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PubMed1983

Actions of GABA, glycine, methionine-enkephalin and beta-endorphin compared with electrical stimulation of nucleus raphe magnus on responses evoked by tooth pulp stimulation in the medial reticular formation in the cat.

In decerebrate, cerebellectomized cats, a comparison was made between the effects of electrical stimulation in nucleus raphe magnus (NRM) and iontophoretic application of GABA, glycine, met-enkephalin and beta-endorphin on the responses of neurones in the medial brain stem reticular formation to tooth pulp stimulation. NRM stimulation, GABA, glycine and enkephalin produced a short lasting inhibition of tooth pulp evoked responses whilst the time course of the inhibition produced by beta-endorphin was much slower, often lasting up to 1 h following a 3-7 min ejection period. The effects of GABA and glycine could be antagonised by iontophoresis of bicuculline and strychnine respectively whilst intravenous injection of naloxone antagonised the inhibition induced by the opioid peptides. In most neurones tested, inhibition of tooth pulp evoked responses by NRM stimulation was blocked by iontophoretic application of bicuculline but not by strychnine or naloxone (i.v.). We conclude that GABA may act as a transmitter which mediates the inhibitory effects of NRM on the responses of reticular neurones to tooth pulp stimulation. Thus GABA may be involved in stimulation produced analgesia.

Animals↗

PubMed1984

Inhibition of primate spinothalamic tract neurons by stimulation in periaqueductal gray or adjacent midbrain reticular formation.

Recordings were made from spinothalamic tract (STT) cells in the lumbosacral enlargement of anesthetized monkeys. The cells were identified by antidromic activation from the contralateral ventral posterior lateral nucleus of the thalamus. Electrical stimulation at sites within the periaqueductal gray, the adjacent midbrain reticular formation, or the deep layers of the tectum were found to inhibit the activity of STT cells. In general, midbrain stimulation inhibited the background discharges and the responses of wide dynamic range cells evoked by innocuous and noxious cutaneous stimulation (29 of 37 cases). However, for six cells, midbrain stimulation preferentially inhibited the responses to noxious stimulation. The evoked responses of all 10 high-threshold cells were inhibited. In only two cases was midbrain stimulation ineffective, and no excitatory effects were observed. The mean latency to onset of inhibition resulting from midbrain stimulation was 24.9 +/- 7.2 ms (n = 35). The amount of inhibition produced by midbrain stimulation was graded with stimulus intensity. For example, trains of stimuli (333 Hz) at 50 microA produced a mean inhibition to 81.7 +/- 16.6% of control, while 200 microA resulted in a mean inhibition to 36.3 +/- 21.7%. Not only was the inhibition increased by the use of stronger current intensities, but the duration of inhibition was prolonged. Midbrain stimulation inhibited the responses of STT cells to volleys in both the A-fibers and the C-fibers of the sural nerve. However, there was a selective action in that the responses to C-fiber volleys were more strongly inhibited than were the responses to A-fiber volleys. Lesions placed in the white matter of the upper cervical spinal cord reduced the inhibition produced by stimulation in either the midbrain or the nucleus raphe magnus. The extent to which the inhibition was reduced was proportional to the extent of the cord lesions. However, even when there was an interruption of the entire lateral funiculus on the side of an STT cell and of the dorsal quadrant of the contralateral side, there was still substantial inhibition following stimulation in either brain stem site. It is concluded that while part of the inhibition is mediated by pathways descending in the dorsal lateral funiculus (DLF), at least some depends on pathways coursing through the ventral spinal cord. Inhibition of STT cells may contribute to the neuronal mechanism of the analgesia that results from stimulation in the periaqueductal gray matter in awake, behaving animals.

Animals↗

PubMed2004

Kynurenate in the pontine reticular formation inhibits acoustic and trigeminal nucleus-evoked startle, but not vestibular nucleus-evoked startle.

The startle reflex is elicited by acoustic, trigeminal or vestibular stimulation, or by combinations of these stimuli. Acoustic startle is mediated largely by ibotenate-sensitive neurons in the ventrocaudal pontine reticular formation (PnC). In these studies we tested whether startle elicited by stimulation of different modalities is affected by infusion of the non-selective glutamate antagonist, kynurenate, into the PnC. In awake rats, startle responses evoked by either acoustic or spinal trigeminal nucleus stimulation were inhibited by kynurenate, but not saline, infusions, with the most effective placements nearest PnC. In chloral hydrate-anesthetized rats, kynurenate in the PnC reduced trigeminal nucleus-evoked hindlimb EMG responses, but not vestibular nucleus-evoked startle. Kynurenate in the vestibular nucleus had no effect on trigeminal nucleus-evoked startle. These results indicate that trigeminal nucleus stimulation evokes startle largely through glutamate receptors in the PnC, similarly to acoustic startle, but vestibular nucleus-evoked startle is mediated through other pathways, such as the vestibulospinal tract.

Animals↗

PubMed1990

Functional organization within the medullary reticular formation of intact unanesthetized cat. I. Movements evoked by microstimulation.

1. The present article described the various patterns of movement evoked in the limbs and neck by microstimulation (33-ms trains, 330 Hz, 0.2-ms pulses at less than or equal to 35 microA) of the medullary reticular formation (MRF) of seven chronically implanted, unanesthetized, intact cats. Altogether 878 loci were stimulated in 83 penetrations. However, as stimulation in the more lateral regions of the MRF was less effective, the results are based on stimulation in 592 loci made in 56 penetrations at distances of between 0.5 and 2.5 mm lateral to the midline. 2. Of these 592 loci, movement of one or more parts of the body was evoked from a total of 539 (91%) sites. Most of these movements were compound in nature, involving movement of one or more limbs as well as the head. Discrete movements were observed only with respect to the head; limb movements were always accompanied by head movement. In addition, hindlimb movements were always accompanied by forelimb movements, although the inverse was generally not true. 3. The most common effects of the stimulation were as follows: a turning of the head to the ipsilateral side (79% of stimulated sites); flexion of the ipsilateral elbow (41%); and extension of the contralateral elbow (45%). Effects in the hindlimbs were more variable and less frequent, with the majority of the effective loci causing flexion of the ipsilateral knee (9%) together with extension of the contralateral knee (8%). In total, including both flexion and extension, 18% of the stimulated sites caused movement of the ipsilateral hindlimb and 11% of the contralateral hindlimb. 4. Although movements of the head were obtained from the whole extent of the brain stem, movements of the forelimbs showed a dorsoventral organization with flexion of the ipsilateral elbow being evoked from the more dorsal regions of the brain stem, whereas contralateral elbow extension was evoked more frequently from the ventral regions. There was a large area of overlap from which movements of both limbs could be obtained simultaneously. Movements of the hindlimbs were more frequently evoked from central and ventral areas of the brain stem and from the most rostral aspect of the explored region. 5. In examining the combinations of movements evoked by the MRF stimulation, it was found that the most commonly evoked pattern was movement of the head to the stimulated side together with flexion of the ipsilateral forelimb and extension of the contralateral forelimb (26.5% of sites).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1984

Role of mesencephalic reticular formation in cholinergic-induced catalepsy and anticholinergic reversal of neuroleptic-induced catalepsy.

The present experiments investigate the brain sites involved in the elicitation of catalepsy by cholinergic agonists and neuroleptics. Microinjection of acetylcholine chloride (50 micrograms) in combination with eserine (2.5 micrograms) into the ventral mesencephalic reticular formation (MRF) elicited catalepsy. Microinjection of atropine sulfate (5 micrograms) into the same sites reversed the catalepsy of rats treated with haloperidol (1.5 mg/kg) 2 h earlier, but did not reverse morphine-induced (30 mg/kg, 1 h) catalepsy. Haloperidol (25 micrograms) injected into the nucleus accumbens septi (NAS) resulted in catalepsy as severe as that caused by an identical injection into the caudate nucleus. Catalepsy caused by intraNAS haloperidol occurred with a shorter latency than that resulting from intracaudate haloperidol, and was reversed by systemic scopolamine (0.4 mg/kg). On the basis of these results it is suggested that the ventral MRF is a site for the elicitation of catalepsy by cholinergic agonists and for the reversal of neuroleptic-induced catalepsy by anticholinergics, and that neuroleptic-induced catalepsy involves blockade of dopamine receptors in both the NAS and caudate nucleus.

Acetylcholine↗

PubMed1980

[Anticonvulsive effect of stimulation of the mesencephalic reticular formation in animals with experimental photogenic epilepsy].

Experimental photogenic epilepsy in rats was induced by injections of microdoses of tetanus toxin into the lateral geniculate body (LGB). One day after injection the animals developed epileptic paroxysms (EP) which were seen at 10--15-minute intervals. Under these conditions the mesencephalic reticular formation (MRF) was continuosly stimulated for 40 min (at a frequency of 0.2 Hz, 0.8 B). In 4 out of 12 animals EP completely ceased both during MRF stimulation and for 1--2 hours following stimulation. In 6 animals, the frequency of EP decreased. Inhibition of EP was not followed by cessation of interparoxysmal discharges. Participation of MRF in the genesis of photogenic stimulation is discussed.

Animals↗

PubMed2004

Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex.

The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (P<0.01) decrease (-28%) in ACh release in the frontal association cortex, a significant (P<0.01) decrease (-23%) in respiratory rate, and a significant (P<0.01) increase (223%) in time to righting after anesthesia. Additional in vitro studies used the [(35)S]guanylyl-5'-O-(gamma-thio)-triphosphate ([(35)S]GTPgammaS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain. In vitro treatment with carbachol (1 mM) caused a significant (P<0.01) increase in [(35)S]GTPgammaS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration-dependent and blocked by atropine, indicating that the carbachol-stimulated [(35)S]GTPgammaS binding was mediated by muscarinic cholinergic receptors. Together, the in vitro and in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.

Acetylcholine↗

PubMed1984

Differential effect of antiepileptic and non-antiepileptic drugs on the reticular formation.

The effect of the antiepileptic drugs carbamazepine and phenytoin, and of the non-antiepileptic drug baclofen, was compared on various inhibitory and excitatory mechanisms in the feline trigeminal nucleus. Baclofen resembled carbamazepine and phenytoin in depressing segmental excitatory and facilitating segmental inhibitory mechanisms. However, baclofen facilitated the periventricular and periaqueductal inhibition of the trigeminal nucleus, while carbamazepine and phenytoin depressed these descending inhibitory mechanisms. Baclofen also resembles carbamazepine and phenytoin in its effectiveness in trigeminal neuralgia, but baclofen is not a clinically effective antiepileptic agent. Our experiments indicate that the ability to depress the reticular formation of the diencephalon and midbrain is an important characteristic of antiepileptic drugs. This suggests that the reticular core is involved in the spread and generalization of seizures.

Action Potentials↗

PubMed1984

The effect of lesions in the mesencephalic reticular formation upon conditioned avoidance responses in rat. II. Lesions of the area cuneiformis.

Hooded rats of the Long-Evans strain were not able to acquire a conditioned avoidance response (CAR) in a jump test when they were injured by bilateral symmetric lesions in the area cuneiformis (CU) of the mesencephalic reticular formation. The acquisition of a simple CAR in a Y-maze was not impaired irrespective of the size of the lesion. However, lesioned rats ran significantly slowlier to the maze exit in simple and discrimination tasks and displayed more erroneous runs in dark-light discrimination sessions. These deficits were not observed when rats with small lesions in the anterior CU (CU-1 group) had preoperatively learnt the dark-light discrimination, but they were observed when preoperatively trained rats were injured by caudally extended lesions (CU-2 group). After preoperative training CU-1 rats had a great retention deficit in the jump test compared with no deficit in a sham-operated group. They were unable to relearn the task, whereas rats with dorsally extended lesions including the nucleus commissurae posterioris (NCP-CU group) had less deficit and relearnt the CAR in the jump test. Animals of this group performed an enhanced number of intertrial responses and showed increased arrest reactions with goal-directed attention evoked by the conditioned stimulus. The results indicate - together with the observed behavioural syndrome of disturbed locomotion, reduced orienting responses and exploratory behaviour - that the CU is an important structure for the integration of goal-directed behaviour.

Animals↗

PubMed1993

Microdialysis of the pontine reticular formation reveals inhibition of acetylcholine release by morphine.

BACKGROUND: Systemically administered morphine inhibits rapid eye movement (REM) sleep; however, the neuronal mechanisms through which morphine disrupts REM sleep remain poorly understood. Recently, the authors have shown that morphine-mediated REM sleep inhibition is localized to a specific region of the pontine reticular formation: the gigantocellular tegmental field (FTG). Because cholinergic neurotransmission in the FTG is known to play a role in REM sleep generation, the present study examined the hypothesis that systemically administered morphine would cause decreased acetylcholine release in the FTG. METHODS: Microdialysis probes were stereotaxically positioned in the FTG of six barbiturate-anesthetized cats to measure acetylcholine release. Cholinergic input to the FTG arises from the laterodorsal (LDT) and pedunculopontine tegmental (PPT) brain stem nuclei. By electrically stimulating the LDT and PPT, it was possible to measure stimulation-evoked acetylcholine release in the FTG. Morphine sulfate (MSO4) was administered intravenously (500 micrograms.kg-1). High performance liquid chromatography with electrochemical detection was used to measure stimulation-evoked acetylcholine release in the FTG before and after the systemic administration of morphine sulfate. RESULTS: Acetylcholine release in the pontine FTG was depressed significantly (P < 0.01) by systemic morphine sulfate. Acetylcholine release without electrical stimulation of the LDT and PPT averaged 0.6 +/- 0.18 (mean +/- SD) pmol/10 min of dialysis. Before morphine sulfate was administered, electrical stimulation of cholinergic LDT and PPT neurons increased acetylcholine release within the FTG to 1.9 +/- 0.76 pmol/10 min. After morphine sulfate was administered, there was a 37% decrease in acetylcholine release within the FTG to average values of 1.2 +/- 0.63 pmol/10 min. There was no significant effect of morphine sulfate on spontaneous acetylcholine release in the absence of LDT and PPT stimulation. CONCLUSIONS: Because FTG levels of acetylcholine release increase during REM sleep, the present results are consistent with the hypothesis that diminished acetylcholine release in the pontine FTG comprises one mechanism by which morphine inhibits REM sleep.

Acetylcholine↗

PubMed1986

Immunohistochemical evidence of plasticity of gamma-aminobutyric acid neurons in the red nucleus and adjacent reticular formation after contralateral cerebellectomy in the adult cat.

A comparative mapping of gamma-aminobutyric acid neurons identified by means of glutamic acid decarboxylase (GAD) immunohistochemistry was performed in the red nucleus (RN) in both intact and hemicerebellectomized adult cats (21 days postoperative). In the deafferented RN (contralateral to the lesion) as well as in the adjacent dorsolateral reticular formation, a marked increase in the number of GAD-positive perikarya was observed. In this mesencephalic area, some neurons may therefore increase their endogenous levels of immunodetectable GAD, as a response to cerebellar deafferentation. This can be viewed as one of the events contributing to functional recovery.

Animals↗

PubMed2006

Role of the parvicellular reticular formation in facilitating the jaw-opening reflex in rats by stimulation of the red nucleus.

In a previous study, we have shown that electrical and chemical stimulation of the red nucleus (RN) facilitates the jaw-opening reflex (JOR). The RN sends projection fibers bilaterally, with contralateral dominance, to the part of the parvicellular reticular formation (RFp) containing premotor neurons projecting to the trigeminal motor nucleus. This implies that RN-induced facilitation of the JOR might be mediated via last-order neurons in the RFp. Here, we address this issue by investigating whether microinjection of lidocaine or l-glutamate into the RFp affects RN-induced modulation of the JOR. Experiments were performed on rats anesthetized with urethane-chloralose. The JOR was evoked by electrical stimulation of the inferior alveolar (IA) nerve and was recorded as an electromyographic response from the anterior belly of the digastric muscle. Conditioning stimulation was delivered unilaterally to the RN 12 ms before the IA test stimulation. We found that local injections of 2% lidocaine (0.5 microl) into the RFp, contralateral to the RN, significantly (P < 0.05) reduce RN-induced facilitation of the JOR, whereas corresponding injections of 0.1 mM l-glutamate (0.5 microl) significantly (P < 0.05) increase it. These results suggest that the facilitatory effect of RN stimulation on the JOR is mediated partly by a relay in the RFp.

Anesthetics, Local↗

PubMed1990

Differentiation of the brain stem reticular formation in the triturus, Triturus pyrrhogaster.

The brain stem of the triturus was observed to be initially composed exclusively of the mantle layer. A few days before hatching, a narrow marginal layer differentiated peripherally. At the time of hatching, the marginal layer was clearly visible throughout the brain stem, except for in a medial region of the optic tectum. Approximately one week after hatching, a few cells migrated into the marginal layer, and almost simultaneously, a few fibers in that layer were myelinated. Cells migrating into the marginal layer formed reticular neurons as well as the raphe nuclei and superficial cellular layers of the optic tectum. As the development proceeded, the number of myelinated fibers in the marginal layer increased, and cells in that layer, especially reticular neurons, were seen to be embedded among numerous myelinated fibers, assuming the characteristic features of the reticular formation.

Animals↗

PubMed2000

Isoflurane action in the spinal cord blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats.

BACKGROUND: Isoflurane depresses the electroencephalographic (EEG) activity and exerts part of its anesthetic effect in the spinal cord. The authors hypothesized that isoflurane would indirectly depress the EEG and subcortical response to noxious stimulation in part by a spinal cord action. METHODS: Depth electrodes were inserted into the midbrain reticular formation (MRF) and thalamus of six of seven isoflurane-anesthetized goats, and needle-electrodes were placed into the skull periosteum. In five of seven goats, an MRF microelectrode recorded single-unit activity. The jugular veins and carotid arteries were isolated to permit cranial bypass and differential isoflurane delivery. A noxious mechanical stimulus (1 min) was applied to a forelimb dewclaw at each of two cranial-torso isoflurane combinations: 1.1+/-0.3%-1.2+/-0.3% and 1.1+/-0.3-0.3+/-0.1% (mean +/- SD). RESULTS: When cranial-torso isoflurane was 1.1-1.2%, the noxious stimulus did not alter the EEG. When torso isoflurane was decreased to 0.3%, the noxious stimulus activated the MRF, thalamic, and bifrontal-hemispheric regions (decreased high-amplitude, low-frequency power). For all channels combined, total (-33+/-15%), delta(-51+/-22%), theta (-33+/-19%), and alpha (-26+/-16%) power decreased after the noxious stimulus (P<0.05); beta power was unchanged. The MRF unit responses to the noxious stimulus were significantly higher when the spinal cord isoflurane concentration was 0.3% (1,286+/-1,317 impulses/min) as compared with 1.2% (489+/-437 impulses/min, P<0.05). CONCLUSIONS: Isoflurane blunted the EEG and MRF-thalamic response to noxious stimulation in part via an action in the spinal cord.

Anesthetics, Inhalation↗

PubMed1983

NADPH-diaphorase: a selective histochemical marker for the cholinergic neurons of the pontine reticular formation.

Choline acetyltransferase immunohistochemistry has identified a large group of cholinergic neurons in the pontine tegmentum. By combined immunohistochemical and enzyme histochemical studies this particular cholinergic cell group was found to contain an enzyme, NADPH-diaphorase, that can be visualized histochemically. Thus NADPH-diaphorase histochemistry provides a simple, reliable method to selectively stain the cholinergic neurons of the brainstem reticular formation. The resolution obtained by this novel histochemical technique is similar to that found with the Golgi stain, and it should therefore be of great value in morphological studies of this cholinergic cell group.

Animals↗

PubMed1979

Combined dynamics of EEG and evoked potentials. II. Studies of simultaneously recorded EEG-EPograms in the auditory pathway, reticular formation, and hippocampus of the cat brain during sleep.

This study is carried out on single (not averaged) recordings combining the spontaneous activity preceding the stimulus onset and the EP recorded upon acoustical stimulation. These recordings, which we call EEG-EPograms, are measured simultaneously from different subdural structures, such as the auditory cortex, medial geniculate nucleus, inferior colliculus, reticular formation and the hippocampus of the cat brain during the slow wave sleep stage. Using a combined analysis procedure (C.A.P.), the relevant frequency components of spontaneous EEG and EPs, recorded simultaneously from these brain nuclei, are analyzed according to the consistent selectivity bands depicted by the determined amplitude-frequency characteristics for the SWS-stage. In parallel with the results which we obtained for the waking stage, these analyses provide also the following information: (1) there is an important congruency in the time courses of simultaneous response components in common frequency bands, especially in the alpha and beta frequency ranges; (2) there exist significant coupling and synchrony between the evoked amplitude enhancements in the simultaneously recorded single response components; (3) the inter-nuclei coherency in the brain's electrical activity is enormously increased upon stimulation;(4) the evoked response magnitude can be predicted, with reasonable accuracy, from the spontaneous activity preceding the stimulus. All these findings are discussed with reference to those obtained for the waking stage.

Animals↗

PubMed2004

Amygdaloid axon terminals are in contact with trigeminal premotor neurons in the parvicellular reticular formation of the rat medulla oblongata.

After ipsilateral injections of biotinylated dextran amine (BDA) into the central nucleus of the amygdala (ACe) and cholera toxin B subunit (CTb) into the motor trigeminal nucleus (Vm) in the rat, numerous BDA-labeled axons with bouton-like varicosities were distributed bilaterally with a clear-cut ipsilateral dominance in the parvicellular reticular formation (RFp), where many CTb-labeled neurons existed bilaterally with slightly ipsilateral dominance. The prominent overlapping distribution of these labeled axons and neurons was found in the RFp region just ventral to the nucleus of the solitary tract and medial to the spinal trigeminal nucleus throughout the caudalmost part of the pons and the rostral half of the medulla oblongata. Within the neuropil of the RFp region in the rostral half of the medulla oblongata, BDA-labeled axons made symmetrical synaptic contacts predominantly with the dendrites and additionally with the somata of RFp neurons, some of which were labeled with CTb. These data suggest that output signals from the ACe may be transmitted disynaptically to the Vm via the RFp neurons in the medulla oblongata for the control of jaw movements.

Amygdala↗

PubMed1979

Combined dynamics of EEG and evoked potentials. I. Studies of simultaneously recorded EEG-EPograms in the auditory pathway, reticular formation, and hippocampus of the cat brain during the waking stage.

This study is carried out on single (not averaged) recordings combining the spontaneous activity preceding the stimulus onset and the EP recorded upon acoustical stimulation. These recordings, which we call EEG-EPograms, are measured simultaneously from different subdural brain structures, such as the auditory cortex, medial geniculate nucleus, inferior colliculus, reticular formation and the hippocampus of awake cats. Using a combined analysis procedure (C.A.P.), the relevant frequency components of spontaneous EEG and EPs, recorded simultaneously from these brain nuclei, are analyzed according to the consistent selectivity bands depicted by the determined amplitude-frequency characteristics. These analyses provide us the following information: (1) there is an important congruency in the time courses of simultaneous response components in common frequency bands, especially in the alpha and beta frequency ranges; (2) there exist significant coupling and synchrony between the evoked amplitude enhancements in the simultaneously recorded single response components; (3) the inter-nuclei coherency in the brain's electrical activity is enormously increased upon stimulation; (4) the evoked response magnitude can be predicted, with reasonable accuracy, from the spontaneous activity preceding the stimulation. The strong dependence of the response magnitude on the stimulus-preceding EEG is explained by means of a model network consisting of a population of relaxation oscillators, which can be brought to different states of synchrony and asynchrony. Some suggestions and comments are also made for investigators working toward theories of signal transmission in the brain.

Animals↗