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At least 523 records · Page 29Linked to original sources

PubMed1988

Effects of thalamic parafascicular stimulation on the periaqueductal gray and adjacent reticular formation neurons. A possible contribution to pain control mechanisms.

To investigate the mechanism of analgesic effect of electrical stimulation of the thalamic parafascicular nucleus (Pf), we studied modulations of neuronal activities in the periaqueductal gray (PAG) and the adjacent reticular formation (RF) in response to Pf electrical and peripheral noxious stimulations in the rat. Extracellular single unit activities were recorded from 129 neurons in the PAG and adjacent RF under light halothane anesthesia. Pf stimulation caused neuronal responses in approximately 80% of the PAG and adjacent RF neurons, and noxious stimulation in 75%, with predominant excitatory responses to either stimulation. When the responses to the two stimuli were tested in the same neurons (n = 69), 91% responding to noxious stimuli also responded to Pf stimuli, again with predominant excitatory responses to either stimulation. The PAG and adjacent RF neurons that were verified antidromically to project to the nucleus raphe magnus (NRM), showed a similar pattern of response (n = 20). These results suggest that a sizeable population of neurons in the PAG and adjacent RF receives excitatory effects from the Pf and noxious afferents, and that part of these neurons projects to the NRM, which inhibits the dorsal horn cells of the spinal cord (the descending pain suppression system). Thus, part of the mechanism of the analgesic effects of Pf stimulation is due to activation of the descending pain suppression system by exciting the PAG and adjacent RF neurons. A possible role of noxious afferents on the negative feedback to pain mediation through this descending system also has to be considered.

Animals↗

PubMedDate not supplied

A case of progressive supranuclear palsy with fibrillary gliosis of the midbrain and pontine reticular formation.

An autopsy case of progressive supranuclear palsy with onset at age 53 and a clinical course of 7 years is reported. The clinico-pathological characteristics of the case were as follows: Fibrillary gliosis of the midbrain and pontine reticular formation corresponded clinically to personality changes: The patient had formerly been irascible and became extremely mild-mannered. He showed lack of spontaneity and initiative and slowing of thought processes, taking him longer than normal to find words and ideas. Gliosis of the nucleus ventralis lateralis of the thalamus was secondary to the degeneration of the cerebellar dentate nucleus and the globus pallidus from which they receive fibers. Neurofibrillary tangles were found in the cerebral cortex.

Cerebral Cortex↗

PubMedDate not supplied

Phase relationships between the rhythmic activity of cortical structures of the rabbit at different midbrain reticular formation stimulation frequencies.

An investigation of the phase shifts between rhythmic constituents of the electrical activity of the hippocampus, somatosensory, motor, and visual areas of the neocortex of the rabbit during an increase in the frequency of stimulation of the reticular formation from 60 to 1000 imp/sec revealed the fluctuating character of the decrease in the phase shift in the theta range in pairings involving the visual area and of its increase in the remaining pairings. In the delta range, at the same time, an increase was observed in the phase angle in pairings between the hippocampus, somatosensory, and motor areas at a stimulation frequency above 200 imp/sec, while in the alpha range the changes in the phase shift were variously directed in character.

Alpha Rhythm↗

PubMedDate not supplied

[Effect of stimulation of rostral portions of the midbrain reticular formation on the cat motor cortex].

Evoked potentials and responses of 139 neurones in the sensorimotor cortex (the lateral third of the posterior sigmoid gyrus) to electrical stimulation of the dorsolateral (DL) and the ventromedial (VM) areas of the mesencephalic reticular formation (MRF) were investigated in cats in acute and chronic experiments. Latencies of the cortical unit responses (in the form of single and multiple discharges) to MRF stimulation varied from 4 to 36 msec for VM (maxima of distribution: 4--10 and 18--24 msec); those for DL were from 4 to 26 msec (maxima of distribution: 4--6 and 14--16 msec). Responses to both DL and VM stimulation were observed in 29 neurones. As for MRF, its effects (mono-and polyvalent) were found in cortical neurones responding to limb electrocutaneous stimulation as well. At 7--10 days after coagulation of the ipsilateral connection between MRF and the pons, persistence of the cortical response main components was recorded, the long-latency part being slightly reduced.

Animals↗

PubMed2000

c-Fos expression in GABAergic, serotonergic, and other neurons of the pontomedullary reticular formation and raphe after paradoxical sleep deprivation and recovery.

The brainstem contains the neural systems that are necessary for the generation of the state of paradoxical sleep (PS) and accompanying muscle atonia. Important for its initiation are the pontomesencephalic cholinergic neurons that project into the pontomedullary reticular formation and that we have recently shown increase c-Fos expression as a reflection of neural activity in association with PS rebound after deprivation in rats (Maloney et al. , 1999). As a continuation, we examined in the present study c-Fos expression in the pontomedullary reticular and raphe neurons, including importantly GABAergic neurons [immunostained for glutamic acid decarboxylase (GAD)] and serotonergic neurons [immunostained for serotonin (Ser)]. Numbers of single-labeled c-Fos+ neurons were significantly increased with PS rebound only in the pars oralis of the pontine reticular nuclei (PnO), where numbers of GAD+/c-Fos+ neurons were conversely significantly decreased. c-Fos+ neurons were positively correlated with PS, whereas GAD+/c-Fos+ neurons were negatively correlated with PS, suggesting that disinhibition of reticular neurons in the PnO from locally projecting GABAergic neurons may be important in the generation of PS. In contrast, through the caudal pons and medulla, GAD+/c-Fos+ cells were increased with PS rebound, covaried positively with PS and negatively with the electromyogram (EMG). In the raphe pallidus-obscurus, Ser+/c-Fos+ neurons were positively correlated, in a reciprocal manner to GAD+/c-Fos+ cells, with EMG, suggesting that disfacilitation by removal of a serotonergic influence and inhibition by imposition of a GABAergic influence within the lower brainstem and spinal cord may be important in the development of muscle atonia accompanying PS.

Animals↗

PubMed1986

Spinal neurons which project to the periaqueductal gray and the medullary reticular formation via axon collaterals: a double-label fluorescence study in the rat.

Fluorescent retrograde double-labeling methods were used in which Fast blue and Nuclear yellow or Diamidino yellow dihydrochloride were injected into the midbrain periaqueductal gray (PAG) and medullary reticular formation (MRF). Double-labeled neurons were most frequently observed in the lateral part of lamina V, in laminae VII, VIII and X and in the lateral cervical and lateral spinal nuclei. The data demonstrate that some spinal neurons project to both the PAG and the MRF via axon collaterals.

Amidines↗

PubMed1983

Role of ventral mesencephalic reticular formation and related noradrenergic and serotonergic bundles in turning behaviour as investigated by means of kainate, 6-hydroxydopamine and 5,7-dihydroxytryptamine lesions.

A unilateral kainate (KA) infusion (2 x 0.15 micrograms, 2 x 0.25 micrograms) in the ventral mesencephalic reticular formation (MRF) resulted in spontaneous contraversive turning lasting only a few days. Upon challenge with apomorphine (0.5 mg/kg s.c.) or amphetamine (5 mg/kg i.p.) the contraversive turning could be reinstated. The incidence, as well as the intensity, of the drug-induced response decreased over the 45 days of observation. KA infused in the ventral MRF induced typical lesions after doses of 2 x 0.15 micrograms but resulted in demyelination after 2 x 0.25 micrograms. These lesions failed to reduce noradrenaline (NA), serotonin (5 HT) or dopamine (DA) in various forebrain areas. Unilateral lesion of ascending NA projections by 6-OHDA infusion (4 micrograms) within the NA bundles coursing in the mesencephalon or near the locus coeruleus, failed to induce motor asymmetries. Unilateral selective lesion of the ventral NA bundle by local 6-OHDA (2 micrograms) infusion also failed to induce motor asymmetries, either spontaneously or in response to dopaminergic drugs. Unilateral lesion of ascending 5-HT projections by the tegmental infusion of 5,7-dihydroxytryptamine (10 micrograms) also failed to induce motor asymmetries in response to dopaminergic drugs but resulted in contraversive circling in response to 5-hydroxytryptophan. These data indicate that intrinsic neurones of the ventral MRF play a role in turning behaviour and exclude, in contrast with previous studies, a role of NA or 5-HT projections in the contraversive turning responses to DA receptor agonists obtained after lesions of the ventral MRF.

5,7-Dihydroxytryptamine↗

PubMed2004

Acetylcholine release in the pontine reticular formation of C57BL/6J mouse is modulated by non-M1 muscarinic receptors.

Pontine acetylcholine (ACh) contributes to the regulation of electroencephalographic and behavioral arousal in all mammals so far investigated. The mouse is recognized as a powerful model for pharmacogenomics but the synaptic mechanisms regulating ACh release in mouse pontine reticular formation have not been characterized. Drug delivery by microdialysis was used in isoflurane-anesthetized C57BL/6J (B6) mice (n=33) to test the hypothesis that muscarinic autoreceptors modulate ACh release in the pontine reticular nucleus, oral part (PnO). Dialysis delivery of tetrodotoxin to the PnO significantly decreased ACh by 58% below control levels, confirming that measured ACh reflected neurotransmitter release. The muscarinic antagonist scopolamine increased ACh release in the PnO by 21% (3 nM), 48% (10 nM), 56% (30 nM), and 104% (100 nM). The muscarinic agonist bethanechol dialyzed into the PnO significantly decreased ACh release by 60% compared with control. Dialysis delivery of relatively subtype selective muscarinic antagonists to the PnO revealed the following order of potency for increasing ACh release: scopolamine (3 nM)>AF-DX 116 (100 nM)=pirenzepine (100 nM). These data support the conclusion that ACh release in PnO of B6 mouse is modulated by non-M1 muscarinic receptors.

Acetylcholine↗

PubMed1991

Neurotoxic lesion of the mesencephalic reticular formation and/or the posterior hypothalamus does not alter waking in the cat.

In order to re-evaluate the role of two putative waking systems, we injected a neural cell body toxin, ibotenic acid (IA) (45 micrograms/microliters), into the mesencephalic reticular formation (MRF) and/or the posterior hypothalamus (PH). On the one hand, when the cell body destruction was only restricted to the MRF, the IA microinjection was followed by a temporary high voltage and slow neocortical electroencephalogram (EEG) during the first 24 postoperative hours and by a subsequent long term increase in waking which lasted 8-12 h. After the first postoperative day, there were no motor disturbances, no aphagia nor adypsia, no alteration of cortical activation and no modification of thermoregulation or of the sleep-waking cycle. On the other hand, the IA microinjection into the PH induced a hypothermia during the first postoperative night and a dramatic transient hypersomnia immediately after the disappearance of the anesthesia (14-24 h after the IA injection). On the third day, all cats recovered control level of paradoxical sleep (PS), slow wave sleep (SWS) and cerebral temperature. They presented normal motor behavior but they were not able to eat by themselves during the first postoperative week. Finally, when the lesions of the MRF and the PH were realized in one single operation, the cats were first motionless in a comatose state for 2-3 days. This state was accompanied by a transitory hypothermia and the suppression of a spontaneous or evoked cortical low voltage fast activity. However, from the 2nd postoperative week, both behavioral and EEG waking re-occurred. By contrast, the two successive operations (MRF followed by PH) did not induce a comatose state. We did not observe any deficit in motor behavior, and the sleep-waking cycle was quite normal as from the second postlesion day. In the MRF-PH-lesioned cats, the injection of alpha-methyl-p-tyrosine (150 mg/kg) induced a large decrease in waking and a moderate increase in PS. In the MRF-lesioned cats, IA produced a large area of cell body loss, centered in the MRF, that extended from levels A2 to A6 of stereotaxic planes and sometimes encroached upon the red nucleus and the substantia nigra. In the PH-lesioned cats, the histological analysis revealed a great loss of cell bodies in the PH extended from levels A8 to A12.5. The damage included the lateral and posterior hypothalamic areas and sometimes the tuberomamillary nucleus. In MRF- and PH-lesioned cats, the cell body loss extended from levels A2 to A12.5.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1977

[Monsynaptic influences from the reticular formation and muscle afferents following axotomy of motor neurons in rats].

Lumbar motoneurons were studied by means of intracellular recording in intact rats and after section of the appropriate ventral roots. In normal motoneurons monosynaptic EPSPs evoked by stimulation of the reticular formation and Ia group muscle afferents showed no difference in amplitude (3.92 +/- 0.17 mV and 3.86 +/- 0.19 mV), but revealed statistically significant difference in time-to-peak (0.71 +/- 0.05 msec and 0.83 +/- 0.06 msec). The membrane potential, the duration and the amplitude of the actionpotentials, and the generation of antidromic actionpotentials showed no difference between normal and axotomized motoneurons. The partial responses were not recorded in axotomized motoneurons. Monosynaptic reticulo-spinal and Ia EPSPs of axotomized motoneurons exhibited longer time-to-peak than those in normal motoneurons. Besides, Ia EPSPs were significantly reduced in amplitude. The changes of monosynaptic reticulo-spinal and Ia EPSPs cannot be explained exclusively by the alterations of the synapses located on the soma and proximal dendrites.

Animals↗

PubMed1978

[Effects of diazepam on evoked potential recorded from basal medial amygdaloid nucleus, lateral hypothalamus and midbrain reticular formation (author's transl)].

The evoked potential in the lateral hypothalamus (LH) recorded by stimulation of basal medial amygdaloid nucleus (Abm) showed a triphasic pattern and diazepam (2 mg/kg, i. p.) decreased the late component. The evoked potential in the midbrain reticular formation (MRF) recorded by stimulation of Abm showed a fast component with a relatively short latency followed by a biphasic late component and diazepam decreased the late component. Though the evoked potential in the Abm recorded by stimulation of LH showed a triphasic pattern, diazepam had no influence on the amplitude. Diazepam increased markedly the amplitude of evoked potential in the MRF recorded by stimulation of LH. Diazepam was ineffective on the evoked potential in the Abm recorded by stimulation of MRF. Diazepam decreased markedly the late component of evoked potential in the LH recorded by stimulation of MRF. These results suggest that the depression of emotional behavior by diazepam may be particularly related to the fact that the evoked potential in the LH recorded by stimulation of Abm was decreased by diazepam.

Amygdala↗

PubMed2004

Responses of feline medial medullary reticular formation neurons with projections to the C5-C6 ventral horn to vestibular stimulation.

Prior studies have shown that the vestibular system contributes to adjusting respiratory muscle activity during changes in posture, and have suggested that portions of the medial medullary reticular formation (MRF) participate in generating vestibulo-respiratory responses. However, there was previously no direct evidence to demonstrate that cells in the MRF relay vestibular signals monosynaptically to respiratory motoneurons. The present study tested the hypothesis that the firing of MRF neurons whose axons could be antidromically activated from the vicinity of diaphragm motoneurons was modulated by whole-body rotations in vertical planes that stimulated vestibular receptors, as well as by electrical current pulses delivered to the vestibular nerve. In total, 171 MRF neurons that projected to the C5-C6 ventral horn were studied; they had a conduction velocity of 34+/-15 (standard deviation) m/sec. Most (135/171 or 79%) of these MRF neurons lacked spontaneous firing. Of the subpopulation of units with spontaneous discharges, only 3 of 20 cells responded to vertical rotations up to 10 degrees in amplitude, whereas the activity of 8 of 14 neurons was affected by electrical stimulation of the vestibular nerve. These data support the hypothesis that the MRF participates in generating vestibulo-respiratory responses, but also suggest that some neurons in this region have other functions.

Analysis of Variance↗

PubMed1980

Conative regulation of cortical activity by the reticular formation, hypothalamus, and thalamus.

Evolution of neural regions suggests the requirement for a common format for information units exchanged among regions. Short-term memory experiments suggest a format of six or seven items. A similar number of configurations of primary cerebral interactions is proposed, associated with arousal, sleep, approach, withdrawal, perseveration, alert scanning, and commanded by the reticular formation. A comparable number of basic states (feeding, mating, grooming, shelter-seeking, fighting, etc.) is proposed as operating within these configurations, under regulation by the hypothalamus. Conative variables from this region are transformed into patterns of regulation for local cortical populations by the thalamus. Elaboration of these configurations and states by higher structures leads to new forms of cortical activity only loosely coupled to brain stem systems.

Adaptation, Physiological↗

PubMed1987

Reduced behavioural inhibition after lesions in the dorsomedial pontine reticular formation of rats.

Male hooded rats of the Long-Evans strain were investigated in an open field (OF), in an Y-maze and in a pole-climbing (jump) test before and after small bilateral symmetric lesions of the dorsomedial pontine reticular formation, medial from the locus coeruleus including lateral parts of the central gray. Postoperative values of ambulatory activity were increased above 300%. This hyperactivity in the OF was characterized by weakened habituation in the OF, increased locomotor speed, increased climbing rate, whereas horizontal exploratory activity was significantly decreased. The preoperatively learnt Y-maze avoidance tasks were correctly performed after lesions without any retention deficit and without errors in brightness-discrimination. The postoperative acquisition of a jump test avoidance task was impossible because the lesioned rats did not find the escape possibility in spite of a great number of variant jumps. They never showed tendencies of arrest behaviour ("learned helplessness"). The syndrome is characterized by weakened behavioural inhibition of incorrect or redundant responses.

Animals↗

PubMed1990

Partial involvement of monoamines and opiates in the inhibition of rat spinal nociceptive neurons evoked by stimulation in midbrain periaqueductal gray or lateral reticular formation.

In rats anesthetized with sodium pentobarbital, we tested the effects of systemic or intrathecal administration of the opiate antagonist naloxone, the serotonergic antagonist methysergide, or the adrenergic antagonist phentolamine, on inhibition produced by electrical stimulation in midbrain periaqueductal gray (PAG) or lateral reticular formation (LRF) of the responses of single lumbar dorsal horn neurons to noxious heating (50-54 degrees C, 10 s) of hindpaw skin. Systemically administered naloxone (1-10 mg/kg i.v.) reduced (greater than 20% below predrug inhibition) inhibition from PAG and/or LRF in 5/12 units and had no effect in the remainder. Systemic methysergide (2-6 mg/kg i.v.) selectively reduced PAG-evoked inhibition in 6 units, while inhibitions from both PAG and LRF stimulation were reduced in one unit and unaffected in 8 units. Systemic phentolamine (2-4 mg/kg) reduced LRF-evoked inhibition in 4 units, while inhibitions from PAG and LRF were reduced in one unit and unaffected in 5. Intrathecally applied methysergide reduced or abolished PAG-evoked inhibition in 8/16 units and reduced or abolished LRF-evoked inhibition in 6/14 units. Reductions in the level of inhibition were reversible in one-half of the cases, whereas they persisted for over 2 h in the remainder. The mixed effects of both systemically and intrathecally administered drugs suggest that monoamines and opiates may be partly involved in spinal inhibitory mechanisms activated from the midbrain.

Animals↗

PubMed1992

Voltammetrically determined differences in changes evoked by KCl microinjections on catecholamine levels in the reticular formation and corpus striatum of the rat.

Using a microelectrode with carbon filaments and the voltammetric technique, changes evoked in the catechol oxidation current (CA.OC) and multiple unit activity (MUA) by microinjection of 3-5 microliters 0.5 mol.l-1 KCl were studied in the reticular formation (RF) of the medulla oblongata of anaesthetized rats; the effect of KCl stimulation of the RF and corpus striatum (S) on the CA.OC in these structures was compared. The microinjection of KCl in the vicinity of the working electrode in the RF caused depression of MUA which began 2-3 s after administration, persisted for up to 6 min after and then diminished, reaching control values within 9 min. The voltammetric signal was first recorded in the 1st min after microinjection, when there was an evident decrease in the CA.OC value (59% of the control value); this effect reached its maximum 7 min after administration (a mean drop to 23% of the control), while at the end of the experiment (i.e. after 24 min) CA.OC values had risen to 45-80% of the control value. The response in the S had a biphasic character, however. Immediately after the microinjection (1st min), the mean CA.OC value rose to 626% of the control, while in the second phase (3-10 min) it was seen to fall below the control values (means 21-63% of the control). The differences in the changes evoked by K+ depolarization in the concentration of catecholamines in the RF and S microenvironment are discussed from the aspect of the existence of different pools of the transmitter and other regional differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Effects of an apovincaminic acid derivative VA-045 on neuronal activity in rat brain stem reticular formation.

Extracellular single unit and spontaneous cortical electroencephalographic (ECoG) recordings were made in the brain stem reticular formation (RF) and the frontal cortex, respectively, of urethane-anesthetized rats. VA-045, an apovincaminic acid derivative had no significant effects on the spontaneous firing rate of the RF neurons and ECoG. Closed head injury (CHI) was induced by dropping a 400 g weight through a tube from 70 cm on a steel helmet placed on the vertex. CHI led to a reduction in the firing rate of RF neurons and ECoG synchronization. VA-045 dose-dependently reversed the CHI-induced decrease in the firing rate of RF and led to ECoG desyncronization. Clonidine, an alpha 2 adrenoceptor agonist, and scopolamine, a muscarinic receptor antagonist, also reduced the firing rate of RF neurons and led to ECoG synchronization. VA-045 dose-dependently antagonized the effects of clonidine, but not the effects of scopolamine on RF neuronal activity and ECoG. Thus, VA-045 has an ameliorating effect on the CHI-induced depression of neuronal activity in the RF. A central alpha 2 adrenoceptor antagonistic action may be involved.

Animals↗

PubMed2007

Taste-evoked Fos expression in nitrergic neurons in the nucleus of the solitary tract and reticular formation of the rat.

The current investigation used double labeling for NADPHd and Fos-like immunoreactivity to define the relationship between nitric oxide synthase-containing neural elements and taste-activated neurons in the nucleus of the solitary tract (NST) and subjacent reticular formation (RF). Stimulation of awake rats with citric acid and quinine resulted in significant increases in the numbers of double-labeled neurons in both the NST and RF, suggesting that some medullary gustatory neurons utilize nitric oxide (NO) as a transmitter. Overall, double-labeled neurons were most numerous in the caudal reaches of the gustatory zone of the NST, where taste neurons receive inputs from the IXth nerve, suggesting a preferential role for NO neurons in processing gustatory inputs from the posterior oral cavity. However, double-labeled neurons also exhibited a preferential distribution depending on the gustatory stimulus. In the NST, double-labeled neurons were most numerous in the rostral central subnucleus after either stimulus but had a medial bias after quinine stimulation. In the RF, after citric acid stimulation, there was a cluster of double-labeled neurons with distinctive large soma in the parvicellular division of the lateral RF, subjacent to the rostral tip of NST. In contrast, in response to quinine, there was a cluster of double-labeled neurons with much smaller soma in the intermediate zone of the medial RF, a few hundred micrometers caudal to the citric acid cluster. These differential distributions of double-labeled neurons in the NST and RF suggest a role for NO in stimulus-specific gustatory autonomic and oromotor reflex circuits.

Animals↗