Changes in centrally released arginine vasopressin by stimulation of the medullary reticular formation]

It has been reported that after 40 minutes of stimulation of the medullary reticular formation (MORF), widespread significant increase by 1.4% to 2.8% in brain water content occurs in white matter of the injured hemisphere. Recent studies indicate that centrally released arginine vasopressin (AVP) influences water permeability of the brain in both normal and pathological conditions. The present study was carried out to clarify the effect of electrical stimulation of MORF on centrally released AVP. The cats were divided into three groups. In group A (16 cats), electrical stimulation of MORF (1msec, 5V, 50Hz) was carried out for 80 minutes in normal cats. In group B (11 cats), stimulation was started 17 hours after cold injury under the same conditions and carried out for 80 minutes. In group C (10 cats), angiotensin II was administered to elevate blood pressure to the same degree as during MORF stimulation 17 hours after cold injury. AVP concentrations in the cerebrospinal fluid (CSF), plasma and brain tissue of the injured and non-injured white matter were measured by radioimmunoassay. Plasma osmolality was also determined by the freezing point depression method. Normal values (mean +/- S. D.) of CSF and plasma AVP were 4.0 +/- 2.2 and 9.9 +/- 3.6 pg/ml respectively. Plasma AVP and osmolality did not show significant changes before and at the end of experiments in all groups. There were no significant changes in CSF AVP by induced hypertension for 80 minutes (Group C). Stimulation of the medullary reticular formation resulted in significant and progressive increase in CSF AVP in normal and injured brain (Group A, B).(ABSTRACT TRUNCATED AT 250 WORDS)     

Behavioral relations of medullary reticular formation cells

The movement correlates of unit activity in medullary reticular formation cells were observed in unrestrained cats. Fifty-four percent of these cells had “laterally asymmetrical” movement relations and 38% had “laterally symmetrical” movement relations. All cells that discharged in relation to active lateral movement of the spinal column discharged preferentially in relation to ipsilateral movements, while all cells responding to passive lateral movement discharged preferentially in relation to contralateral movement. Cells related to movements of the vertebral column in the vertical plane and a small number of units related to facial, laryngeal, paw, and other movements were also found. The specific motor relations of reticular formation cells may explain the findings of previous lesion, stimulation, and recording studies.     

Synaptic responses of neurons of the lateral medullary reticular formation to stimulation of the locomotor strip in the cat

Intracellular recording of neuronal responses in the lateral medullar reticular formation to stimulation of locomotor points located rostrally and caudally of the obex was made in mesencephalic uncurarized cats. Of 114 neurons with synaptic responses to the rostral point stimulation by current up to 30 microA 40 neurons were excited antidromically from the caudal point.     

Noxious cardiac input onto neurons in medullary reticular formation

Responses of reticular formation neurons to electrical stimulation of cardiopulmonary afferents as well as cardiac application of bradykinin were determined. Experiments were performed in chloralose anesthetized, vagotomized and sino-aortic denervated cats paralyzed with pancuronium. The medial reticular formation in the medulla was explored with microelectrodes until single neurons responding to electrical stimulation of the cardiac nerve were isolated. Electrical stimulation evoked an early (latency less than 40 ms) burst only (most common), both an early burst and a late burst, or a late (latency greater than 90 ms) burst only (least common) from medullary neurons. Cells were subsequently tested for responses to epicardial or intracardiac administration of bradykinin. Of the 62 neurons tested, one-third responded to bradykinin. Cells typically exhibited a bursting pattern of spontaneous activity; bradykinin enhanced the duration and intensity of the bursts. Neurons were also tested for somatic, visual and auditory input. Most cells were excited by somatic as well as auditory stimuli, while a fewer number also received visual input. Furthermore, most cells responsive to epicardial bradykinin also received these other inputs. The neurons recorded in this study may mediate cardiac pain, cardiovascular reflexes, alerting responses, and/or arousal responses.     

Role of medullary lateral reticular formation in baroreflex coronary vasoconstriction

We have recently identified a polysynaptic pathway traversing discrete regions of the hypothalamus, midbrain, and medulla, along which site-specific electrical and chemical activation produces coronary vasoconstriction as part of a sympathoexcitatory response. We tested for the potential functional significance of this pathway by examining the hypothesis that a medullary component is involved in carotid baroreflex induced coronary vasoconstriction. Coronary flow velocity was measured with a Doppler probe in anesthetized cats. Following vagotomy and propranolol, bilateral carotid occlusion produced an increase in mean arterial pressure (56 +/- 14%, means +/- S.E.M.) and in coronary vascular resistance (51 +/- 13%) which was greater than that (29 +/- 6%) expected from the concurrent rise in arterial pressure during aortic constriction. Bilateral microinjections of lidocaine into the medullary lateral reticular formation attenuated the reflex increase in pressure (11 +/- 2%) and virtually abolished the rise (8 +/- 2%) in coronary resistance. After one hour recovery, carotid occlusion again increased aortic pressure (56 +/- 13%) and coronary vascular resistance (47 +/- 15%). Microinjections of lidocaine outside this medullary region did not impair the coronary vasoconstrictor response to carotid occlusion. We conclude that the medullary lateral reticular formation contains neural elements which participate in baroreflex-induced changes in arterial pressure and coronary vascular resistance. Components of the previously described central coronary vasoconstrictor pathway may play a role in pathophysiological conditions associated with increased coronary vasomotor tone.     

Enkephalin and serotonin innervation of somatostatin-immunoreactive medullary reticular formation neurones

Somatostatin cells in the rat medullary reticular formation (Md) have been studied using peroxidase-antiperoxidase immunocytochemistry. Large fusiform and multipolar somatostatin immunoreactive cells were observed in the ventral subnucleus (MdV) running in a band close to the border with the dorsal subnucleus (MdD). In the same region somatostatin-, serotonin- and enkephalin-immunoreactive fibres occur and double staining revealed that these all contact the somatostatin-immunoreactive cells, with enkephalin making a particularly dense innervation.     

Bunina bodies in neurons of the medullary reticular formation in amyotrophic lateral sclerosis

Summary To determine how often Bunina bodies (BBs) appear in the medullary reticular formation (MRF) in amyotrophic lateral sclerosis (ALS), we microscopically examined 20 serial sections of MRFs from each of nine autopsied ALS cases, which had BBs in the lower motor neurons, including those of cranial motor nuclei. In 1 of them, the pontine tegmentum was examined in the same way. In 8 cases one to several BB-containing neurons in the MRF were seen. The case in which the pontine tegmentum was also investigated exhibited several neurons with BBs in this region. Some of the BBs in the MRFs were confirmed by electron microscopy. Thus, this study demonstrates the common appearance of BBs, although the number is small, in the MRF, indicating that pathological processes that undermine the lower motor neurons in ALS in some way also affect neurons other than motor neurons in this condition.Supported in part by the Research Committee of CNS Degenerative Diseases, the Ministry of Health and Welfare of Japan     

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.     

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 iontophoressed 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 ofindividual 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. These results suggest that morphine's effect on neuronal activity in the MRF when microinjected in the PAG is not mediated by an enkephalinergic interneuron. The implications of these results on the role of the MRF in opiate-induced antinociception are discussed.     

Global increase in cerebral metabolism and blood flow produced by focal electrical stimulation of dorsal medullary reticular formation in rat

We sought to determine whether the increases in local cerebral blood flow (LBCF) elicited by focal electrical stimulation within the dorsal medullary reticular formation (DMRF), are secondary to or independent of, increased local cerebral glucose utilization (LCGU).Rats were anesthetized (chloralose), paralyzed, artificially ventilated and arterial pressure and blood gases controlled. LCBF and LCGU were determined in two separate groups of animals, using the autoradiographic [¹⁴C]iodoantipyrine and [¹⁴C]2-deoxyglucose methods, respectively. In unstimulated controls, LCBF (n= 5) and LCGU (n= 5) were linearly related (r = 0.780; P < 0.001) in the 27 brain regions studied. During DMRF stimulation LCGU increased significantly in 21 of the 27 regions, including cerebral cortex (up to 168% of control), thalamic nuclei (up to 161%) and selected ponto-medullary regions (e.g. parabrachial complex: 212%; vestibular complex: 147%). Along with LCGU, LCBF rose significantly in 25 regions (sensory motor cortex: 163%; anterior thalamus: 161%; parabrachial complex: 186%). Correlation analysis demonstrated that, during DMRF stimulation, the close relationship between LCBF and LCGU is preserved (r = 0.845; P < 0.001) and that, in addition, the increase in LCBF (δ LCBF) is proportional to the increase in LCGU (δ LCGU) (δLCGU+ 6.92; r = 0.7729; P < 0.001).Excitation of neurons or fibers within DMRF increases brain metabolism globally and blood flow secondarily. The DMRF appears to modulate cerebral metabolism globally, by as yet undefined pathways.