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Biomedical subjects

F C Barone

Publications and source records attributed to F C Barone.

At least 109 records · Page 6Linked to original sources
PubMed1991

Quantitative comparison of magnetic resonance imaging (MRI) and histologic analyses of focal ischemic damage in the rat.

Hemispheric swelling and area of infarction, two parameters of cerebral focal ischemic damage, were identified and quantified from T2-weighted magnetic resonance imaging (MRI) two days after occlusion of the middle cerebral artery (MCAO) in spontaneously hypertensive rat (SHR) brains. Results were compared with these measures quantified from 2,3,5-triphenyltetrazolium hydrochloride (TTC)- and hematoxylin and eosin (H&E)-stained histologic sections in the same brains. The degree of hemispheric swelling and infarct size determined by MRI were highly correlated to the measurements as determined in the TTC- and H&E-stained tissues. These results demonstrate that the focal ischemic damaged area and associated tissue swelling identified by MRI is quantitatively similar to, and thus, is representative of actual tissue damage/changes that can be identified by gross or histologic examination.

Animals↗
PubMed1991

Human lower oesophageal sphincter relaxation is associated with raised cyclic nucleotide content.

Increases in cyclic adenosine monophosphate and cyclic guanosine monophosphate content accompany relaxation of isolated strips of opossum and canine lower oesophageal sphincter muscle. The aim of this investigation was to characterise these responses in isolated muscle from the human lower oesophageal sphincter. Electrical stimulation of enteric neurons produced a frequency dependent relaxation of the human lower oesophageal sphincter that was sensitive to tetrodotoxin. Furthermore, as previously shown in the opossum and canine lower oesophageal sphincter, cyclic guanosine monophosphate content was significantly raised in muscle strips frozen during maximum electrical field stimulation whereas cyclic adenosine monophosphate content was unchanged. In addition, sodium nitroprusside (EC50 = 0.1 microM) produced a concentration dependent relaxation of human lower oesophageal sphincter, significantly increased cyclic guanosine monophosphate content, but did not alter cyclic adenosine monophosphate content. Zaprinast (M&B 22948) and SK&F 94120, selective inhibitors of cyclic guanosine monophosphate and cyclic adenosine monophosphate phosphodiesterases, respectively, both relaxed human lower oesophageal sphincter with a potency similar to that seen in the dog or opossum lower oesophageal sphincter. Finally, the 8-bromo analogues of both cyclic adenosine monophosphate (EC50 = 420 microM) and cyclic guanosine monophosphate (EC50 = 100 microM) relaxed the human lower oesophageal sphincter. These studies suggest that in the human, as well as the canine and opossum lower oesophageal sphincter, increases in cyclic nucleotide content are associated with relaxation and increases in cyclic guanosine monophosphate are associated with the relaxation induced by stimulation of enteric neurons.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Carvedilol (Kredex) reduces infarct size in a canine model of acute myocardial infarction.

Carvedilol (Kredex) is a multiple action, antihypertensive agent that may also prove to be useful in the treatment of angina and congestive heart failure. Carvedilol combines in one molecule both beta-adrenoceptor blocking and vasodilating activities. Inasmuch as beta-adrenoceptor blocking agents are known to be cardioprotective and thereby reduce infarct size, it is logical to assume that carvedilol, likewise, would possess this desirable activity. Furthermore, the additional vasodilating activity of carvedilol could contribute to further reductions in infarct size by reducing myocardial work (and therefore myocardial oxygen demand) through reductions in both afterload and myocardial wall tension. As such, we have investigated the ability of carvedilol to reduce infarct size in a canine model of acute myocardial infarction. Carvedilol (1 mg/kg i.v.) or its vehicle, dimethylformamide, were administered 15 min before left circumflex coronary artery (LCX) occlusion. Following 1 h of LCX occlusion, dogs were reperfused through a critical stenosis and then allowed to recover for 24 h. Carvedilol-treated animals exhibited a 78% reduction in infarct size compared to vehicle controls, such that the percentage of the left ventricle infarcted was reduced significantly from 16.2 +/- 4.1% in control animals to 3.6 +/- 1.3% in animals treated with carvedilol (p = 0.017, n = 6). Stained tissue sections of the left ventricle were photographed, digitized and color-enhanced using an Image Analysis Computer System, and three-dimensional reconstruction of the left ventricle, including the infarcted areas, was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Inhibition of neuronally induced relaxation of canine lower esophageal sphincter by opioid peptides.

Opioid peptides have profound effects on gut motility. To assess their actions on enteric neurons regulating sphincteric smooth muscle, the ability of several opioid agonists to antagonize the neuronally induced relaxation of canine lower esophageal sphincter smooth muscle was examined. Opioid peptides selective for mu (FK 33-824) or delta [( D-Pen2,D-Pen5]enkephalin) receptors produced a concentration dependent inhibition of electrical field stimulation (EFS)-induced relaxation. In contrast, neither kappa (ketocycloclazine) or sigma (SK & F 10047) opioid agonists were potent inhibitors of EFS-induced relaxation. This inhibition was relatively selective for opioid agonists since BHT 933 (alpha 2 adrenoceptor agonist) and SK & F 89124 (D2 dopamine agonist) did not inhibit EFS-induced relaxation. Furthermore, naloxone antagonized the effects of both FK 33-824 and DPDPE. These functional data suggest that opioid receptors are present on sphincteric intrinsic inhibitory neurons and that stimulation of these neuronal receptors can regulate lower esophageal sphincter relaxation.

Animals↗
PubMed1990

Oral activity of the growth hormone releasing peptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 in rats, dogs and monkeys.

The purpose of this study was to evaluate the growth hormone (GH) releasing activity of orally administered His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6, SK&F 110679) in rats, dogs and monkeys. Rats were administered GHRP-6 orally by gavage or parenterally through femoral artery catheters. Blood was collected before and after GHRP-6 administration for estimation of plasma GH and comparison of GH changes resulting from enteral and parenteral administration of the peptide. GHRP-6 was administered to dogs intravenously (i.v.) through cephalic vein catheters, intragastrically (i.g.) through esophagostomy tubes or intraduodenally (i.d.) through vascular access ports, and blood was collected before and after peptide administration for estimation of plasma GH. Cynomolgus monkeys were administered GHRP-6 i.g., and blood was collected from abdominal aorta for estimation of changes in plasma GH. Enteral activity of GHRP-6 was observed in all 3 species tested. In rats, ED50's for enteral and parenteral administration of GHRP-6 were 4 mg/kg and 28 micrograms/kg, respectively. Thus in rats, enterally administered GHRP-6 was 0.7% as bioactive as the parenterally administered peptide. In dogs GHRP-6 was slightly less potent than in rats, with ED50's for i.g. and i.v. administration approximately 15 mg/kg and 125 micrograms/kg, respectively. However, enteral potency of GHRP-6 in dogs was 0.8% of parenteral potency, and thus, comparable to that in rats. Additionally, comparison of plasma GH levels following i.g. vs i.d. administration in dogs suggested greater activity by the i.d. route. Monkeys were the species most sensitive to enterally administered GHRP-6, with plasma GH increased in those receiving i.g. doses as low as 0.3 mg/kg and an ED50 of 0.75 mg/kg compared to 4 and 15 mg/kg in rats and dogs, respectively. The results of this study demonstrate that GHRP-6 releases GH when administered directly into the gastrointestinal tract. Although enteral activity is approximately 1% of parenteral activity, GHRP-6 is potent, especially in primates which require relatively low doses to provoke GH release. These data suggest that orally active GHRP-6 may provide a practical therapeutic alternative to parenterally administered peptides such as GHRH, especially if enteral activity is enhanced with appropriate formulation.

Administration, Oral↗
PubMed1990

Cold-restraint stress increases rat fecal pellet output and colonic transit.

Increased fecal pellet output that occurs during cold-restraint stress (CRS) was evaluated systematically. Free-feeding rats, which exhibit a reduced occurrence of gastric ulcers under these conditions, were studied. CRS significantly increased fecal pellet production and fluid content. However, the fecal output produced during CRS was not associated with increased gut secretory activity or somatic motor activity associated with cold restraint and did not occur in anesthetized animals. Cold and restraint stress were additive in producing increased fecal output. Significant dose-related decreases in fecal output were produced by drugs that decrease gut transit (i.e., B-HT 920, clonidine, Lomotil, loperamide, and lidamidine). Anticholinergic-antisecretory drugs, antidepressants, and tranquilizers had little effect on fecal output or fluid content. Changes in gastrointestinal transit did not contribute to the increased fecal output during CRS. Transit in the lower small intestine was not altered, but the cecum tended to empty more contents into the large intestine during CRS. Colonic transit was dramatically affected by CRS, which eliminated retrograde transit and produced the evacuation of the majority of colonic contents. The increased colonic transit produced by CRS was decreased in a dose-related fashion by hexamethonium, nifedipine, loperamide, and B-HT 920. In several time-response and drug-inhibition studies during CRS, both fecal pellet output and colonic transit were affected similarly. These data indicate that CRS appears to change central nervous system output to the colon and that it alters colonic smooth muscle motility in a manner that facilitates colonic transit and evacuation. Small intestinal transit is not involved in this phenomenon and is regulated differently during CRS.

Animals↗
PubMed1989

Cholecystokinin stimulates neuronal receptors to produce contraction of the canine colon.

The motor effects of cholecystokinin 26-33-amide (CCK octapeptide; CCK-OP) and several purported CCK receptor antagonists on canine colonic circular muscle were determined in pentobarbital anesthetized dogs. Intravenous injections of CCK-OP had no effect on colonic motility at doses that contracted the gallbladder, stomach and duodenum. CCK-OP delivered by intraarterial injection to a small segment of the proximal colon produced a dose related increase in colonic motility with one-half maximum response at 12 ng/Kg and maximum response at 50 ng/Kg. The effects of intraarterial injections of several established CCK-receptor antagonists on proximal colonic responses to intraarterial injections of CCK-OP were determined. Proglumide, 10 mg/Kg, did not produce colonic contractions itself, but antagonized CCK-OP-induced responses. Carbobenzyloxy (CBZ)-CCK27-32-amide antagonized CCK-OP-induced colonic responses and also had no effect on basal colonic motility (0.1-1 and 5 micrograms/Kg). Neither compound antagonized acetylcholine- induced colonic responses. Butoxycarbonyl (BOC)-CCK31-33-amide increased basal colonic motility, but did not alter CCK-OP-induced responses at doses of 0.1 and 0.2 mg/Kg. Dibutyryl-cGMP at a dose of 0.1 mg/Kg did not affect basal motility or CCK-OP-induced contractions. At a dose of 1.0 mg/kg it increased basal colonic motility but did not affect CCK-OP-induced contractions. Pentagastrin increased colonic motor activity only at a dose of 5 micrograms/Kg, i.a., a much higher dose than effective doses of CCK-OP. The mechanism of CCK-OP-induced colonic motor effects also was determined. Atropine sulfate, 100 micrograms/Kg, i.v. significantly reduced both intraarterial acetylcholine-and CCK-OP-induced maximum colonic contractions. Tetrodotoxin, at intravenous doses that completely block neuronal activity, did not affect maximum acetylcholine-induced contractions but practically eliminated maximum CCK-OP-induced maximum colonic responses. In conclusion, intraarterial CCK-OP produces circular muscle contraction of the canine proximal colon that is mediated by stimulation of specific CCK receptors which produce the release of acetylcholine from cholinergic enteric neurons. Proglumide and CBZ-CCK27-32-amide are effective CCK receptor antagonists at these colonic neuronal receptors.

Acetylcholine↗
PubMed1987

Effects of KC 2450 on the lower esophageal sphincter in vivo and in vitro.

The effect of KC 2450 (racemic 3,5-cis-3-methylamino-2,3,4,5-tetrahydro-1-benzoxepine-5-ol hydrochloride) on lower esophageal sphincter pressure in pentobarbital-anesthetized dogs was determined and compared to the effect of metoclopramide. The ED20 value (i.e. the dose that increased lower esophageal sphincter pressure 20 mm Hg) was 0.72 (0.45-1.04) mg/kg i.v. for KC 2450, significantly different from 2.18 (1.30-3.42) mg/kg i.v. for metoclopramide (P less than 0.01). The superior potency of KC 2450 over metoclopramide also was demonstrated at a dose of 2 mg/kg i.v.; KC 2450 produced an increase in sphincter pressure of 43.2 +/- 4.4 mm Hg and metoclopramide produced an increase in sphincter pressure of only 28.5 +/- 5.4 mm Hg (P less than 0.05). Intraduodenally administered KC 2450 increased lower esophageal sphincter pressure at a threshold dose of 2 mg/kg with 10 mg/kg producing an increase in pressure of 53.2 +/- 9.9 mm Hg. KC 2450-induced increases in sphincter pressure were not affected by bilateral cervical vagotomy or ketanserin, but were eliminated by atropine and reduced by neuronal blockade using tetrodotoxin (TTX). KC 2450 effects also were determined in isolated circular strips of lower esophageal sphincter muscle. KC 2450 produced a concentration-related increase in canine (EC50 = 27 microM) and opossum (EC50 = 199 microM) sphincter muscle strip tension. The KC 2450 concentration-response curve was antagonized by atropine in canine and opossum sphincter muscle strips. Neuronal blockade of canine sphincter muscle with TTX antagonized the KC 2450 concentration-response curve in a non-competitive manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

DA1 receptor mediates dopamine-induced relaxation of opossum lower esophageal sphincter in vitro.

The objective of the present experiments was to determine the specific receptor subtype through which dopamine (DA) receptor agonists relax the lower esophageal sphincter in vitro. Opossum lower esophageal sphincter smooth muscle strips were placed in oxygenated Krebs' solution containing propranolol and cocaine. The tissues were placed at a tension that gave maximum relaxation to electrical field stimulation and were then pretreated with phenoxybenzamine. The effects of DA, and the DA receptor agonists epinine and apomorphine were determined. In addition, agonist responses were studied in the presence of the selective DA2 receptor antagonist domperidone, a mixed DA1/DA2 receptor antagonist metoclopramide, and the selective DA1 receptor antagonists bulbocapnine and SK&F 83566. The DA agonists relaxed the smooth muscle strips in the following order of potency: DA greater than epinine greater than apomorphine. Domperidone did not antagonize DA- or apomorphine-induced relaxation. Metoclopramide failed to alter DA-induced relaxation. Bulbocapnine and SK&F 83566 significantly inhibited the relaxation induced by DA. These data indicate that DA-induced lower esophageal sphincter relaxation in vitro is mediated by DA1 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

Effects of calcium channel entry blockers, nifedipine and nilvadipine, on colonic motor activity.

The effects of the dihydropyridine calcium channel entry blockers nifedipine and nilvadipine on colonic contractions were determined in vitro and in vivo. In circular muscle strips prepared from the canine proximal colon, cumulative concentration-response curves were generated to potassium chloride (KCl), acetylcholine (ACh) and substance P, and the effects of electrical field stimulation were determined. Responses to KCl and ACh were examined in circular muscle strips prepared from the monkey proximal and distal colon. Nifedipine (10(-8) - 10(-6) M) significantly decreased KCl-induced contractions, whereas equimolar concentrations of nilvadipine were less effective at modifying these responses. Both calcium channel entry blockers produced similar significant decreases in ACh, substance P and electrical field stimulation contractions. In anesthetized dogs, strain gauge force transducers were oriented to record proximal colonic circular muscle contractions. Colonic contractions to i.a. infusions of ACh, cholecystokinin-(26-33) and substance P were produced in a small segment of the proximal colon. Nifedipine and nilvadipine (200 micrograms/kg i.v.) significantly decreased maximal ACh contractions. Nilvadipine also decreased maximum cholecystokinin-(26-33) and substance P contractions. Both calcium channel entry blockers decreased systolic and diastolic blood pressure significantly at 100 micrograms/kg i.v. These results indicate that nifedipine and nilvadipine are equieffective at reducing colonic contractile activity to a variety of colonic stimulants and illustrate the importance of extracellular calcium in the mediation of colonic motility

Acetylcholine↗
PubMed1985

Direct effects of androgens on lateral hypothalamic neuronal activity in the male rat: I. A microiontophoretic study.

Unit neuronal activity in the lateral hypothalamic-medial forebrain bundle region (LHA-MFB) of the male rat is modified following an increase of plasma testosterone level. In order to determine possible direct action of hormones on LHA-MFB neurons, unit discharge frequencies were recorded during local microiontophoresis of testosterone and estradiol, and electroosmotic application of cholesterol. Thirteen cells did not respond, 9 were nonspecifically depressed by all the steroids tested, 13 were excited by both sex-steroids, and 11 were specifically activated by testosterone. The short latencies of the responses suggest a direct effect of steroids on the plasma membrane sites.

Action Potentials↗
PubMed1985

Total intestinal aganglionosis.

Total Intestinal Aganglionosis is a rare, uniformly fatal condition with absence of ganglia from the duodenum to the rectum. A neonate with this extreme form of Hirschsprung's disease is presented with a review of 12 previously reported cases. Smooth muscle strips from this infant's gastrointestinal tract demonstrated viable cholinergic receptors, absence of intrinsic neuronal innervation, and colonic contractile activity to the purported peptidergic neurotransmitter cholecystokinin. Four aspects of total intestinal aganglionosis are noteworthy: (1) one-third of patients presented between four and eight days of age after passing meconium on the first day of life; (2) at laparotomy, no intestinal distention, obstruction, or transition zone was evident; (3) hypertrophic nerve fibers seen in classic Hirschsprung's disease were absent in one-quarter of patients; and (4) a high incidence of affected siblings occurred in the previously reported cases. This form of Hirschsprung's disease may represent a distinct entity with autosomal recessive inheritance and significant risk for recurrence.

Acetylcholine↗
PubMed1984

Effects of neurotransmitters and vagus nerve stimulation on diencephalic and mesencephalic neuronal activity.

The effects of microiontophoretically applied neurotransmitters and cervical vagus nerve stimulation on neuronal discharge frequency was determined for cells located in the lateral hypothalamus-lateral preoptic area (LH-LPA), medial hypothalamus, thalamus-zona incerta area, and midbrain of anesthetized rats. Seven barrel electrodes were utilized to record simultaneously from and apply gamma aminobutyric acid (GABA), dopamine, glutamate, acetylcholine and norepinephrine to single neurons. Microiontophoretically applied GABA resulted in similar decreases in neuronal discharge frequency in all central areas tested. Thalamus-zona incerta cells were the most sensitive to GABA and required the lowest ejection current for threshold responses. Dopamine application resulted in increases and decreases in hypothalamic and mesencephalic neuronal discharge frequency. Thalamus-zona incerta neurons were the most sensitive to dopamine and exhibited only decreased activity during its application. Glutamate application resulted in a non-specific excitation of neurons. Acetylcholine induced increases and decreases in neuronal discharge frequency. Thalamus-zona incerta cells were the most sensitive to acetylcholine application. Hypothalamic neurons were the most sensitive to norepinephrine induced decreases in neuronal activity and effects in this area persisted for a prolonged period after norepinephrine was applied. Neuronal discharge frequency was significantly increased during vagus nerve stimulation in all central areas studied. Only hypothalamic neurons also exhibited decreased activity during vagus nerve stimulation. Results are discussed in terms of previous neurochemical and neurophysiological data and in terms of the importance of vagal afferents in the control of central neuronal activity.

Animals↗
PubMed1984

Vagal and gastric connections to the central nervous system determined by the transport of horseradish peroxidase.

Horseradish peroxidase (HRP, Sigma Type VI) crystals were encased in a parafilm envelope and applied to the transected central ends of the left and right cervical vagus nerves and the anterior and posterior esophageal vagus nerves of adult male hooded rats. Injections of 30% HRP were made into the muscle wall of the fundus and antrum regions of the stomach. After 48 hr survival time, animals were perfused intracardially with a phosphate buffer plus sucrose wash followed by glutaraldehyde and paraformaldehyde fixative. The brain stem, spinal cord and corresponding dorsal root ganglia, superior cervical sympathetic ganglion, and the nodose ganglion were removed and cut into 50 micron sections. All tissue was processed with tetramethylbenzidine (TMB) for the blue reaction according to Mesulum and counterstained with neutral red. Sequential sections were examined under a microscope. Labeled neurons and nerve terminals were identified using bright and dark field condensers and polarized light. In tissue from animals that had HRP applied to the cervical vagus nerves, retrogradely labeled neurons were identified ipsilaterally in the medulla located in the dorsal motor nucleus of the vagus (DMN) and the nucleus ambiguus (NA). Labeled cells extended from the DMN into the spinal cord in ventral-medial and laminae X regions C1 and C2 of cervical segments. Many neurons were labeled in the nodose ganglion. Anterogradely labeled terminals were observed throughout and adjacent to the solitary nucleus (NTS) dorsal to the DMN and intermixed among labeled neurons located in the DMN. In tissue from animals that had HRP applied to the esophageal vagus nerves, similar labeling was observed. However, fewer neurons were identified in the NA, the nodose ganglion, and only in laminae X of the cervical spinal cord segments C1 and C2. Also, very little terminal labeling was observed in and adjacent to the NTS. Labeled neurons in tissue from animals that had HRP injected into the stomach wall were observed bilaterally in the DMN, nodose ganglion, and only in laminae X at the C1 and C2 levels of the spinal cord. Labeled neurons also were observed in the dorsal root ganglia of the thoracic cord. These data indicate that cervical cord and NA neurons are important in the supradiaphragmatic motor innervation by the vagus. Also, many afferents to the NTS originate above the diaphragm. In addition, some afferents from the stomach enter the central nervous system via the thoracic spinal cord.

Animals↗
PubMed1984

Effects of hindbrain stimulation on lower esophageal sphincter pressure in the cat.

Lower esophageal sphincter (LES) pressure was measured in anesthetized cats during electrical stimulation of the dorsal motor nucleus of the vagus (DMV) and nucleus ambiguus (NA). Stimulation parameters were varied to determine maximal changes in LES pressure and upper gastrointestinal motor responses. LES pressure decreased significantly during DMV and NA stimulation. The LES preferentially was affected over other upper gastrointestinal locations. Bradycardia and increases in blood pressure occurred with stimulation of both nuclei. LES pressure changes could be demonstrated in the absence of other gastrointestinal responses by decreasing hindbrain stimulation parameters. Cervical vagotomy completely eliminated hindbrain stimulation-induced changes in LES pressure, upper gastrointestinal motor activity, and heart rate. Similar frequency-LES pressure response relationships were observed for DMV and NA stimulation, with maximum changes occurring at 25 Hz. Changes in LES pressure occurred at shorter stimulation pulses (0.05 vs. 0.5 ms) and at lower stimulating current strength (30 vs. 60 microA) during DMV as compared with NA stimulation. In addition, stimulation of areas adjacent to the DMV and NA also significantly altered LES pressure, indicating that a large portion of the cat hindbrain associated with the vagal motor nuclei is involved in LES pressure control.

Animals↗
PubMed1983

Limbic connections to the lateral preoptic area: a horseradish peroxidase study in the rat.

Horseradish peroxidase, 13% Sigma Type VI, was administered iontophoretically to the lateral preoptic area (LPA) of male hooded rats. Animals were perfused intracardially on the following day and brains were removed and sliced in the coronal plane into 50 microns sections. Alternate sections were processed with DAB and BDH for the brown and blue reaction products and later examined by bright and dark field microscopy for the presence and location of retrogradely labeled neurons. Results indicate that there are a significant number of limbic efferent connections to the LPA. Afferents to the LPA originate in the prefrontal corex, nucleus accumbens, diagonal band and olfactory structures, lateral and medial septum, stria hypothalamic tract and stria terminalis, the magnocellular and medial preoptic nuclei, along the extent of the medial forebrain bundle in the LPA and LH, anterior and basolateral amygdala, ventromedial caudate-putamen, stria medullaris and lateral habenula, the stellatocellular-periventricular, ventromedial, arcuate and anterior hypothalamic nuclei, the perifornical area, zona incerta, ventral medial thalamic area, ventral tegmental area of Tsai, interpeduncular nucleus, reticular zone of the substantia nigra, mesencephalic periaqueductal gray and reticular formation, all aspects of the raphe nuclei and the locus coeruleus. Results are discussed in terms of known anatomical and neurophysiological data and the similar limbic inputs observed for lateral hypothalamic neurons which are found along the extent of the medial forebrain bundle.

Animals↗
PubMed1981

Mesencephalic reticular formation stimulation effects on hypothalamic neuronal activity.

The effects of mesencephalic reticular formation (RF) single pulse, 0.5 msec and 0-500 microA, stimulation on lateral preoptic-lateral hypothalamic (LPA-LH) neuronal activity were determined in anesthetized rats. In addition, the effects of LH stimulation on neural activity in the RF and periaqueductal gray (PAG) were evaluated. Recordings from 117 neurons indicate reciprocal connections between the LPA-LH and the mesencephalon. Stimulation of the RF affected 70% of the LPA-LH neurons tested. Short latency decreases in activity predominated indicating an inhibitory synaptic input from the RF to the LPA-LH. Short latency increases in discharge frequency were observed infrequently. Stimulation of the LH affected only 32% of the mesencephalic neurons tested. Short latency decreases in activity were usually observed indicating reciprocal inhibitory synaptic connections between the LPA-LH and the RF and periaqueductal gray. Antidromic responses verified these interconnections and revealed relatively slow conduction velocities of approximately 1.0 m/sec. Results are discussed in terms of the involvement of the LPA-LH and RF in sensorimotor functions, spinal motor excitability, and ingestive behavior.

Action Potentials↗