SEARCH · PubMed Health

Results for “Reticular Formation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

PubMed1981

Serotonergic mediation of descending inhibition from midbrain periaqueductal gray, but not reticular formation, or spinal nociceptive transmission in the cat.

Electrical stimulation in the midbrain periaqueductal gray (PAG) and lateral midbrain reticular formation (LRF) strongly suppresses the responses of spinal dorsal horn neurons to noxious heating of the skin. The possible role of serotonin (5-hydroxytryptamine, 5-HT) was investigated by quantitatively comparing certain parameters of descending inhibition from PAG and LRF in normal cats [14,15] and cats whose central 5-HT levels had been reduced by pretreatment with p-chlorophenylalanine (PCPA, 300 or 500 mg/kg i.p., 72 h prior to acute experiment). Single lumbar dorsal horn neuronal responses to noxious radiant heating of glabrous footpad skin(50 degrees C, 10 sec, 1/3 min) were recorded in normal and PCPA-pretreated cats anesthetized with sodium pentobarbital and N2O. Inhibition of neuronal heat-evoked responses during midbrain stimulation (mean frequency 30 Hz, up to 800 microA current intensity) was expressed as percent of the unit's control response in the absence of midbrain stimulation. Inhibition by PAG stimulation of units from cats pretreated with 300 mg/kg PCPA (mean inhibition at 450 microA to 60% of control in 12 units) was not detectably different from that in control (non-pretreated) cats. However, inhibition by PAG stimulation was significantly weaker in units from cats pretreated with 500 mg/kg PCPA (mean to 83.4% of control in 9 units). In the latter group, mean current threshold for inhibition was higher, and slope of current-intensity plots lower, than in the control and 300 mg/kg PCPA pretreatment groups. In contrast, mean inhibition by LRF stimulation was enhanced in the 300 and 500 mg/kg PCPA treatment groups in a dose-related manner. In normal (non-pretreated) cats, systemic administration of the putative 5-HT antagonist methysergide (0.07--1 mg/kg) reduced or abolished inhibition by PAG stimulation in each of 8 units. Low doses of methysergide had little or no effect on inhibition produced by LRF stimulation in 6 units. The results suggest pharmacologically distinct mechanisms of inhibition produced by stimulation in PAG and LRF.

Animals↗

PubMed1994

Microstimulation of the medullary reticular formation during fictive locomotion.

1. The present study was designed to determine the effects of microstimulation of the medullary reticular formation (MRF) on the locomotor activity of the cat in the absence of phasic afferent feedback from the limbs. To this end, both short (33 ms) and long (200 ms) trains of stimuli (trains of 0.2-ms pulses at 330 Hz, 35 microA) were applied at 43 loci in the MRF (P:6-12 mm; L:0.5-1.5 mm), and in 3 loci in the medial longitudinal fasciculus (P7.5, L < 0.5 mm) during fictive locomotion in the decerebrate and paralyzed cat. The locomotor pattern was monitored by recording the activity of representative flexor and extensor muscle nerves from each of the four limbs. 2. Short trains of stimuli evoked transient excitatory and/or inhibitory responses in extensor and flexor nerves of each limb that were incorporated into the locomotor pattern. In the majority of sites, excitatory responses were obtained in the motor nerves to both flexor and extensor muscles of the fore- and hindlimbs. The exception to this rule was the ipsilateral triceps, in which the predominant response was inhibitory. The amplitude of these responses was dependent on the time of the locomotor cycle at which the stimulus was delivered, and it was always maximum during the period of activity of the respective nerve. 3. The shortest latency response in the nerves to different muscles of the forelimb averaged between 5.6 and 7.3 ms; for the hindlimbs the values were between 6.9 and 9.3 ms. 4. Changing the depth at which the stimulation was applied in any one trajectory usually produced changes only in the amplitude of the evoked responses but occasionally also caused a change in the sign of these responses, especially in the most ventral regions of the MRF. 5. At 72% of the loci (31/43), short trains of stimulation also changed the duration of the activity in the recorded nerves. These changes were often (20/31 loci) sufficiently strong to alter the duration of the overall locomotor cycle. If one considers only the largest changes produced at each locus, stimulation during the period of ipsilateral extensor activity produced an average reduction in the ipsilateral locomotor cycle duration of 12.8 +/- 8.8% (mean +/- SD), whereas stimulation when the ipsilateral flexor nerve was active produced an average increase in locomotor cycle duration of 27.1 +/- 20.8%. 6. Long trains of stimuli produced similar but larger effects than the shorter trains and always reset the locomotor rhythm.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1996

Specific binding of [3H]resiniferatoxin by human and rat preoptic area, locus ceruleus, medial hypothalamus, reticular formation and ventral thalamus membrane preparations.

Specific [3H]resiniferatoxin (RTX) binding detects the vanilloid (capsaicin) receptors and provides a biochemical means for exploring their pharmacology. In the present study we demonstrate specific vanilloid (RTX) binding sites in various brain areas not known to be innervated by primary afferent neurons. Specific high-affinity binding of [3H]RTX could be detected in membrane preparations of the posterior ("hypothalamic") and anterior ("septal") parts of the preoptic area, locus ceruleus, medial hypothalamus, brainstem reticular formation and ventral thalamic nuclei from naive rats. The determined levels of binding at 4 nM [3H]RTX were 23.0 +/- 4.5, 7.1 +/- 1.6, 29.9 +/- 2.3, 23.5 +/- 2.4, 9.9 +/- 2.2 and 8.1 +/- 1.9 fmol/mg, respectively; unfortunately, the high levels of non-specific binding (higher than 80%) in the present experiments made it impossible for us to characterize fully the binding properties of the receptors. However, no detectable specific [3H]RTX binding was present in membranes of brain nuclei from rats pretreated with 300 mg/kg capsaicin, a treatment which causes loss of response to capsaicin. Significant specific [3H]RTX binding was also absent in membrane preparations of the midbrain central gray matter, somatosensory cortex and cerebellum either from naive or capsaicin treated rats. In human brain specific [3H]RTX binding measured at 4 nM [3H]RTX showed a pattern of distribution similar to that in the rat brain. The corresponding levels of specific [3H]RTX binding in the preoptic area, locus ceruleus, medial hypothalamus, reticular formation and ventral thalamus were 44.9 +/- 2.4, 50.6 +/- 3.0, 36.1 +/- 2.9, 9.4 +/- 2.8 and 8.4 +/- 2.4 fmol/mg, respectively. Our findings corroborate previous biological evidence that vanilloid receptors are present in brain as well as in sensory afferent neurons.

Animals↗

PubMed1978

Movement induced in cataleptic rats: differential effects produced by electrical stimulation of the lateral hypothalamus, substantia nigra, and reticular formation.

Haloperidol catalepsy can be countered by electrical stimulation of the lateral hypothalamus (LH) and, to a lesser extent, the reticular formation (RH). Substantia nigra (SN) stimulation proved to be least effective in this regard. Dissociation between behavioral arousal and cortical EEG during stimulation of the RF in cataleptic rats was observed.

Animals↗

PubMed1989

Putative nociceptive modulatory neurons in the dorsolateral pontomesencephalic reticular formation.

The present study was undertaken to confirm the dorsolateral pontomesencephalic reticular formation (an area that includes the nucleus cuneiformis (NCF) and nucleus parabrachialis (NPB)) as a sensitive site for stimulation-produced antinociception and to investigate the possibility that there are cells in this region that show a change in activity that can be correlated with the occurrence of a nocifensive reflex (the tail-flick withdrawal response from noxious heat (TF)). Such cells have been previously demonstrated in the rostral ventromedial medulla (RVM). Extracellular single unit recording studies were made at sites from which it was possible to inhibit the TF with currents of 10 microA or less. Cellular response to 3 TF trials at 5 min intervals, and spontaneous activity over a 10 min period, were monitored for each unit. Of the cells encountered, 17% displayed an increase (on-cells) and 4% a decrease (off-cells) in activity that preceded the TF. The remaining cells were unaffected by the TF (neutral cells). On- and off-cells were found throughout the region from which TF suppression was observed but were most concentrated in the areas of the NCF and NPB. The presence of on- and off-cells in the NCF/NPB region as well as the RVM suggests that the input to RVM from NCF/NPB may be important in descending nociceptive modulation.

Action Potentials↗

PubMed1983

Habituation of the acoustic startle response in rats after lesions in the mesencephalic reticular formation or in the inferior colliculus.

Extensive damage to the mesencephalic reticular formation (MRF) in rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. The MRF lesions did not alter initial startle amplitudes, but the animals with lesions were unable to attain as low a long-term asymptote of habituation as could control animals. Subsequent manipulation of stimulus intensity and interstimulus interval revealed no differences in short-term habituation between the two groups. Large lesions to the inferior colliculus (IC) did not disrupt long-term habituation of the acoustic startle response, but these animals were unable to suppress responding as much as controls to intense stimuli presented rapidly. The deficits in long-term habituation following MRF lesions suggested a disruption of an extrinsic, inhibitory mechanism of habituation. The deficits following IC lesions could be due either to a disruption of a short-term habituation mechanism or to an increase in response sensitization produced by the lesions.

Acoustic Stimulation↗

PubMed1981

[Responses of pericruciate cortex neurons to stimulation of the hypothalamus and reticular formation].

Neurons of the pericruciate cortex revealed a high degree of reactivity to stimulation of posterior hypothalamus (HP) and mesencephalic reticular formation (RF)--94 and 88% resp., and a marked convergence of upward discharges from HP and RF (73.5%) in anesthetized and immobilized cats. Latency and unit responses (2.4--4.0 msec) suggested a monosynaptic input from the two subcortical structures. Out of the corticofugal neurons activated antidromically, 27% were of the "divergent" type with collaterals in both the HP and RF and, therefore, reacting antidromically to stimulation of these structures. A predominance of cortical antidromic responses to stimulation of HP suggested a greater corticofugal influence on hypothalamic rather than on reticular neurons (84% and 42.3% resp.). Mean latency of antidromic reaction of cortico--hypothalamic neurons was 2.4 +/- 0.2 msec (0.8--6.0 msec), of cortico--reticular neurons--3.2 +/- 0.3 msec (1.0--6.0 msec). The conduction velocity (12.5 m/sec) was the same for both the HP and RF. Characteristics of neuronal organization of hypothalamo--cortical and reticulo--cortical systems of integration are discussed.

Animals↗

PubMed1991

[Afferent projections of the bulbar locomotor region located in the medial reticular formation of the brain stem].

Afferent projections to the functionally identified bulbar locomotor region which is situated in the medial reticular formation were studied in cats and rats by means of horse-radish peroxidase technique. Cells of origin of such projections were found not only in hypothalamic and mesencephalic locomotor regions but also in the interstitial nucleus of Cajal and adjacent structures and in the ventral part of the caudate nucleus.

Afferent Pathways↗

PubMed1989

Afferent and efferent connections of the cholinoceptive medial pontine reticular formation (region of the ventral tegmental nucleus) in the cat.

Following minor concussive brain injury when there is an otherwise general suppression of CNS activity, the ventral tegmental nucleus of Gudden (VTN) demonstrates increased functional activity (32). Electrical or pharmacological activation of a cholinoceptive region in this same general area of the medial pontine tegmentum contributes to certain components of reversible traumatic unconsciousness, including postural atonia (31, 32, 45). Therefore, in an effort to examine the neuroanatomical basis of the behavioral suppression associated with a reversible traumatic unconsciousness, the afferent and efferent connections of the VTN and putative cholinoceptive medial pontine reticular formation (cmPRF) were studied in the cat using the retrograde horseradish peroxidase (HRP), HRP/choline acetyltransferase (ChAT) double-labeling immunohistochemistry, and anterograde HRP and autoradiographic techniques. Based upon retrograde HRP labeling, the principal afferents to the VTN region of the cmPRF originated from the medial and lateral mammillary nuclei, and lateral habenular nucleus, and to a lesser extent from the interpeduncular nucleus, lateral hypothalamus, dorsal tegmental nucleus, superior central nucleus, and contralateral nucleus reticularis pontis caudalis. Other afferents, which were thought to have been labeled through spread of HRP into the medial longitudinal fasciculus (MLF), adjacent paramedian pontine reticular formation, or uptake by transected fibers descending to the inferior olive, included the nucleus of Darkschewitsch, interstitial nucleus of Cajal, zona incerta, prerubral fields of Forel, deep superior colliculus, nucleus of the posterior commissure, nucleus cuneiformis, ventral periaqueductal gray, vestibular complex, perihypoglossal complex, and deep cerebellar nuclei. In HRP/ChAT double labeling studies, only a very small number of cholinergic VTN afferent neurons were found in the medial parabrachial region of the dorsolateral pontine tegmentum, although the pedunculopontine and laterodorsal tegmental nuclei contained numerous single-labeled ChAT-positive cells. Anterograde HRP and autoradiographic findings demonstrated that the VTN gave rise almost exclusively to ascending projections, which largely followed the course of the mammillary peduncle (16,21) and medial forebrain bundle, or the tegmentopeduncular tract (4). The majority of fibers ascended to terminate in the medial and lateral mammillary nuclei, interpeduncular complex (especially paramedian subnucleus), ventral tegmental area, lateral hypothalamus, and the medial septum in the basal forebrain. Labeling that joined the mammillothalamic tract to terminate in the anterior nuclear complex of the thalamus was thought to occur transneuronally. Some projections were also observed to nucleus reticularis pontis oralis and caudalis, superior central nucleus, and dorsal tegmental nucleus adjacent to the VTN...

Animals↗

PubMed1995

[A case of infarction in the pontine tegmentum involving the bilateral MLF and unilateral paramedian pontine reticular formation].

A 61-year-old man with lesions of the bilateral medial longitudinal fasciculus (MLF) and left paramedian pontine reticular formation (PPRF) caused by an infarction in the pontine tegmentum was reported. On admission, the ocular position of the left eye on forward gaze was fixed at the midline, while the right eye was abducted, and skew deviation was observed. On leftward gaze, neither eye could pass the midline, and on rightward gaze the right eye was abducted with monocular nystagmus, indicating paralytic pontine exotropia. On the fifth day, the bilateral eyes were abducted on forward gaze. On leftward gaze, the left eye was abducted slightly with monocular nystagmus. On rightward gaze, the right eye was abducted with monocular nystagmus. This issue was considered to be walleyed bilateral internuclear ophthalmoplegia (WEBINO). On the 37th day, right MLF syndrome was noted. About 2.5 months later, the disturbances of ocular movement disappeared. T2-weighted MRI showed high signal intensity lesions in the bilateral paramedian portion of the midpontine tegmentum. It suggests that WEBINO is caused by a lesion in the pons, and that paralytic pontine exotropia, one and a half syndrome and WEBINO are considered to be analogous to one another. The associated abnormality of vergence eye movements suggests that these are also generated by the PPRF in the pons.

Cerebellar Ataxia↗

PubMed1986

Brain stem reticular formation neuronal correlates of stimulus significance and behavior during discriminative avoidance conditioning in rabbits.

Multiple-unit activity in the reticular formation of the midbrain and pons was recorded in rabbits during discriminative conditioning of locomotor (wheel-running) avoidance behavior. The conditional stimuli (CS+ and CS-) were pure tones of different auditory frequency, and the unconditional stimulus (US) was a constant-current footshock (1.5-2.5 mA) delivered through the grid floor of the wheel. The pontine, but not the midbrain, sites manifested development during behavioral acquisition, of brief-latency (10-40-ms) discriminative neuronal discharges (i.e., greater discharges to the CS+ than to the CS-). The greatest magnitude of the discriminative discharges in the rostral pontine loci occurred in the first conditioning session. The discriminative response in the caudal loci developed more slowly, and it persisted to the criterial stage of training. Both rostral and caudal pontine loci, during the interval from CS onset to US onset, manifested a progressive build-up of neuronal firing in anticipation of the behavioral response. The occurrence in the rostral and caudal pontine areas, respectively, of early- and late-developing discriminative discharges is analogous to effects observed in past studies in the limbic mesocortical and thalamic systems. These findings provide a basis for establishing the possible functional relatedness or independence of these analogous effects.

Animals↗

PubMed2005

Microinjection of neostigmine into the pontine reticular formation of the mouse: further evaluation of a proposed REM sleep enhancement technique.

Microinjections of cholinergic agonists into the pontine reticular formation (PRF) powerfully induce rapid eye movement sleep (REMS) in cats but have comparatively weaker effects in rats. Recently, the cholinomimetic neostigmine has been reported to strongly enhance REMS following microinjection into the PRF of the mouse. That study used behavioral assessments of locomotion in lieu of electrophysiological measures of muscle tone to identify REMS. We sought to confirm that the behavioral state induced in mice by PRF injections of neostigmine meets standard electroencephalogram (EEG) and electromyogram (EMG) criteria for defining REMS. Cortical EEG, nuchal muscle EMG, and PGO waves were recorded from male C57BL/6N mice with chronic indwelling cannulae for the delivery of neostigmine to the PRF. Recordings were made during midday following injections of neostigmine (8.8 mM, 50 nl), 2 h after lights on (LD 12:12). Neostigmine induced a behavioral state characterized by low amplitude, highly desynchronized cortical EEG with little theta, no PGO waves, and a sustained high muscle tone. Behavioral states meeting standard criteria for slow-wave sleep (SWS) and REMS were significantly suppressed compared to baseline recordings, and REMS onset was delayed by 3 h. Consistent with earlier reports, neostigmine did strongly suppress locomotor activity in open field tests and in the home cage. Due to the failure to meet criteria for defining REMS, we conclude that neostigmine microinjection into the PRF of the mouse induces an abnormal waking state rather than REMS.

Animals↗

PubMed2004

Response of NADPH-diaphorase-exhibiting neurons in the medullar reticular formation to high spinal cord injury.

1. The effect of hemisection of the cervical spinal cord on NADPH-diaphorase staining in the reticular nuclei of the rabbit medulla was investigated using histochemical technique. 2. A quantitative assessment of somal and neuropil NADPH-diaphorase staining was made by an image analyzer in a selected area of each reticular nucleus of the rabbit medulla. 3. On the 7th postsurgery day, the highest up-regulation of somatic NADPH-diaphorase staining was observed in regions regulating cardiorespiratory processes; however, the highest increase of neuropil NADPH-diaphorase staining was found in the reticular nuclei modulating the tonus of postural muscles. 4. The degeneration of non-NADPH-diaphorase-stained neurons was detected throughout the reticular formation of the medulla, but the extent of neuronal death did not correlate with the up-regulation of the NADPH-diaphorase staining in the reticular nuclei of the medulla. 5. The findings provide evidence that NADPH-diaphorase-exhibiting neurons are refractory to the hemisection of the cervical spinal cord and that the neuronal up-regulation of NADPH-diaphorase at the medullar level is probably not a causative factor leading to the death of the reticulospinal neurons.

Animals↗

PubMed1996

Central mesencephalic reticular formation (cMRF) neurons discharging before and during eye movements.

1. One hundred twenty neurons were recorded in the central mesencephalic reticular formation (cMRF) of four rhesus monkeys, trained to make visually guided and targeted saccadic eye movements. Eye movements were recorded with the head fixed, using electrooculography (EOG) or subconjunctival scleral search coils. Seventy-six percent (92/120) of cells discharged before and during contraversive visually guided or targeted rapid eye movements, and 76% of these (70/92) responded during contraversive spontaneous saccades in the dark. cMRF neurons had large contraversive movement fields and either a high (> 10 spikes/s) or low background level of spontaneous activity in the dark. The optimal movement vectors (i.e., saccades with greatest response) were predominantly horizontal, although many had a vertical component. Cells with optimal movement vectors within +/- 25 degrees of pure vertical were more rostral in the MRF and were excluded from the analysis. 2. A subgroup of cMRF neurons (31 of 92) that discharged before and during visually guided saccades were examined for visual sensitivity. Slightly less than one-half of these cells (42%, 13/31) were visuomotor units, i.e., they responded to visual targets in the absence of eye movement. The other 58% (n = 18) did not discharge during the visual probe trial; they were movement-related cells. 3. Microstimulation (threshold 40-60 microA at 333 Hz) at the sites of many of these cMRF neurons produced contraversive saccadic eye movements at short latency (< 40 ms). The amplitude and direction of the elicited saccades were similar to the optimal movement vector determined from single-unit recording. This suggested that cMRF cells recorded at the same locus of electrical microstimulation participated in the network responsible for the production and control of rapid eye movements. 4. The 92 saccade-related neurons were divided into two groups on the basis of their background discharge rate. Firing rates for both low background (28%, n = 26) and high background (72%, n = 66) cells increased approximately 30 ms before contraversive saccades and reached a peak discharge just before saccade onset. The low background neurons had either no activity or generated a few spikes just before the end of ipsiversive saccades. The steady rate of discharge (> 10 spikes/s) of high background neurons was inhibited from approximately 20 ms before ipsiversive saccades until just before saccade end. 5. Cells were also subdivided on the basis of how their discharge rates fell at the end of saccades. Clipped cells (38%, n = 35) had activity that fell sharply with saccade offset. Partially clipped cells (62%, n = 57) had persistent firing in the 100 ms following the saccade that was > 20% higher than the firing during the 100 ms before the saccade. 6. Latencies between the 90% point on the rising edge of the peak discharge and the start of the saccade were < or = 5.3 ms for eye movement-related cells in two monkeys. Longer latencies (11-19 ms) were found when measured between the 10% point on the rising edge of the peak discharge and saccade onset. These latencies were equal to or shorter than those obtained for eye movement-related burst neurons in the intermediate and deep layers of the superior colliculus analyzed similarly. Delays between the peak discharge and peak eye velocity were 13.6-15.1 ms for the same group of cMRF eye movement-related cells. These were significantly shorter than the delays measured for eye movement neurons in the superior colliculus (SC) of one of the monkeys. These findings suggest that the buildup discharge of cMRF neurons occurs early enough before saccades to contribute to saccade triggering. The peak discharge, however, occurs with or after the burst in the SC, suggesting that this portion of the discharge serves a function other than saccade triggering. 7. The number of spikes in bursts associated with eye movement was correlated with saccade parameters.

Animals↗

PubMed2002

Microinjection of an adenosine A1 agonist into the medial pontine reticular formation increases tail flick latency to thermal stimulation.

BACKGROUND: Both pain and the pharmacologic management of pain can cause the undesirable effect of sleep disruption. One goal of basic and clinical neuroscience is to facilitate rational drug development by identifying the brain regions and neurochemical modulators of sleep and pain. Adenosine is thought to be an endogenous sleep promoting substance and adenosinergic compounds can contribute to pain management. In the pontine brain stem adenosine promotes sleep but the effects of pontine adenosine on pain have not been studied. This study tested the hypothesis that an adenosine agonist would cause antinociception when microinjected into pontine reticular formation regions that regulate sleep. METHODS: The tail flick latency (TFL) test quantified the time in seconds for an animal to move its tail away from a thermal stimulus created by a beam of light. TFL measures were used to evaluate the antinociceptive effects of the adenosine A1 receptor agonist N6-p-sulfophenyladenosine (SPA). Pontine microinjection of SPA (0.1 microg/0.25 microl, 0.88 mm) was followed by TFL measures as a function of time after drug delivery and across the sleep-wake cycle. RESULTS: Compared with saline (control), pontine administration of the adenosine agonist significantly increased latency to tail withdrawal (P < 0.0001). The increase in antinociceptive behavior evoked by the adenosine agonist SPA was blocked by pretreatment with the adenosine A1 receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 0.75 ng/0.25 microl, 10 microm). CONCLUSIONS: These preclinical data encourage additional research on the cellular mechanisms by which adenosine in the pontine reticular formation contributes to the supraspinal modulation of pain.

Analgesics↗

PubMed1995

Induction of rapid eye movement sleep by carbachol infusion into the pontine reticular formation in the rat.

Cholinergic regulation of sleep and wakefulness was studied in freely moving rats locally infused with various doses of carbachol into the pontine reticular formation. Induction of REM sleep occurred when carbachol was infused specifically into the posterior oral pontine reticular nucleus (PnO). This effect was observed with 1-10 ng of carbachol, and lasted for at least 6 h. It was antagonized by atropine (100-200 ng) infused into the same site 15 min before carbachol (10 ng), indicating that REM sleep induction resulted from the stimulation of pontine muscarinic receptors. High doses of carbachol (500 ng) did not affect REM sleep but enhanced wakefulness. Cholinergic mechanisms within the PnO may play a critical role in the regulation of REM sleep in the rat.

Animals↗

PubMed1989

Immunohistochemical studies on the development of 5-HT (serotonin) neurons in the nuclei of the reticular formations of human fetuses.

5-HT-positive neurons were detected by the PAP immunohistochemical methods in different nuclei of the reticular formations of human fetuses as early as 10 weeks of gestation. The majority of positive 5-HT cells were located in dorsal raphe and central superior nuclei, and there was a reduction of these neurons per 40-microns section as the fetus aged.

Cell Count↗

PubMed2000

Phenytoin administration reveals a differential role of pontine reticular formation and periaqueductal gray neurons in generation of the convulsive behaviors of audiogenic seizures.

The ventrolateral periaqueductal gray (PAG) and pontine reticular formation (PRF) are implicated in the neuronal network for audiogenic seizures (AGS). The AGS of genetically epilepsy-prone rats (GEPR-9s) culminate in tonic hindlimb extension (TE), and elevated acoustically evoked neuronal firing and burst firing, immediately preceding TE, have been observed in PAG and PRF. This study examined changes in PAG and PRF neuronal firing and behavior in GEPR-9s, following phenytoin administration. Recordings involved 16 PAG and nine PRF neurons in GEPR-9s. Phenytoin in doses (mean, 6. 3 mg/kg) that suppressed TE selectively did not consistently alter PAG neuronal firing. However, these doses of phenytoin resulted in significant (51.6% of control) suppression of PRF neuronal firing. Doses of phenytoin (mean, 8.3 mg/kg), which completely blocked AGS, significantly reduced PAG neuronal firing (64.6% of control), and more greatly suppressed PRF firing (25.8% of control). These results are consistent with a critical role for PRF neurons in generation of TE not evident for PAG. The suppression of PAG and PRF neuronal firing induced by phenytoin with complete seizure blockade is consistent with vital roles for both structures in the seizure network. The differential effects of phenytoin on structures requisite to the seizure network indicate that this experimental approach may be able to identify the most sensitive therapeutic target for anticonvulsant drugs, which could be critical to pharmacological suppression of specific seizure behaviors manifest in various types of convulsions, potentially including human epilepsy.

Action Potentials↗