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PubMedDate not supplied

[Responses of sensomotor cortex neurons of rats to stimulation of the midbrain reticular formation].

High frequency stimulation of the mesencephalic reticular formation produces significant inhibition of neuronal activity in the sensorimotor cortex, the effect being equally observed in both hemispheres. In case of low frequency stimulation, marked difference was observed between the reaction of ipsi- and contralateral neurons. Under these conditions, contralateral neurons produce mainly facilitation responses. In both hemispheres evident predominance of tonic effects was observed which revealed itself in the continuation of the reaction in the poststimulation period. Single shocks applied to the midbrain reticular formation elicited in the cortex the evoked potentials of two types: one with a constant and the other with varying latent periods. The former exhibited a latency of 4-18 msec. Responses with varying latencies were predominant. In general, latent periods were longer in contralateral hemisphere.

Animals↗

PubMed1981

Reticular formation influence on neuronal transmission from perforant pathway through dentate gyrus.

Electrical stimulation of the perforant pathway discharges granule cell synchronously, giving rise to a characteristic evoked potential in the granule cell layer termed here the evoked action potential or EAP. In freely moving rats, we applied 3 pulses of low intensity electrical stimulation to the medullary reticular formation prior to the application of the perforant path pulse. The effect of prior reticular formation stimulation was a marked augmentation of the normal EAP response to the perforant path stimulus. The augmentation was dependent on the behavioral state of the experimental animal (it occurred during slow-wave sleep but not during still, alert behavior) and was eliminated by anesthetic agents. The latency of EAP augmentation effect (minimum effective time interval between application of the reticular formation stimulus and the perforant path pulse) was 13--18 msec. In order to localize the sites in the medullary reticular formation from which EAP augmentation could be elicited, threshold currents for producing the effect were determined during dorso-ventral penetrations of a reticular formation stimulating electrode. EAP augmentation was elicited at low stimulus currents from a relatively broad region of the reticular formation. It was also noted that reticular formation stimulation which produced EAP augmentation always elicited one or more motor responses of the neck, back, face or vibrissae. Subsequent investigation of the pathways underlying these motor responses suggested that the effect of reticular formation stimulation on granule cell excitability was mediated by a polysynaptic pathway, the first segment of which was a projection to cells of nucleus gigantocellularis of the caudal medulla.

Afferent Pathways↗

PubMed1992

Loss of the acoustic startle response following neurotoxic lesions of the caudal pontine reticular formation: possible role of giant neurons.

The effect of the excitotoxic N-methyl-D-aspartate agonist quinolinic acid in the caudal pontine reticular formation on the acoustic startle response was investigated in rats. Bilateral injections of 90 nmol of quinolinic acid led to large lesions in the reticular formation characterized by the loss of all neurons and a marked reduction or even abolition of the acoustic startle response; 18 nmol of quinolinic acid led to smaller lesions characterized by a selective loss of giant neurons within the caudal pontine reticular formation and a reduction of the startle amplitude. The partial correlation analysis revealed that the reduction of the amplitude of the acoustic startle response can be correlated with the loss of the giant neurons (r = 0.575; d.f. = 29; P less than 0.001) but not with the reduction of the number of all neurons (r = 0.207; d.f. = 29; P greater than 0.2) in the caudal pontine reticular formation. These findings were reconciled with electrophysiological and anatomical data indicating that the giant neurons in the caudal pontine reticular formation receive acoustic input and project to motoneurons of the spinal cord. It is concluded that the caudal pontine reticular formation is an important element of the startle pathway and that the giant reticulospinal neurons constitute an important part of the sensorimotor interface mediating this response.

Acoustic Stimulation↗

PubMed1986

An autoradiographic analysis of ascending projections from the medullary reticular formation in the rat.

Ascending projections from the several nuclei of the medullary reticular formation were examined using the autoradiographic method. The majority of fibers labeled after injections of [3H]leucine into nucleus gigantocellularis ascended within Forel's tractus fasciculorum tegmenti which is located ventrolateral to the medial longitudinal fasciculus. Nucleus gigantocellularis injections produced heavy labeling in the pontomesencephalic reticular formation, the intermediate layers of the superior colliculus, the pontine and midbrain central gray, the anterior pretectal nucleus, the ventral midbrain tegmentum including the retrorubral area, the centromedian-parafascicular complex, the fields of Forel/zona incerta, the rostral intralaminar nuclei and the lateral hypothalamic area. Nucleus gigantocellularis projections to the rostral forebrain were sparse. Labeled fibers from nucleus reticularis ventralis, like those from nucleus gigantocellularis, ascended largely in the tracts of Forel and distributed to the pontomedullary reticular core, the facial and trigeminal motor nuclei, the pontine nuclei and the dorsolateral pontine tegmentum including the locus coeruleus and the parabrachial complex. Although projections from nucleus reticularis ventralis diminished significantly rostral to the pons, labeling was still demonstrable in several mesodiencephalic nuclei including the cuneiform-pedunculopontine area, the mesencephalic gray, the superior colliculus, the anterior pretectal nucleus, the zona incerta and the paraventricular and intralaminar thalamic nuclei. The main bundle of fibers labeled by nucleus gigantocellularis-pars alpha injections ascended ventromedially through the brainstem, just dorsal to the pyramidal tracts, and joined Forel's tegmental tract in the midbrain. With the brainstem, labeled fibers distributed to the pontomedullary reticular formation, the locus coeruleus, the raphe pontis, the pontine nuclei, and the dorsolateral tegmental nucleus and adjacent regions of the pontine gray. At mesodiencephalic levels, labeling was present in the rostral raphe nuclei (dorsal, median and linearis), the mesencephalic gray, the deep and intermediate layers of the superior colliculus, the medial and anterior pretectal nuclei, the ventral tegmental area, zona incerta as well as the mediodorsal and reticular nuclei of the thalamus. Injections of the parvocellular reticular nucleus labeled axons which coursed through the lateral medullary tegmentum to heavily innervate lateral regions of the medullary and caudal pontine reticular formation, cranial motor nuclei (hypoglossal, facial and trigeminal) and the parabrachial complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Neural connections of the pontine reticular formation, which connects reciprocally with the nucleus prepositus hypoglossi in the rat.

The pontine reticular formation connected with the nucleus prepositus hypoglossi was studied in the rat using anterograde and retrograde tracer techniques. The area reciprocally connected with the nucleus prepositus hypoglossi was evident in the pontine reticular formation of the rat. The region had intensive reciprocal connections with the ipsilateral subthalamic region, the contralateral pontine reticular formation and the nucleus prepositus hypoglossi. Furthermore, it was confirmed that the region received cholinergic projections mainly from the pedunculopontine tegmental nucleus and the laterodorsal tegmental nucleus, and aminergic projections from the dopaminergic cell groups A13 and A11, noradrenergic cell groups A7, A6 and A5, and the serotoninergic B9 cell group. This region in the rat was considered to be the preoculomotor structure in the function of horizontal gaze corresponding to the paramedian pontine reticular formation in other animals.

Animals↗

PubMed1978

[Ultrastructure of the dendrites of neurons of the brain stem reticular formation in acute hypoxic hypoxia].

In 45 adult rats (Wistar strain) neuronal dendrites of the reticular formation were studied electron microscopically at an acute hypoxic hypoxia. Structural changes in neurons of the reticular formation, were demonstrated to begin, as a rule, in the terminal portions of the dendrites. Dystrophic and destructive changes in dendrites are always more pronounced than in the pericaryon and are not infrequently they terminate in destruction of cytoplasmic islets. Submicroscopic changes in the dendrites are classified according to the dynamics of their development. Taking into consideration a specific role of the neuronal dendrites of the reticular formation under certain physiological conditions, it is possible to conclude that dendritic damage is of major importance in functional disturbance of the reticular formation at hypoxic hypoxia.

Acute Disease↗

PubMed1994

Cholinergic mechanisms in canine narcolepsy--I. Modulation of cataplexy via local drug administration into the pontine reticular formation.

Cataplexy in the narcoleptic canine has been shown to increase after systemic administration of cholinergic agonists. Furthermore, the number of cholinergic receptors in the pontine reticular formation of narcoleptic canines is significantly elevated. In the present study we have investigated the effects of cholinergic drugs administered directly into the pontine reticular formation on cataplexy, as defined by brief episodes of hypotonia induced by emotions, in narcoleptic canines. Carbachol and atropine were perfused through microdialysis probes implanted bilaterally in the pontine reticular formation of freely moving, narcoleptic and control Doberman pinschers. Cataplexy was quantified using the Food-Elicited Cataplexy Test, and analysed using recordings of electroencephalogram, electrooculogram and electromyogram. Cataplexy was characterized by a desynchronized electroencephalogram and a drop in electromyogram and electrooculogram activity. In narcoleptic canines, both unilateral and bilateral carbachol (10(-5) to 10(-3) M) produced a dose-dependent increase in cataplexy, which resulted in complete muscle tone suppression at the highest concentration. In control canines, neither bilateral nor unilateral carbachol (10(-5) to 10(-3) M) produced cataplexy, although bilateral carbachol, did produce muscle atonia at the highest dose (10(-3)). The increase in cataplexy after bilateral carbachol (10(-4) M) was rapidly reversed when the perfusion medium was switched to one containing atropine (10(-4) M). Bilateral atropine (10(-3) to 10(-2) M) alone did not produce any significant effects on cataplexy in narcoleptic canines; however, bilateral atropine (10(-2) M) did reduce the increase in cataplexy produced by systemic administration of physostigmine (0.05 mg/kg, i.v.). These findings demonstrate that cataplexy in narcoleptic canines can be stimulated by applying cholinergic agonists directly into the pontine reticular formation. The ability of atropine to inhibit locally and systemically stimulated cataplexy indicates that the pontine reticular formation is a critical component in cholinergic stimulation of cataplexy. Therefore, it is suggested that the pontine reticular formation plays a significant role in the cholinergic regulation of narcolepsy.

Analysis of Variance↗

PubMedDate not supplied

[Effect of acetylcholine, L-glutamate, serotonin and mezaton, administered microiontophoretically, on spontaneous and evoked activity of midbrain reticular formation neurons].

Spontaneous activity of reticular formation neurons responding to the stimulation of pyramidal tract axons and different peripheral conductors is liable to changes during microiontophoretic exposures to acetylcholine, L-glutamate, serotonin and mesaton. The test neurons showed the highest sensitivity to L-glutamate and acetylcholine. 80% of the neurons responded to exposures to several substances. The time course of evoked reactions in the presence of microiontophoresis of biologically active substances is uncertain in character. Different components of evoked responses might react dissimilarly to microiontophoretic application of the substances. 20% of the neurons manifested significant differences as regards the time course of evoked efferent and afferent responses.

Acetylcholine↗

PubMed1980

Effects of focal electrical stimulation and morphine microinjection in the periaqueductal gray of the rat mesencephalon on neuronal activity in the medullary reticular formation.

Neurons in the medullary reticular formation (MRF; nucleus reticularis gigantocellularis and nucleus reticularis paragigantocellularis) were evaluated for their involvement in the analgesia produced by focal electrical stimulation and microinjection of morphine into the periaqueductal gray region (PAG) of the rat mesencephalon. Analgesia-producing PAG stimulation altered the spontaneous activity of 80% of the neurons in the MRF (both excitation and inhibition were observed) and inhibited the noxious-evoked excitation of 75% of MRF neurons. Microinjection of morphine into the PAG also increased (50%) and decreased (17%) the spontaneous activity of MRF units and inhibited the noxious-evoked excitation of 47% of MRF neurons. These effects were specific for analgesia produced by the PAG manipulations and were partially reversed by naloxone. The role of the MRF in PAG-induced analgesias and the degree of overlap in neuronal systems influenced by intracranial morphine and electrical stimulation is discussed.

Animals↗

PubMed1981

Involvement of caudate nucleus, amygdala or reticular formation in neuroleptic and narcotic catalepsy.

Local injection of haloperidol into the caudate nucleus produced catalepsy in contrast to the weak effects of morphine injected at the same site. Injection of either haloperidol or morphine into the amygdala did not have any cataleptogenic effect. Both haloperidol and morphine produced catalepsy when injected into the reticular formation. Naloxone injected into the reticular formation completely reversed the catalepsy following intraperitoneal morphine but not haloperidol. Pretreatment with alpha-methyl-p-tyrosine potentiated the effect of haloperidol injected into either the reticular formation or caudate nucleus. Phentolamine but not lignocaine or metergoline, injected into the reticular formation also caused a cataleptic response. The results confirm the caudate nucleus as a site for haloperidol catalepsy and in addition, suggest the reticular formation as a primary site for morphine catalepsy and a secondary site for haloperidol catalepsy; additionally a noradrenergic modulation of catalepsy may occur within this brainstem region.

Amygdala↗

PubMed1987

Morphology of pontomedullary raphe and reticular formation neurons in the brainstem of the cat: an intracellular HRP study.

In order to understand better the anatomical substrates underlying processing of sensory information, the cytoarchitecture of neurons in the pontomedullary raphe and reticular formation was investigated following intracellular injections of horseradish peroxidase in the cat. Raphe cells studied were located in the nucleus raphe magnus, nucleus raphe obscurus, and nucleus raphe pallidus. The most prominent type had a smooth, oval cell body and oval dendritic tree with dendrites extending laterally into the adjacent reticular formation. Two other raphe cell types, large cells with a dorsoventral orientation of both cell body and dendritic tree, and very small cells, were rarer. The primary dendritic orientation lay in the coronal plane for all three raphe cell types. Wispy, straight, or clublike spines were located on more distal regions of dendrites, although we also found spineless dendrites. Raphe cells lying near longitudinal fiber pathways exhibited bundling of dendrites around the passing axon fascicles. Reticular formation cells studied were located in the nucleus gigantocellularis, nucleus magnocellularis, nucleus paragigantocellularis dorsalis, and nucleus reticularis paramedianus. Two morphological types were found on the basis of dendritic branching patterns: sparsely branched and densely branched. Most reticular formation cells had round dendritic trees as viewed in the coronal plane and polygonal cell bodies that were medium to large in size. There was no correlation between reticular formation cell morphology and nuclear location. Spines were more common on the densely branched cells, but for both reticular cell types they were usually absent from cell bodies and proximal dendrites. Thus, by using the criteria of dendritic branching and arbor shape along with distance from the midline it was possible to identify raphe cells as distinct from reticular formation cells. In contrast, no morphological characteristics were found that would differentiate cells in the two major median reticular formation nuclei, gigantocellularis and magnocellularis.

Animals↗

PubMed1991

Projections from the rostral parvocellular reticular formation to pontine and medullary nuclei in the rat: involvement in autonomic regulation and orofacial motor control.

The efferent connections of the rostral parvocellular reticular formation to pontine and medullary nuclei in the rat were studied with anterogradely transported Phaseolus vulgaris leucoagglutinin. Dense innervations from the rostral parvocellular reticular formation were found in the mesencephalic trigeminal nucleus, the supratrigeminal area, the motor trigeminal nucleus, the motor trigeminal nucleus, the facial, hypoglossal and parabrachial nuclei and specific parts of the caudal parvocellular reticular formation, including nucleus linearis and the dorsal reticular nucleus of the medulla. The raphe nuclei, nucleus of the solitary tract, inferior olive, dorsal principal sensory, spinal trigeminal nuclei and gigantocellular reticular nucleus and the ventral reticular nucleus of the medulla received moderate projections. In general, the projections from the rostral parvocellular reticular formation were bilateral with an ipsilateral dominance. The dorsal motor vagus and the ambiguus nuclei were not labeled. It is concluded that the rostral parvocellular reticular formation participates in regulation of orofacial motor control and in neural networks for limbic control of metabolic homeostasis.

Animals↗

PubMed1981

[Effect of local cortical exclusion on evoked potentials in the reticular formation occurring in response to somatosensory stimulation].

The evoked potentials in different nuclei of the reticular formation were studied in unanesthetized immobilized rats. Evoked potentials in response to electrical stimulation of the forepaw were registered under normal conditions and during cooling of the somatosensory cortex (S1) in the representation area of one the forepaws. It was found that evoked potentials in the reticular formation change according to the degree of depression of the cortex primary response to the same stimulus during cooling. The peak time of the main negative wave increased from 409-50 ms to 60-80 ms with simultaneous decrease of its amplitude up to complete depression during deep cooling of the cortex. The wave with peak latency 14 ms in the ventral reticular nucleus changed in some manner, but less. Parallel registered evoked potentials in response to the stimulation of another paw were preserved in the same points of the reticular formation without changes or they decreased in their value with preservation of their parameters. Thus, during cooling of the cortex there is a selective change in the reticular formation of that signal, the representation area of which in the cortex is depressed. Obviously, the normal development of both late and early components of reticular evoked potentials to the somatic stimuli requires the inflow of an additional corticofugal signal, formed by transformation of the same signal in the corresponding area of the somatosensory cortex.

Afferent Pathways↗

PubMed1996

Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons.

A large and consistent body of data implicates mesopontine cholinergic neurons in the production of rapid eye movement sleep, and indicates that many rapid eye movement sleep events are mediated by activation of pontine reticular formation neurons. There is anatomical evidence for projections from the mesopontine cholinergic nuclei to the pontine reticular formation, but no study has shown that stimulation of this cholinergic zone produces excitatory postsynaptic potentials in pontine reticular formation neurons. In the present study, intracellular recording were made from 168 pontine reticular formation neurons, identified by antidromic activation from the bulbar reticular formation and by neurobiotin intracellular labeling, in acutely anesthetized cats. The effects of single-pulse electrical stimulation of the laterodorsal tegmental nucleus portion of the ipsilateral mesopontine cholinergic zone were evaluated in these neurons. Under urethane anesthesia this stimulation produced, in 21 of 22 recorded neurons, long-latency excitatory postsynaptic potentials (mean = 3 ms), consistent with the conduction velocity of unmyelinated cholinergic fibers (measured conduction velocity was 2 m/s). This excitatory postsynaptic potential was virtually abolished by intravenous administration of the muscarinic cholinergic receptor blocker scopolamine (n = 40 neurons), and by acute cuts separating the laterodorsal tegmental nucleus and the recorded neurons (n = 40). In contrast, a short-latency excitatory postsynaptic potential (0.7-1.5 ms) was not reduced in amplitude by scopolamine and could still be elicited following acute transverse cuts. Unlike the longer-latency excitatory postsynaptic potential, its amplitude was not reduced by barbiturate anesthesia. These data, suggesting the presence of an excitatory, cholinergic laterodorsal tegmental nucleus projection to the pontine reticular formation, provide further support to other lines of evidence implicating mesopontine cholinergic neurons in the production of rapid eye movement sleep, and are compatible with a model of rapid eye movement sleep generation in which a key element is mesopontine cholinergic input depolarizing and increasing the excitability of reticular core neurons.

Animals↗

PubMed1993

Nicotinic depolarizations of rat medial pontine reticular formation neurons studied in vitro.

Either muscarinic or nicotinic cholinergic activation of the medial pontine reticular formation evokes a behavioral state, indistinguishable in most respects from that of natural rapid eye movement sleep. However, the presence of physiologically relevant nicotonic receptors has not been described. Intracellular current and single electrode voltage clamp recordings were used to analyse the electrophysiological responses of rat medial pontine reticular formation neurons to nicotinic activation in vitro. In response to the nicotonic agonist, 1,1-dimethyl-4-phenylpiperazinium iodine, depolarization in association with an inward current was observed in 70% of the medial pontine reticular formation neurons. This effect was insensitive to the muscarinic antagonist atropine and the nicotinic ganglionic antagonists mecamylamine and hexamethonium. However, the neuromuscular nicotinic antagonist D-tubocurare and dihydro-beta-erythroidine were effective. This is consistent with a cholinergic activation of medial pontine reticular formation neurons evoking a rapid eye movement sleep-like behavioral state, at least in part, by nicotinic receptors on these neurons.

Animals↗

PubMed1982

Heterotopic stimuli-related potential gradients in a small volume of the medullary reticular formation in the cat.

In anaesthetized cats the role of the medullary reticular formation in discriminative functions was studied. We analysed (1). variability of collective reactions of the reticular neurons (extracellular potential gradients recorded bipolarly in three directions by a tetrad of micropipettes with closely-positioned tips in a small volume of the reticular formation) to the same stimulus, and (2). reactions to heterotopic stimuli. The pattern of the potential gradients generated by the stimulation (electrical, natural) of the same spot on the body surface was constant during the time periods studied (up to 30 min). Responses evoked from reciprocally remote receptor areas were manifestly different, at least in one of the depth profiles investigated. It can be concluded that the reticular formation, through its reactions, can differentiate heterotopic stimuli; in this respect it does not operate as a 'nonspecific' system.

Afferent Pathways↗

PubMed1994

Cholinergic regulation of cataplexy in canine narcolepsy in the pontine reticular formation is mediated by M2 muscarinic receptors.

Both rapid eye movement sleep and cataplexy in the narcoleptic canine have been shown to increase after both systemic and local administration of cholinergic agonists in the pontine reticular formation. Furthermore, binding studies indicate an increase in the number of M2 muscarinic receptors in the pontine reticular formation of narcoleptic canines. In the present study we have investigated the receptor subtypes involved in mediating the cholinergic stimulation of cataplexy, as defined by brief periods of hypotonia induced by emotions, within the pontine reticular formation of narcoleptic canines. Specific cholinergic and monoaminergic agonists and antagonists, and excitatory or inhibitory amino-acid neurotransmitter receptor agonists, were perfused through microdialysis probes implanted bilaterally in the pontine reticular formation of narcoleptic canines, and cataplexy was monitored using the Food-Elicited Cataplexy Test and recordings of electroencephalogram, electrooculogram and electromyogram. In narcoleptic canines, bilateral perfusion with oxotremorine (M2 muscarinic) (10(-5)-10(-3) M) in the pontine reticular formation produced a dose-dependent increase in cataplexy, which reached complete muscle atonia (status cataplecticus) during the highest concentration. In control canines bilateral perfusion with oxotremorine (10(-5)-10(-3) M) did not produce any cataplectic attacks, but did produce muscle atonia after the highest concentration. Bilateral perfusion with either McN-A-343 (M1 muscarinic) or nicotine (both 10(-5)-10(-3) M) did not have any effect on cataplexy in either narcoleptic or control canines. The increase in cataplexy in narcoleptic canines produced by local perfusion with carbachol (10(-4) M) followed by equimolar perfusion with a muscarinic antagonist was rapidly reversed by atropine (muscarinic) and gallamine (M2 muscarinic), partially reversed by 4-DAMP (M3/M1 muscarinic) and completely unaffected by pirenzepine (M1 muscarinic). Bilateral perfusion with excitatory, glutamatergic receptor agonists N-methyl-D-aspartate, AMPA (both at 10(-4)-10(-3) M) and kainic acid (10(-5)-10(-4) M) did not have any effect on cataplexy, whereas bilateral perfusion with the inhibitory GABAergic receptor agonist muscimol (10(-4)-10(-3) M) produced a moderate increase in cataplexy in the narcoleptic canines. Bilateral perfusion with numerous monoaminergic compounds, BHT-920 (alpha-2 agonist), yohimbine (alpha-2 antagonist), propranolol (beta antagonist) and prazosin (alpha-1 antagonist), did not have any effect on cataplexy. These findings demonstrate that cholinergic regulation of cataplexy in the narcoleptic canine at the level of the pontine reticular formation is mediated by M2, and possibly M3, muscarinic receptors. The effects of muscimol indicate that the stimulation of cataplexy might be elicited by local neuronal inhibition.

Animals↗

PubMed1992

Serotonin1 and serotonin2 receptors hyperpolarize and depolarize separate populations of medial pontine reticular formation neurons in vitro.

The action of serotonin on medial pontine reticular formation neurons was examined using intracellular electrophysiological methods in rat brainstem slices in vitro. A hyperpolarization associated with a decrease in input resistance was elicited by serotonin in 34% of the neurons, and a depolarization associated with an increase in input resistance was produced in 56% of the neurons. Both responses persisted in the presence of tetrodotoxin. The hyperpolarization resulted from a steady-state increase in outward current which varied with the external potassium concentration in a manner consistent with a conductance increase primarily to this ion. This response was mimicked by the serotonin1 agonist, 5-carboxamidotryptamine, as well as by the serotonin1a agonist, 8-hydroxy-dipropyl aminotetralin hydrobromide, and was blocked by spiperone, an antagonist of serotonin1 sites. The depolarization resulted from a steady-state decrease in outward current which varied with external potassium. The depolarization was mimicked by the serotonin2 agonist, alpha-methyl-5-hydroxytryptamine, and was blocked by the serotonin2 antagonist, ketanserin. Neither of these agents had any effect upon serotonin-induced hyperpolarizations. In conclusion, the excitability of medial pontine reticular formation neurons is influenced by serotonin acting to increase or decrease potassium conductance(s). These opposing effects reflect actions on distinct serotonin receptor subtypes that are segregated to distinct populations of medial pontine reticular formation neurons.

Animals↗