. Type II (A-current) PPN cells from 12-16 day old offspring of treated animals had a 1/2max Ih amplitude of (mean +/- SE) 4.1 +/- 0.9 mV, while 17-21 day cells had a higher 1/2max Ih of 9.9 +/- 1.1 mV (p < 0.0001). Cells from 12-16 day old control brainstems had a 1/2max Ih of 1.3 +/- 0.1 mV, which was lower (p < 0.05) than in cells from prenatally treated offspring; while 17-21 day old cells from controls had a 1/2max Ih of 3.3 +/- 0.3 mV, which was also lower (p < 0.01) than in cells from prenatally treated offspring. In addition, changes in resting membrane potential [control -65. +/- 0.9 mV (n=32); exposed -55.0 +/- 1.4 mV (n = 27) (p < 0.0001)], and action potential (AP) threshold [control -56.5 +/- 0.7 mV (n = 32), exposed -47.0 +/- 1.4 mV (n = 27) (p < 0.0001)], suggest that prenatal exposure to cigarette smoke induced marked changes in cells in the cholinergic arm of the RAS, rendering them more excitable. Such data could partially explain the differences seen in individuals whose parents smoked during pregnancy, especially in terms of their hypervigilance and increased propensity for attentional deficits and cognitive/behavioral disorders.

Animals↗

PubMed2006

Restoration of frequency-dependent depression of the H-reflex by passive exercise in spinal rats.

STUDY DESIGN: Hyper-reflexia, measured as a decrease of low frequency-dependent depression of the H-reflex, is known to occur in both humans and animals after spinal cord injury (SCI). Previous studies have shown that passive exercise for 3 months could be used to restore low frequency-dependent depression of the H-reflex after SCI. OBJECTIVE: To determine the effects of various periods of time on the ability of passive exercise to restore low frequency-dependent depression of the H-reflex. SETTING: Spinal Cord Injury Mobilization Program of the Center for Translational Neuroscience, the research arm of the Jackson T Stephens Spine and Neuroscience Institute, Little Rock, AR, USA. METHODS: Adult rats underwent complete spinal cord transection at the T10 level. The hindlimbs were passively exercised in different groups of rats for 1 h/day, 5 days/week for 15, 30, 45, 60, or 90 days, and low frequency-dependent depression of the H-reflex was tested. RESULTS: Statistically significant low frequency-dependent depression of the H-reflex was evident by 30 days of exercise, although numerical reductions were seen even at 15 days. There was a linear decrease in low frequency-dependent depression of the H-reflex with duration of passive exercise. CONCLUSIONS: Passive exercise can restore frequency-dependent depression of spinal reflexes in a time-dependent manner if used following complete spinal transection.

Animals↗

PubMed2005

Induction of long-lasting depolarization in medioventral medulla neurons by cholinergic input from the pedunculopontine nucleus.

Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states by activation of such descending targets as the caudal pons and the medioventral medulla (MED). Previously, PPN stimulation was reported to induce prolonged responses (PRs) in intracellularly recorded caudal pontine neurons in vitro. The present study used intracellular recordings in semihorizontal slices from rat brain stem (postnatal days 12-21) to determine responses in MED neurons following PPN stimulation. One-half (40/81) of MED neurons showed PRs after PPN stimulation. MED neurons with PRs had shorter duration action potential, longer duration afterhyperpolarization, and higher amplitude afterhyperpolarization than non-PR MED neurons. PR MED neurons were significantly larger (568 +/- 44 microm2) than non-PR MED neurons (387 +/- 32 microm2). The longest mean duration PRs and maximal firing rates during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. The muscarinic cholinergic agonist carbachol induced depolarization in all PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked carbachol- and PPN stimulation-induced PRs in all MED neurons tested. These findings suggest that PPN stimulation-induced PRs may be due to activation of muscarinic receptor-sensitive channels, allowing MED neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs in large MED neurons using parameters known best to induce locomotion.

Animals↗

PubMed2005

Nicotine suppresses the P13 auditory evoked potential by acting on the pedunculopontine nucleus in the rat.

We identified a potential novel site of action for nicotine (NIC) since (a) systemic injection of NIC led to a dose-dependent decrease in the amplitude of the sleep state-dependent, vertex-recorded, P13 midlatency auditory evoked potential (generated by the reticular activating system, RAS), (b) localized injections of a nicotinic receptor antagonist into the pedunculopontine nucleus (PPN, the cholinergic arm of the RAS) blocked the effects of systemic NIC on the P13 potential (a measure of level of arousal), and (c) localized injection of a nicotinic receptor agonist into the PPN also led to a decrease in the amplitude of the P13 potential, an effect blocked by PPN injection of a nicotinic receptor antagonist. There were minor changes in the manifestation of the startle response (SR) at the concentrations used; however, NIC did decrease the hippocampal N40 potential, although its effects were not affected by antagonist or agonist injections into the PPN. These results suggest a potential mechanism underlying the anxiolytic effects of NIC-suppression of the cholinergic arm of the RAS.

Acoustic Stimulation↗

PubMed2004

The P50 midlatency auditory evoked potential in patients with chronic low back pain (CLBP).

OBJECTIVE: Patients with Chronic Low Back Pain (CLBP) show arousal, attentional and cognitive disturbances. The sleep state-dependent P50 midlatency auditory evoked potential was used to determine if patients with CLBP [with and without co-morbid depression (DEP)] show quantitative disturbances in the manifestation of the P50 potential. METHODS: P50 potential latency, amplitude and habituation to repetitive stimuli at 250, 500 and 1000ms interstimulus intervals (ISIs) was recorded, along with the McGill Pain Questionnaire-Short Form (MPQ-SF). CLBP subjects (n=42) were compared with Controls (n=43), and with subjects with DEP only (n=6). Of the CLBP subjects, 20/42 had clinical depression (CLBP+DEP); 8/20 were taking anti-depressant medication (CLBP+DEP+med), the others were not (CLBP+DEP-med). RESULTS: There were no differences (ANOVA) in age, sex or P50 potential latency, although there was a trend towards increased latencies in CLBP groups. P50 potential amplitude was lower in CLBP groups, but not in sub-groups, again indicating a trend. P50 potential habituation was decreased in the DEP only subjects at the 250m ISI, and decreased in CLBP+DEP-med subjects at the 500ms ISI. This difference was not present in CLBP+DEP+med subjects. The MPQ-SF revealed that patients with CLBP and CLBP+DEP-med showed lower pain scores than CLBP+DEP+med patients. CONCLUSIONS: There is decreased habituation of the P50 potential habituation in unmedicated patients with CLBP+DEP compared to Controls. SIGNIFICANCE: Patients with CLBP+DEP-med may be less able to disregard incoming sensory information, including painful sensations, but anti-depressant medications help correct this deficit. However, their perception of pain may be increased by medication.

Acoustic Stimulation↗

PubMed2004

Developmental changes in pedunculopontine nucleus (PPN) neurons.

The developmental decrease in rapid-eye-movement (REM) sleep in man occurs between birth and after puberty. We hypothesize that if this decrease in REM sleep does not occur, lifelong increases in REM sleep drive may ensue. Such disorders are characterized by hypervigilance and sensory-gating deficits, such as are present in postpubertal onset disorders like schizophrenia, panic attacks (a form of anxiety disorder), and depression. The decrease in REM sleep in the rat occurs between 10 and 30 days of age. We studied changes in size and physiological properties of pedunculopontine nucleus (PPN) cells involved in the control of arousal, i.e., waking and REM sleep. During the largest decrease in REM sleep (12-21 days), cholinergic PPN neurons doubled in cell area, the hypertrophy peaking at 15-16 days, then decreasing in area by 20-21 days. Noncholinergic PPN cells did not change in area during this period. We confirmed the presence of two populations of PPN neurons based on action potential (AP) duration, with the proportion of short-AP-duration cells increasing and long AP duration decreasing between 12 and 21 days. Most cholinergic and noncholinergic cells had short AP durations. Afterhyperpolarization (AHP) duration became segregated into long and short AHP duration after 15 days. Cells with short AP duration also had short AHP duration. The proportion of PPN cells with Ih current increased gradually, peaking at 15 days, then decreased by 21 days. These changes in morphological and physiological properties are discussed in relation to the developmental decrease in REM sleep.

Action Potentials↗

PubMed2004

The feline fictive startle response and its related potential in the pedunculopontine nucleus.

The human P1/P50 midlatency auditory evoked potential and the auditory startle response (SR) have been used for investigating sensory gating and sensorimotor modulation which is impaired in various psychiatric diseases. In the present study, we demonstrated that auditory stimulation was capable of eliciting excitation of flexor and extensor neurograms from the hindlimb nerves in the paralyzed decerebrate cat, a phenomenon which corresponds to a "fictive" startle response (FSR). Previous studies have shown that the SR consists of distinct excitatory components, "early" and "late", separated by an inhibitory phase. However, in the FSR, unlike the SR in the intact preparation, the "late" excitatory phase never occurred. Recordings from the pedunculopontine nucleus (PPN) simultaneously with the FSR revealed the presence of an auditory evoked potential at a 20-25 ms latency, presumably the depth-recorded equivalent of the vertex-recorded wave A, which has been shown to be the feline equivalent of the human P1 potential. The depth-recorded wave A appeared to share neurological substrates with the excitatory phase of the FSR, since both responses were facilitated in a similar manner by increasing stimulus duration. We previously reported that, in the intact rat, the vertex-recorded P13 potential, the putative rodent equivalent of the human P1 potential, is generated, at least in part, by outputs of the PPN, and that the P13 potential shares neurological substrates with the "early" excitatory phase of the SR. Taken together, the results of the present study indicate that, along with the SR and the P13 potential in the intact rat, the FSR and the depth-recorded wave A in the paralyzed cat may be unique animal models for further examining, in the absence of neural structures rostral to the precollicular decerebration, the cellular basis of startle behavior.

Acoustic Stimulation↗

PubMed2003

Development of REM sleep drive and clinical implications.

Rapid eye movement (REM) sleep in the human declines from approximately 50% of total sleep time ( approximately 8 h) in the newborn to approximately 15% of total sleep time (approximately 1 h) in the adult, and this decrease takes place mainly between birth and the end of puberty. We hypothesize that without this developmental decrease in REM sleep drive, lifelong increases in REM sleep drive may ensue. In the rat, the developmental decrease in REM sleep occurs 10-30 days after birth, declining from >70% of total sleep time in the newborn to the adult level of approximately 15% of sleep time during this period. Rats at 12-21 days of age were anesthetized with ketamine and decapitated, and brain stem slices were cut for intracellular recordings. We found that excitatory responses of pedunculopontine nucleus (PPN) neurons to N-methyl-D-aspartic acid decrease, while responses to kainic acid increase, over this critical period. During this developmental period, inhibitory responses to serotonergic type 1 agonists increase but responses to serotonergic type 2 agonists do not change. The results suggest that as PPN neurons develop, they are increasingly activated by kainic acid and increasingly inhibited by serotonergic type 1 receptors. These processes may be related to the developmental decrease in REM sleep. Developmental disturbances in each of these systems could induce differential increases in REM sleep drive, accounting for the postpubertal onset of a number of different disorders manifesting increases in REM sleep drive. Examination of modulation by PPN projections to ascending and descending targets revealed the presence of common signals modulating ascending arousal-related functions and descending postural/locomotor-related functions.

Action Potentials↗

PubMed2002

Effects of pedunculopontine nucleus (PPN) stimulation on caudal pontine reticular formation (PnC) neurons in vitro.

Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states. Previously, PPN stimulation was reported to induce prolonged responses (PRs) in extracellularly recorded PnC neurons in the decerebrate cat. The present study used intracellular recordings in semihorizontal slices from rat brain stem (postnatal days 12-21) to determine responses in PnC neurons following PPN stimulation. Two-thirds (65%) of PnC neurons showed PRs after PPN stimulation. PnC neurons with PRs had higher amplitude afterhyperpolarizations (AHP) than non-PR (NPR) neurons. Both PR and NPR neurons were of mixed cell types characterized by "A" and/or "LTS," or neither of these types of currents. PnC cells showed decreased AHP duration with age, due mostly to decreased AHP duration in NPR cells. The longest mean duration PRs were induced by stimulation at 60 and 90 Hz compared with 10 or 30 Hz. Maximal firing rates in PnC cells during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. BaCl2 superfusion blocked PPN stimulation-induced PRs, suggesting that PRs may be mediated by blockade of potassium channels, in keeping with increased input resistance observed during PRs. Depolarizing pulses failed to elicit, and hyperpolarizing pulses failed to reset, PPN stimulation-induced PRs, suggesting that PRs may not be plateau potentials. Pharmacological testing revealed that nifedipine superfusion failed to block PPN stimulation-induced PRs; i.e., PRs may not be calcium channel-dependent. The muscarinic cholinergic agonist carbachol induced depolarization in most PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked PPN stimulation-induced PRs in some PnC neurons, suggesting that some PRs may be due to muscarinic receptor activation. The nonspecific ionotropic glutamate receptor antagonist kynurenic acid failed to block PPN stimulation-induced PRs, as did the metabotropic glutamate receptor antagonist (R, S)-alphamethyl-4-carboxyphenylglycine, suggesting that PRs may not be mediated by glutamate receptors. These findings suggest that PPN stimulation-induced PRs may be due to increased excitability following closing of muscarinic receptor-sensitive potassium channels, allowing PnC neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs using parameters known best to induce locomotion. This mechanism may be related to switching from one state to another (e.g., locomotion vs. standing or sitting, waking vs. non-REM sleep or REM sleep).

Action Potentials↗

PubMed2001

Pedunculopontine stimulation induces prolonged activation of pontine reticular neurons.

Extracellular and intracellular recordings were carried out from neurons in the region of the pontine reticular formation at the transition between the nucleus reticularis pontis oralis and caudalis, and in the pontis caudalis. Responses were studied after stimulation of the mesopontine cholinergic pedunculopontine nucleus in precollicular-postmammillary transected, paralyzed preparations. Recordings of neurographic activity in hindlimb flexor and extensor nerves served to detect changes in fictive locomotion and muscle tone induced by pedunculopontine nucleus stimulation or occurring spontaneously. Short duration trains of pedunculopontine nucleus stimulation induced long lasting responses, on average over 12s in duration, in one-third of pontine reticular neurons. These prolonged responses were stimulation frequency-dependent such that the longest durations were induced by stimulation at 20-60Hz. In some cells, stimulation at lower (10Hz) or higher (100Hz) frequencies induced responses of shorter duration or were absent, while in others, higher frequencies prolonged the excitatory effects of pedunculopontine nucleus stimulation. We conclude that these stimulation frequency-dependent effects may be related to the modulation of postural muscle tone and locomotion by the pedunculopontine nucleus.

Action Potentials↗

PubMed2000

Cholinergic modulation of the sleep state-dependent P13 midlatency auditory evoked potential in the rat.

Injections into the pedunculopontine nucleus (PPN) of the cholinergic receptor agonist, carbachol (CAR), were found to reduce the amplitude of the vertex-recorded, sleep state-dependent P13 midlatency evoked potential in a dose- and time-dependent manner. This effect was blocked or reduced by pretreatment with the muscarinic receptor antagonist, scopolamine, injected into the PPN.

Acetylcholine↗

PubMed2000

Serotonergic modulation of the P13 midlatency auditory evoked potential in the rat.

The vertex-recorded, sleep state-dependent P13 midlatency auditory evoked potential in the rat may be generated, in part, by pedunculopontine nucleus (PPN) projections. Injections into the PPN of the 5-HT(1A) serotonin receptor agonist, 8-hydroxy-2-di-n-propylaminotetralin hydrobromide (DPAT), were found to reduce the amplitude of the P13 potential in a dose- and time-dependent manner. The suppressive effect of DPAT was blocked or reduced by pretreatment with the 5-HT(1A) serotonin receptor antagonist, Pindobind. These results show that the P13 potential can be modulated by known inhibitory serotonergic inputs to the PPN.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2000

Locus coeruleus involvement in the effects of immobilization stress on the p13 midlatency auditory evoked potential in the rat.

1. Adult male rats were prepared for recording midlatency auditory evoked responses from the vertex (Vx, P13 potential) and auditory cortex (ACx, P7 potential). 2. The P13 potential is the rodent equivalent of the human P1 or P50 potential, which exhibits decreased sensory gating in posttraumatic stress disorder. 3. Immobilization (IMB) stress for 60 min led to a significant decrease in P13 potential amplitude and sensory gating of the potential for the first 30-40 min of IMB. 4. The effects of IMB on the P13 potential were reduced by pre-treatment with the alpha-2 adrenergic receptor blocker yohimbine (YOH). 5. Injections of corticotropin releasing factor (CRF) into the locus coeruleus (LC), but not injections dorsal or ventral to the LC, induced a dose-dependent decrease in P13 potential amplitude and sensory gating. 6. The effects of CRF were blocked by cotreatment with the CRF receptor antagonist alpha-helical CRF (alpha-h CRF). 7. The effects of IMB on the P13 potential were mimicked by injections of the alpha-2 adrenergic receptor agonist dexmedetomidine (DEX) into the pedunculopontine nucleus (PPN). 8. The effects of DEX injections into PPN were reduced by pre-treatment with the alpha-2 adrenergic receptor blocker YOH. 9. The effects of IMB on P13 potential amplitude and sensory gating may be mediated in part via CRF activation of LC, which sends inhibitory alpha-2 adrenergic projections to PPN, a major source of the P13 potential.

Adrenergic alpha-Antagonists↗

PubMed2000

Effect of age on sensory gating of the sleep state-dependent P1/P50 midlatency auditory evoked potential.

The P1/P50 midlatency auditory evoked potential is a sleep state-dependent waveform present during waking and rapid eye movement (REM) sleep and absent during slow-wave sleep. The P50 potential was studied in normal male and female subjects of various ages including post-pubertal adolescents (12-19 yrs), young adults (24-39 yrs), middle-aged adults (40-55 yrs) and older adults (55-78 yrs). There were no statistically significant differences in the mean peak amplitude or mean peak latency of the P50 potential between males and females or between age groups. Using a paired stimulus paradigm, the degree of sensory gating of the P50 potential was tested at three different interstimulus intervals (ISIs), 250, 500 and 1000 msec. There were no statistically significant differences in the sensory gating of the P50 potential between males and females. However, there was a significant decrease in sensory gating of the P50 potential in the adolescent group compared to each of the other age groups at the 250 msec ISI, but not at the 500 or 1000 msec ISI. These results suggest the presence of decreased sensory gating in normal adolescents compared to normal, older age groups.

Adolescent↗

PubMed1999

Sensory gating of the P13 midlatency auditory evoked potential and the startle response in the rat.

The human P1/P50 midlatency auditory evoked potential and the startle response (SR) have been used as measures of sensory and sensorimotor gating, respectively. In the present study, both prepulse and paired stimulus paradigms were used in order to investigate the relationship between sensory gating mechanisms of the P13 potential, the putative rodent equivalent of the P1 potential, and those of the SR. In addition, these were compared to the properties of the N40 potential, another measure of sensory gating. Simultaneous recordings from the vertex (P13 potential and N40 potential) and neck musculature (SR) showed that (1) in a prepulse paradigm, increasing the intensity of the prepulse or decreasing the interstimulus interval resulted in increased inhibition of the P13 potential, N40 potential (to a lesser degree) and the SR (to a greater degree), (2) when using a low signal-to-noise ratio between the prepulse intensity and the background level, prepulse inhibition of the SR was reduced or absent while that of the P13 potential was present, (3) the amplitude of the 'prepulse evoked' P13 potential was significantly correlated with prepulse inhibition of the P13 potential, the N40 potential and the SR, (4) in a paired identical stimulus paradigm, decreasing the interstimulus interval resulted in increased habituation of the P13 potential, N40 potential (to a lesser degree) and the SR, and (5) increasing the intensity of the paired stimulation resulted in increased habituation of the P13 potential and the N40 potential (to a lesser degree), but not of the SR. These results demonstrate the presence of prepulse inhibition of the P13 potential, the N40 potential and the SR in a parallel manner, but show certain specific differences in their responses to parametric changes.

Acoustic Stimulation↗

PubMed1999

Midlatency auditory-evoked potentials in the rat: effects of interventions that modulate arousal.

The vertex-recorded P13 midlatency auditory-evoked potential in the rat shows the same characteristics as the P1 potential in the human, namely, sleep-state dependence, rapid habituation and blockade by the cholinergic antagonist scopolamine. The P13 potential appears to be generated, at least in part, by projections of the pedunculopontine nucleus, the cholinergic arm of the reticular activating system. On the other hand, the auditory cortex-recorded P7 potential appears to be of primary cortical origin. Simultaneous recordings from the vertex and the auditory cortex showed that (1) the P13 potential was suppressed by administration of the anesthetics ketamine, pentobarbital or halothane in a dose-dependent manner, but the P7 potential was not; (2) the P13 potential was suppressed by intragastric injections of ethanol in a dose-dependent manner, but the P7 potential was not; (3) the amplitude of the P13 potential was negatively correlated with blood ethanol levels; (4) both the P13 and P7 potentials were still present following injections of the neuromuscular blocker pancuronium bromide; and (5) both the P13 and P7 potentials were decreased by diffuse brain injury induced by a weight-drop device in a weight-dependent manner. These findings suggest that the P13 potential is more sensitive than the P7 potential to changes in arousal and that the P13 and P7 potentials are not of myogenic but of neural origin.

Anesthetics↗

PubMed1999

Effects of fetal spinal cord tissue transplants and cycling exercise on the soleus muscle in spinalized rats.

Studies were carried out to determine if an intraspinal transplant (Trpl) of fetal spinal cord tissue or hind limb exercise (Ex) affected the changes in myosin heavy chain (MyHC) composition or myofiber size that occur following a complete transection (Tx) of the lower thoracic spinal cord of the adult rat. In one group of animals, transplants were made acutely, whereas in a second group, daily cycling exercise was initiated 5 days after injury, with animals in both groups being sacrificed 90 days after injury. The soleus muscle is normally composed of myofibers expressing either type I (90%) or type IIa (10%) MyHC. Following a spinal transection, expression of type I MyHC isoform decreased (18% of myofibers), type IIa MyHC expression increased (65% of myofibers), and the majority of myofibers (80%) expressed type IIx MyHC. Most myofibers coexpressed multiple MyHC isoforms. Compared with Tx only, with Ex or with Trpl, there was a decrease in the number of myofibers expressing type I or IIa isoforms but little change in expression of IIx MyHC. Myofibers expressing the IIb isoform appeared in several transplant recipients but not after exercise. Transection resulted in atrophy of type I myofibers to approximately 50% of normal size, whereas myofibers were significantly larger after exercise (74% of control) and in Trpl recipients (77% of control). Type IIa myofibers also were significantly larger in Trpl recipients compared with the Tx only group. Overall, the mean myofiber size was significantly greater after exercise and in Trpl recipients compared with myofibers in Tx only animals. Thus, although neither strategy shifted the MyHC profile towards the control, both interventions influenced the extent of atrophy observed after spinalization. These data suggest that palliative strategies can be developed to modulate some of the changes in hind limb muscles that occur following a spinal cord injury.

Animals↗