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At least 127 records · Page 7Linked to original sources

PubMed1991

[Drug treatment of various diseases, primarily of those caused by disorders of the reticular formation of the brain stem].

The author holds that a great number of failures and poor results in the treatment of organic or functional nervous and somatic diseases result from ignoring the role of brain stem reticular formation interacting with vegetative innervation and limbic formations. The disturbances of this reticular formation often contribute to the development of a pathological process due to enhancement or inhibition of the neuromediatory reticular systems. Drugs are proposed able to produce a selective positive action on neuromediatory systems of the reticular formation. Such approach may bring about responses in severe neurogenic and somatic affections.

Autonomic Nervous System Diseases↗

PubMed1985

Octanoic acid-induced coma and reticular formation energy metabolism.

The medium chain fatty acid octanoic acid was injected i.p. into 20-22 g Swiss-Albino mice at a dose of 15 mumol/g. This dose produced a reproducible response consisting of a 3-4 min period of drowsiness, followed by coma. These mice as well as suitable controls were sacrificed by rapid submersion in liquid N2, or by microwave irradiation in a 7.3 kW microwave oven. Tissue from the reticular formation and the inferior colliculus was prepared for microanalysis of the energy metabolites glucose, glycogen, ATP and phosphocreatine. Results from this study showed a selective effect on energy metabolism in cells of the reticular formation. Both glucose and glycogen were elevated in the coma and precoma state. In addition, ATP and phosphocreatine were decreased in the reticular formation during coma. These results show a selective effect of octanoic acid on energy metabolism in the reticular formation both in the precoma stage, and during overt coma. The selective vulnerability of the reticular formation to metabolic insult may act in a beneficial manner to the animal by inducing coma. This lowers the overall demand for energy, thereby placing the animal in a milieu in which there is an increased chance for correction of the perturbation.

Adenosine Triphosphate↗

PubMed1987

The origin of brainstem afferents of the paramedian pontine reticular formation in the cat.

Transcannular microinjections of horseradish peroxidase (HRP) were made into the paramedian pontine reticular formation (PPRF) in adult cats to determine the origin of the principal sources of inputs to this important preoculomotor center for the production of saccadic eye movements. Retrogradely labeled cells were observed in numerous oculomotor-related structures, including the prerubral field (rostral interstitial nucleus of the medial longitudinal fasciculus), nucleus of Darkschewitsch, nucleus of the posterior commissure, deep superior colliculus, supraoculomotor ventral periaqueductal gray, contralateral paramedian pontine reticular formation, pontine raphe and dorsal medial pontine tegmentum medial to the abducens nucleus (purported to contain omnipause neurons), cell group Y, and the perihypoglossal complex (nucleus prepositus hypoglossi). Other sources of afferents to the region included the zona incerta, lateral and medial habenular nuclei, medial hypothalamus, medial mammillary nucleus, nucleus cuneiformis, medial medullary reticular formation, and the medial and lateral cerebellar nuclei. The results are discussed in terms of the potential influence of these nuclei on the control of eye movement.

Afferent Pathways↗

PubMed1988

The origin of projections from the medullary reticular formation to the spinal cord, the diencephalon and the cerebellum at different stages of development in the North American opossum: studies using single and double labeling techniques.

We have employed the retrograde transport of horseradish peroxidase alone or conjugated to wheat germ agglutinin, to label neurons within the medullary reticular formation which project to the spinal cord, the diencephalon and the cerebellum at different stages of development in the North American opossum. At selected ages, the fluorescent markers Fast Blue and Diamidino Yellow were also used in double-labeling experiments to determine if single neurons innervate both the spinal cord and diencephalon or the spinal cord and cerebellum, presumably via axonal collaterals. The opossum was employed because it is born in a very immature state, 12 days after conception, and is thus available for injections at early stages of development. At all ages studied, the location of retrograde labeling within the medullary reticular formation after spinal, diencephalic or cerebellar placements of horseradish peroxidase or its conjugate appeared similar to that obtained in the adult animal. Such results suggest that the origin of projections from the medullary reticular formation to the areas injected is specified early in development. At some ages, however, the labeling density appeared greater than in the adult animal. When either Fast Blue or Diamidino Yellow was injected into the spinal cord and the other marker was placed into the diencephalon at such ages, relatively few neurons of the medullary reticular formation were double-labeled. When one marker was injected into the spinal cord and the other was placed within the cerebellum, no double-labeled neurons were found. These results indicate that at the ages studied, relatively few neurons of the medullary reticular formation provide collateral innervation to either the spinal cord and diencephalon or the spinal cord and cerebellum. Similar conclusions have been reached previously for the adult opossum. We have interpreted our results to suggest that the organization of reticular projections, at least to the areas injected, may not be shaped by the selective elimination of axonal collaterals as in certain other areas of the brain.

Amidines↗

PubMed1983

Steroid anaesthesia: alphadione depresses multiunit activity in the mesencephalic reticular formation.

Cortical EEG and multiunit activity (MUA) of the mesencephalic reticular formation (MRF), area hypothalami anterior (AH) and the nucleus amygdalae basalis (AMY) were studied before and after different doses of alphadione (Althesin) and hexobarbitone (Evipan-Natrium) given to cats with chronically implanted electrodes. Non-anaesthetic doses of alphadione (0.15 ml/kg; 0.3 ml/kg; 0.6 ml/kg and 1.2 ml/kg i.p.) had sedative effects decreasing selectively the MUA in the MRF. In doses of 2.0 ml/kg, 2.4 ml/kg and 3.0 ml/kg i.p., alphadione induced anaesthesia which was associated with a rapid decrease of MUA in the MRF and by a gradual decrease of activity in the AH and AMY. The i.p. dose of 3.0 ml/kg abolished MUA responses of the reticular formation to acoustic, visual and somatic stimulation but failed to block responses to pain. Deep anaesthesia with lasting analgesia could be maintained by i.v. infusion (0.075 ml/kg/min). This procedure blocked the responsiveness to painful stimulation while pharyngeal and laryngeal reflexes were maintained. Hexobarbitone in a dose of 20.0 mg/kg i.p. did not produce anaesthesia in the cat. Administration of 40.0 mg/kg i.p. resulted in a rapid decrease of MUA in the MRF, AH and AMY, MUA responses to each stimulation were abolished and the pharyngeal reflex was blocked.

Alfaxalone Alfadolone Mixture↗

PubMed1992

Giant neurons in the caudal pontine reticular formation receive short latency acoustic input: an intracellular recording and HRP-study in the rat.

The reticular formation is composed of heterogeneous cell populations with multiple functions. Among these multiple functions is the processing of sensory information in the context of behavior. The purpose of the present study was to identify and characterize neurons in the reticular formation of the rat that receive auditory input. In order to do so, we combined intracellular electrophysiology in vivo with intracellular injection of horseradish peroxidase, enabling us to correlate electrophysiology unequivocally with anatomy at the single cell level. We found that many neurons in the caudal pontine reticular nucleus (PnC), which we analyzed intracellularly, responded to acoustic stimuli and were excited at short latency (mean EPSP latency: 2.6 ms; mean spike latency: 5.2 ms). This short latency suggests a direct input from the cochlear nucleus, the first central nucleus of the auditory pathway. The morphology revealed that the acoustically driven PnC neurons have very large somata (mean diameter: 44.0 microns). They can therefore be referred to as "giant PnC neurons." Complex dendritic arbors extended from these neurons into the reticular formation and thus formed a large membrane surface for the integration of multimodal inputs. Most of the giant PnC neurons sent their axons caudally into the medial longitudinal fasciculus and can therefore be regarded as reticulospinal neurons. The results demonstrate that the giant reticulospinal PnC neurons are in a position to transmit acoustic information very quickly to spinal cord neurons and to receive converging input from other parts of the brain. They are thus good candidates for participation in the mediation and modulation of acoustically elicited behaviors, such as the short latency acoustic startle response.

Acoustic Stimulation↗

PubMed1983

Paralemniscal reticular formation: response of cells to a noxious stimulus.

Extracellular single unit recordings were made in the paralemniscal reticular formation in adult male rats. A majority of the cells studied were characterized as nociceptive because a noxious stimulus evoked a change (either an increase or decrease) in their spontaneous firing rates. Norepinephrine (NE) administered microiontophoretically usually mimicked the response to the noxious stimulus (foot pinch). After a neuron had been characterized with respect to its response to NE and the noxious stimulus, horseradish peroxidase (HRP) was iontophoretically ejected from the micropipette. Following iontophoresis of HRP into the paralemniscal reticular formation, retrograde and orthograde labeling was observed in the periaqueductal gray and the nucleus raphe magnus. These data support a possible role of the paralemniscal reticular formation in an endogenous analgesic system.

Animals↗

PubMed1981

Effect of morphine administered in the periaqueductal gray and at the recording locus on nociresponsive neurons in the medullary reticular formation.

Neurons in the medullary reticular formation (MRF) contained within the nuclei reticularis gigantocellularis and reticularis paragigantocellularis were evaluated for their responses to morphine administered in the periaqueductal gray (PAG) and iontophoresed at the recording site. Morphine had a predominant excitatory effect on neurons in the MRF whether microinjected in the PAG or iontophoresed at the recording locus. Although morphine generally excited neurons in the MRF when administered at either site, examination of individual neurons for their responses to both modes of administration of morphine indicated that the effect produced by morphine administered in the PAG was rarely mimicked by morphine iontophoresed at the recording locus. Moreover, morphine administered in the PAG markedly attenuated the noxious evoked excitatory response of MRF neurons, an effect not reliably produced by morphine iontophoresed in the MRF when microinjected in the PAG is not mediated by an enkephalinergic interneurons. The implications of these results on the role of the MRF in opiate-induced antinociception are discussed.

Animals↗

PubMed1962

Functional organization of the brain stem reticular formation and sensory input.

Injections of 20 microg of adrenaline, dissolved in 10, microl of Tyrode solution, directly into the brain stem reticular formation, are followed by a transient increase in the amplitude of the cortical-evoked response obtained from single-shock stimulation of the optic chiasma, while injections of the same amount of acetylcholine produce a transient decrease. Furthermore, injections of procaine in the medial region of the rostral pontine reticular formation are followed by a long-lasting increase in the amplitude of these evoked responses, while the same injections at mesencephalic levels produce a marked decrease. These findings are interpreted in terms of the presence, in the reticular formation, of two antagonistic ascending systems: one adrenergic, the other cholinergic, whose tonic activity originates in the mesencephalic tegmentum in one case and in the caudal regions of the brain stem in the other.

Acetylcholine↗

PubMed1984

Distribution of corticospinal neurons with collaterals to lower brain stem reticular formation in cat.

The fluorescent retrograde double-labeling technique has been used to determine whether corticospinal neurons in the cat sensorimotor cortex distribute collaterals to the lower brain stem reticular formation. In this study the fluorescent tracers Nuclear Yellow and Diamidino Yellow 2HCl were used in combination with Fast Blue. One tracer was injected unilaterally in the spinal cord and the other was injected ipsilaterally in the bulbar medial reticular formation. The distribution of the retrogradely labeled neurons was studied in the contralateral hemisphere. In the sensorimotor cortex a large population of neurons was found which were labeled from the spinal cord and were double-labeled from the brain stem. These branching neurons were concentrated in the rostromedial part of the area 4 and the adjoining lateral part of area 6. In this region the percentages of corticospinal neurons which were double-labeled from the brain stem ranged from 5% laterally to 30% medially. In two cats it was demonstrated by means of the anterograde transport of HRP that the corticobulbar fibers from this region which must include the corticospinal collaterals are distributed to the reticular formation of the lower brain stem. In view of the fact that the double-labeled neurons are concentrated in the anterior part of the motor cortex, those branching neurons are in all likelihood involved in the control of neck, back and shoulder movements. This control is probably exerted by way of two routes i.e. by way of the direct corticospinal connections to spinal interneurons, and by way of the indirect cortico-reticulospinal connections established by the cortical fibers to the bulbar reticular formation. The present findings suggest that this dual control may be exerted by one and the same cell.

Animals↗

PubMed1996

Injection of a GABA antagonist into the mesopontine reticular formation abolishes haloperidol-induced catalepsy in rats.

THE pedunculopontine nucleus and its adjacent structure of the mesopontine reticular formation are known as a mesencephalic locomotor region, since either electrical or chemical stimulation of these regions induces locomotion in decerebrate animals. In parkinsonism, it is presumed that the pedunculopontine nucleus is under GABAergic overinhibition from the basal ganglia. To reveal the behavioural effects of GABAergic disinhibition of the mesopontine reticular formation in parkinsonism, picrotoxin, a GABAA antagonist, (5 or 10 ng/ 0.25 microliter) or vehicle was injected unilaterally into the mesopontine reticular formation of rats via implanted cannulae after induction of catalepsy using haloperidol (1.5 mg kg-1, i.p.). Injection of the larger dose of picrotoxin, but not the smaller dose nor the vehicle, abolished the catalepsy with or without spontaneous locomotor activity. The present result suggests that the disinhibition of the brainstem output structures contributes to the recovery of mobility in the cataleptic state induced by blocking the dopaminergic transmission of the basal ganglia.

Animals↗

PubMed1987

Motoneuron properties during motor inhibition produced by microinjection of carbachol into the pontine reticular formation of the decerebrate cat.

It is well established that cholinergic agonists, when injected into the pontine reticular formation in cats, produce a generalized suppression of motor activity (1, 3, 6, 14, 18, 27, 33, 50). The responsible neuronal mechanisms were explored by measuring ventral root activity, the amplitude of the Ia-monosynaptic reflex, and the basic electrophysiological properties of hindlimb motoneurons before and after carbachol was microinjected into the pontine reticular formation of decerebrate cats. Intrapontine microinjections of carbachol (0.25-1.0 microliter, 16 mg/ml) resulted in the tonic suppression of ventral root activity and a decrease in the amplitude of the Ia-monosynaptic reflex. An analysis of intracellular records from lumbar motoneurons during the suppression of motor activity induced by carbachol revealed a considerable decrease in input resistance and membrane time constant as well as a reduction in motoneuron excitability, as evidenced by a nearly twofold increase in rheobase. Discrete inhibitory postsynaptic potentials were also observed following carbachol administration. The changes in motoneuron properties (rheobase, input resistance, and membrane time constant), as well as the development of discrete inhibitory postsynaptic potentials, indicate that spinal cord motoneurons were postsynaptically inhibited following the pontine administration of carbachol. In addition, the inhibitory processes that arose after carbachol administration in the decerebrate cat were remarkably similar to those that are present during active sleep in the chronic cat. These findings suggest that the microinjection of carbachol into the pontine reticular formation activates the same brain stem-spinal cord system that is responsible for the postsynaptic inhibition of alpha-motoneurons that occurs during active sleep.

Action Potentials↗

PubMed2003

Dialysis delivery of an adenosine A1 receptor agonist to the pontine reticular formation decreases acetylcholine release and increases anesthesia recovery time.

BACKGROUND: Adenosine modulates cell excitability, acetylcholine release, nociception, and sleep. Pontine cholinergic neurotransmission contributes to the generation and maintenance of electroencephalographic and behavioral arousal. Adenosine A(1) receptors inhibit arousal-promoting, pontine cholinergic neurons, and adenosine enhances sleep. No previous studies have determined whether pontine adenosine also modulates recovery from anesthesia. Therefore, the current study tested the hypotheses that dialysis delivery of the adenosine A(1) receptor agonist N6-p-sulfophenyladenosine (SPA) into the pontine reticular formation would decrease acetylcholine release and increase the time needed for recovery from halothane anesthesia. METHODS: A microdialysis probe was positioned in the pontine reticular formation of halothane-anesthetized cats. Probes were perfused with Ringer's solution (control) followed by the adenosine A(1) receptor agonist SPA (0.088 or 8.8 mm). Dependent measures included acetylcholine release and a numeric assessment of recovery from anesthesia. An intensive, within-subjects design and analysis of variance evaluated SPA's main effect on acetylcholine release and anesthetic recovery. The adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 microm) was coadministered with SPA to test for antagonist blocking of SPA's effects. RESULTS: SPA significantly (P < 0.0001) decreased acetylcholine release in the pontine reticular formation and significantly (P < 0.0001) delayed recovery from anesthesia. Coadministration of SPA and DPCPX caused no decrease in acetylcholine release or delay in postanesthetic recovery. Dialysis delivery of SPA into the cerebellar cortex confirmed that the SPA effects were site-specific to the pontine reticular formation. CONCLUSION: The results provide a novel extension of the sleep-promoting effects of adenosine by showing that pontine delivery of an adenosine A(1) receptor agonist delays resumption of wakefulness following halothane anesthesia. This extension is consistent with a potentially larger relevance of the current findings for efforts to specify neurons and molecules causing physiologic and behavioral traits comprising anesthetic states. These data support the conclusion that adenosine A(1) receptors in medial regions of the pontine reticular formation, known to modulate sleep, also contribute to the generation and/or maintenance of halothane anesthesia.

Acetylcholine↗

PubMed2000

Infusion of adenylyl cyclase inhibitor SQ22,536 into the medial pontine reticular formation of rats enhances rapid eye movement sleep.

Microinjection of cholinergic and adenosinergic agonists into the medial pontine reticular formation of rats produces long lasting increases in the time spent in rapid eye movement sleep. Several G-protein-coupled muscarinic and adenosinergic receptors share a common action of inhibition of adenylyl cyclase and inhibition of cyclic adenosine monophosphate. Inhibition of cyclic adenosine monophosphate has been implicated in the mechanism of rapid eye movement sleep induction in the cat. We sought to determine whether a direct inhibitor of adenylyl cyclase microinjected into the rat reticular formation at sites where muscarinic and adenosinergic agonists are effective in producing long lasting elevations in rapid eye movement sleep also result in similar effects on the sleep/wake cycle. The caudal, oral pontine reticular formation was unilaterally infused with 60 nl volumes of carbachol (0.1-1.1mM) and N(6)-cyclohexyladenosine (0.1mM) each within 1h of lights on. Sites effective for significantly elevating rapid eye movement sleep for the 8h following microinjection of both receptor agonists were additionally injected with the adenylyl cyclase inhibitor, SQ22,536 (0.1M). Pontine injections of SQ22,536 resulted in significant mean increases in rapid eye movement sleep time and rapid eye movement sleep period frequency at all of these sites. As with the receptor agonists, SQ22,536 did not alter latency to rapid eye movement sleep onset. Rapid eye movement sleep amounts were observed to be significantly elevated by SQ22,536 at two days, but not at four days, following a single microinjection. These data implicate inhibition of cyclic adenosine monophosphate in the pons of the rat as a mechanism involved in the long-term modulation of rapid eye movement sleep. This mechanism may underlie the homeostatic regulation exhibited by this sleep-state.

Adenine↗

PubMed1989

Cholinergic activation of medial pontine reticular formation neurons in vitro.

Direct microinjection of cholinergic compounds into pontine reticular formation furnishes an excellent phenomenological model of the rapid eye movement phase of sleep (REM), but the mechanisms underlying this effect and whether they mimic the cellular events of natural REM remain unknown. Data presented here from intracellular recordings in vitro in the rat demonstrate that two-thirds of medial pontine reticular formation neurons respond to application of 0.5-1.0 microM carbachol with a depolarization characterized by a decreased conductance and a linear I/V curve. The resultant mimicry of REM cellular events by carbachol extends to membrane potential depolarization, increased cellular excitability, enhancement of PSPs from reticular stimulation, and the absence of a burst discharge pattern. The presence of these effects with tetrodotoxin and their blockade by atropine imply a direct, muscarinic cholinergic mediation. Other neurons tested responded with either a biphasic hyperpolarization-depolarization or a hyperpolarization. The hyperpolarization was associated with an increased conductance which exhibited pronounced inward rectification, an effect novel for cholinergic agonists in vertebrate CNS but described in heart cells.

Action Potentials↗

PubMed1980

Reciprocal connections between substantia nigra and medullary reticular formation in the rat.

Electrophysiological analysis shows reciprocal connections between substantia nigra and medullary reticular formation (nucleus reticularis giganto celullaris). The nigro-reticular connection appears to be monosynaptic, as shown by antidromic activation, and comprises an ipsi and a contralateral component. Its effect is mainly inhibitory. The reticulonigral component produces mainly excitatory effects and includes fibres from nucleus giganto celullaris and nucleus parvocelullaris in the medullary reticular formation.

Afferent Pathways↗

PubMed1995

Distribution of Fos-like immunoreactivity in the caudal medullary reticular formation following noxious facial stimulation in the rat.

To investigate the topographic organization of nociceptive neurons in the caudal medullary reticular formation, the distribution of cells that exhibit c-fos expression was examined following a unilateral noxious facial stimulus: subcutaneous injection of formalin into the vibrissal pad of awake rats. Labelling for Fos-like immunoreactivity was present in a somatotopic distribution in a region of the lateral reticular formation adjacent to trigeminal nucleus caudalis, which corresponds approximately to lamina V of the medullary dorsal horn. Labelling in adjacent regions of the reticular formation showed no somatotopy but was predominantly ipsilateral. Contralateral labelling was concentrated ventrolaterally around the lateral reticular nucleus and dorsally near the nucleus of the solitary tract.

Animals↗

PubMedDate not supplied

Effect of stimulation of bulbar reticular formation on long latency discharges in the region of nucleus centralis lateralis of thalamus.

Electrical stimulation of medial medullary reticular formation of rabbits was found to have marked inhibitory effect on nociceptive discharges of neurons in the region of centrolateral nucleus of thalamus. Among the 32 nociceptive units tested, 15 showed the inhibitory effect, 3 the facilitatory, and 14 no effect. Comparison between the effect of direct stimulation of medial medullary reticular formation and that of the electric needling on the same neurons revealed a general resemblance of the two in many respects. These findings suggest that the nucleus reticularis gigantocellularis in medial bulbar reticular formation may serve as an important relay station in the transmission of the analgesic effect of acupuncture.

Acupuncture Therapy↗