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PubMed1983

Reversal of morphine-induced catalepsy by naloxone microinjections into brain regions with high opiate receptor binding: a preliminary report.

The relationship between opiate binding density and morphine-induced catalepsy was estimated via dose-response analysis of the brain sites in which naloxone microinjections reversed the catalepsy induced by intraperitoneal morphine. One-hundred forty-one experimentally naive male Long-Evans rats were implanted with chemical microinjection guide cannulae aimed for various high-to-moderate binding density areas within caudate nucleus, central gray matter, thalamus, hypothalamus, amygdala, and frontal cortex as well as low density sites in pyriform cortex and various fiber tracts. Overall, 48 out of 91 animals microinjected with naloxone in brain sites having high-to-moderate density of opiate binding showed reversal of the cataleptic response. Dose-response effects were found in all 6 high-to-moderate density sites: ranging from 85% reversals at 100 mcg naloxone over all sites to 34% reversals at 0.01 mcg naloxone. There were no reversals out of 38 naloxone microinjection in brain sites having a low density of opiate binding and no reversals out of 18 saline microinjections in either high-to-moderate or low opiate binding density loci. These results suggest a role for limbic and basal ganglia portions of the opiate system in a motor aspect of narcotic action. We speculate that these loci may also play a role in the motor expression of the response to the analgesic and euphoric actions of morphine to supplement actions mediated through periventricular structures.

Animals↗

PubMed1992

Measurement of the distribution of [3H]bicuculline microinjected into the rat hypothalamus.

The purpose of this study was to measure the distribution of a radiolabeled drug [3H]bicuculline methylchloride ([3H]BMC) following microinjection into the supraoptic nuclei (SON) and the dorsal hypothalamus of conscious rats. The anteroposterior (AP) distribution was measured using liquid-scintillation counting while computer-assisted densitometry was used to measure the mediolateral (ML) and dorsoventral (DV) distribution of silver grains on autoradiograms. Following a 50-nl microinjection into the SON, 90% of the detected tracer was found within 0.6 +/- 0.1 mm (n = 5) of the injection site. Using the same volume, the pattern of distribution of 90% of the detected tracer in the SON was not significantly altered when rats received a microinfusion over 10 min (n = 5) or a bolus microinjection with a 10 min waiting period (n = 6) prior to death. Following a 100-nl microinfusion over 20 min into the dorsal hypothalamus, 90% of the detected radiolabel was found within 0.6 +/- 0.1 mm (n = 7) of the injection site, in a spherical pattern of distribution. Although caution must be used in extrapolating these results to other drugs, these data suggest that intraparenchymal microinjections of 50- and 100-nl volumes are suitable for drug localization in studies using microinjection techniques for conscious rats.

Animals↗

PubMed1995

Substance P and serotonin independently affect intragastric pressure when microinjected into the nucleus raphe obscurus of the rat.

We have recently shown that microinjection of substance P (SP) into the nucleus raphe obscurus (NRO) of the rat decreases intragastric pressure, whereas microinjection of serotonin (5-HT) increases it. The purpose of the present study was to investigate whether there exists a functional interaction between SP and 5-HT in the NRO of the rat in their effects on gastric motor function. This was accomplished by microinjection of SP (135 pmol) and 5-HT (0.6 and 6 nmol) into the NRO in a rapid, sequential order in alpha-chloralose-anesthetized rats, while monitoring intragastric pressure and pyloric and greater curvature motilities. Substance P evoked significant decreases in intragastric pressure when microinjected into the NRO after vehicle and after 5-HT (at both 0.6 and 6 nmol). There was no difference in the magnitude of the SP effect after 5-HT when compared to the response after vehicle. Serotonin at a dose of 6 nmol, but not at a dose of 0.6 nmol, elicited significant increases in intragastric pressure when microinjected after vehicle or after SP, and there was no difference between the responses to 5-HT with respect to the initial treatment. We conclude that SP and 5-HT act independently in the NRO of the rat to affect intragastric pressure.

Animals↗

PubMed1994

Effects of microinjection of N-methyl-D-aspartic acid into the nucleus tractus solitarii on cerebral blood flow in anesthetized rats.

N-Methyl-D-aspartic acid (NMDA) (10 pmol in 100 nl of 0.9% sodium chloride solution) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized, paralyzed and artificially ventilated rats, and cerebral blood flow (CBF) was determined using a combination of labeled microspheres. Moderate hypertension within the upper limit of cerebral autoregulation was induced by blood transfusion in order to measure CBF at normotension. Arterial blood pressure (ABP) was decreased by unilateral microinjection into the NTS in these rats but remained within normotensive range. The CBF in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) decreased from 38 +/- 4 (mean +/- S.E.M) to 27 +/- 4 ml.min-1.(100 g)-1(n = 9). The cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) increased from 2.6 +/- 0.3 to 4.1 +/- 0.7 mmHg per [ml.min-1.(100 g)-1]. Blockade of NMDA receptors in the NTS with D,L-2-amino-5-phosphonovalerate (AP5, 500 pmol) abolished the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 9). Blockade of non-NMDA receptors in the NTS with 6,7-dinitro-quinoxaline-2,3-dione (DNQX, 100 pmol) had little effect on the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 10). Microinjection of the vehicle solution into the NTS had no effects on cerebral circulation (n = 7). Cerebral autoregulation was well maintained at moderate hypertension induced by blood transfusion and at normotension returned from moderate hypertension following controlled hemorrhage (n = 8). These results suggest that the NMDA receptors in the NTS may be involved in the control of cerebral circulation.

2-Amino-5-phosphonovalerate↗

PubMed1989

Bombesin microinjected into the dorsal vagal complex inhibits vagally stimulated gastric acid secretion in the rat.

Medullary sites of action for bombesin-induced inhibition of gastric acid secretion were investigated in urethane-anesthetized rats with gastric fistula. Unilateral microinjection of bombesin or vehicle into the dorsal vagal complex was performed using a glass micropipet and pressure ejection of 100 nl volume; gastric acid output was measured every 10 min by flushing the stomach. Microinjection of vehicle into the dorsal vagal complex did not alter gastric acid secretion (1.9 +/- mumol/10) from preinjection levels (2.9 +/- 0.8 mumol/10 min). Microinjection of the stable thyrotropin-releasing hormone (TRH) analog, RX 77368, at a 77 pmol dose into the dorsal vagal complex stimulated gastric acid secretion for 100 min with a peak response at 40 min (24.1 +/- 3.2 mumol/10 min). Concomitant microinjection of RX 77368 (77 pmol) with bombesin (0.6-6.2 pmol) into the dorsal vagal complex dose dependently inhibited by 35-86% the gastric acid response to the TRH analog. Bombesin (6.2 pmol) microinjected into the dorsal vagal complex inhibited by 17% pentagastrin infusion-induced stimulation of gastric acid secretion (13.2 +/- 0.8 mumol/10 min) whereas intracisternal injection induced a 69% inhibition of the pentagastrin response. These results demonstrate that the dorsal motor complex is a sensitive site of action for bombesin-induced inhibition of vagally stimulated gastric secretion. However, other medullary sites must be involved in mediating the inhibitory effect of intracisternal bombesin on pentagastrin-stimulated gastric acid secretion.

Animals↗

PubMed1988

Intrahypothalamic microinjection of calcitonin prevents stress-induced gastric lesions in rats.

Injection of salmon calcitonin into the lateral ventricle or the cisterna magna was reported to potently inhibit gastric lesions induced by cold restraint stress. The forebrain sites of action were investigated using unilateral microinjection of salmon calcitonin prior to exposing conscious pylorus-ligated rats to cold restraint stress for 2 hr. Calcitonin (100 ng), microinjected in 100 nl volume by pressure ejection from glass micropipette positioned into the lateral or ventromedial hypothalamus or the paraventricular nucleus, prevented the development of gastric lesions whereas microinjections into the caudate putamen, the cerebral cortex or the hippocampus were ineffective. The antiulcerogenic effect of lateral hypothalamic injection was dose dependent and specific since calcitonin gene-related peptide, tested under the same conditions, had no effect. Microinjection of calcitonin at 100 ng dose into the ventromedial hypothalamus did not modify gastric secretion whereas microinjection into the lateral hypothalamus or the paraventricular nucleus induced 75-82% inhibition of gastric acid output in pylorus-ligated rats exposed to restraint stress. These results demonstrate that the hypothalamus including the lateral, ventromedial and paraventricular nuclei are responsive sites of action for calcitonin-induced inhibition of cold restraint stress ulcers. The antiulcerogenic effect may be related to suppression of gastric acid secretion along with other mechanisms that remain to be elucidated.

Animals↗

PubMed1994

Complementation of xeroderma pigmentosum cells by microinjection of mRNA fractionated under denaturing conditions: an estimation of sizes of XP-E and XP-G mRNA.

Excision repair deficiencies in groups A and G xeroderma pigmentosum (XP) cells are transiently complemented after microinjection of HeLa poly(A)+RNA, but those in groups D and F are not complemented (Legerski et al., 1984). We tested XP cells belonging to the seven complementation groups, A-G, and Cockayne's syndrome (CS) cells belonging to the two complementation groups, A and B, for transient correction by microinjection of total poly(A)+RNA from HeLa cells. Among the XP cells, unscheduled DNA synthesis (UDS) was increased only in XP-A cells by microinjection of total poly(A)+RNA. However, UDS was increased in XP-E and XP-G cells as well as in XP-A cells by microinjection of concentrated poly(A)+RNA fractionated on a 5-25% sucrose density gradient containing methylmercuric hydroxide. The sizes of XP-E and XP-G mRNA were estimated to be 1.5-2.7 kb and 2.0-3.8 kb, respectively, by comparison to internal marker RNAs including 18S rRNA, 28S rRNA, HPRT mRNA and XPAC mRNA. RNA synthesis recovery after UV exposure in CS cells was not increased by microinjection of either total poly(A)+RNA or fractionated RNA. These results provide estimates of the sizes of XP-E and XP-G proteins and will facilitate molecular cloning of DNA repair genes, especially of XP-E and XP-G genes.

Centrifugation, Density Gradient↗

PubMed2005

Hemodynamic and respiratory responses to microinjection of ATP into the intermediate and caudal NTS of awake rats.

The nucleus tractus solitarii (NTS) is the site of integration of the peripheral chemoreceptor afferents in the brainstem. Previous studies from our laboratory have shown that microinjection of ATP into the intermediate NTS produced increases in arterial pressure and bradycardia. In the present study, we evaluated the hemodynamic and respiratory responses to microinjection of ATP into the intermediate and caudal commissural NTS. In the same group of rats the responses were compared with cardiorespiratory responses to chemoreflex activation (KCN, i.v.). The data show that microinjection of ATP into the intermediate NTS produced pressor and bradycardic responses similar to those observed in response to chemoreflex activation but apnoea instead of tachypnoea. Microinjection of ATP into caudal commissural NTS produced increase in arterial pressure and tachypnoea similar to the chemoreflex but a minor bradycardia. The data show that microinjection of ATP into different sub-regions of the NTS produces a diverse pattern of hemodynamic and respiratory responses and suggest the involvement of this purine in the neurotransmission of the cardiovascular reflex in the NTS.

Adenosine Triphosphate↗

PubMed2005

Respiratory and autonomic responses to microinjection of NMDA and AMPA into the commissural subnucleus of the NTS of awake rats.

The changes in mean arterial pressure (MAP) and respiratory frequency (RF) in response to microinjection of NMDA or AMPA into the commissural subnucleus of the NTS (comNTS) at the calamus scriptorius level of awake rats were evaluated. Under tribromoethanol anesthesia, the rats received guide-cannulae in direction of the NTS and a catheter was inserted into the femoral artery for measurement of arterial pressure. Changes in RF were evaluated with the rats inside a plethysmographic chamber. Randomly microinjections of 5 doses of NMDA (0.001, 0.01, 0.1, 1.0 and 2 nmol/50 nL; n = 10) or AMPA (1, 5, 10, 25 and 50 pmol/50 nL; n = 8) into the comNTS were performed at 15 min intervals and produced a dose-dependent increase in MAP [NMDA (3 +/- 2, 4 +/- 3, 25 +/- 4, 41 +/- 4 and 51 +/- 4 mm Hg) and AMPA (0 +/- 1, 14 +/- 4, 17 +/- 3, 27 +/- 5 and 34 +/- 3 mm Hg)]. Microinjection of NMDA (1 nmol/50 nL; n = 7) or AMPA (50 pmol/50 nL; n = 4) into the comNTS produced a long lasting apnea. The pressor responses to microinjection of NMDA or AMPA into the comNTS were blocked by prazosin, a alpha(1)-adrenoceptor antagonist, indicating that the increase in arterial pressure in both cases was sympathetically mediated. The data show that microinjection of NMDA and AMPA into the comNTS produced pressor response and apnea, indicating that both ionotropic l-glutamate receptors may play a role in the neurotransmission/neuromodulation of the autonomic and respiratory components of the cardiovascular reflexes at this level.

Analysis of Variance↗

PubMed2006

Antinociceptive tolerance revealed by cumulative intracranial microinjections of morphine into the periaqueductal gray in the rat.

The periaqueductal gray (PAG) appears to play a key role in morphine antinociception and tolerance. The objective of this manuscript is to develop a cumulative dose microinjection procedure so the hypothesized role of the PAG in morphine antinociceptive tolerance can be assessed using dose-response analysis. Rats were implanted with a guide cannula into the ventrolateral PAG. Microinjection of cumulative half log doses of morphine (0.32, 1, 3.2, and 10 micro g/0.4 micro l) produced antinociception on the hot plate test only at the two highest doses. Microinjection of quarter log doses of morphine into the PAG (1, 1.8, 3.2, 5.6, and 10 micro g/0.4 micro l) resulted in an ED(50) for antinociception of 1.8 mug. Systemic administration of the opioid antagonist naloxone increased the morphine ED(50) to 9.0 micro g. Repeated microinjections of saline into the PAG had no effect on nociception. Pretreatment with twice daily injections of morphine, either systemically (5 mg/kg, s.c.) or into the PAG (5 micro g/0.4 micro l), for 2 days produced a two-fold increase in the ED(50) for morphine antinociception. These data validate the use of an intracranial cumulative dose procedure to assess morphine potency and demonstrate that microinjection of morphine into the PAG is sufficient to produce tolerance.

Analgesics, Opioid↗

PubMed1998

Antinociception produced by microinjection of morphine in the rat periaqueductal gray is enhanced in the foot, but not the tail, by intrathecal injection of alpha1-adrenoceptor antagonists.

Antinociception produced by microinjection of morphine in the ventrolateral periaqueductal gray is mediated in part by alpha2-adrenoceptors in the spinal cord dorsal horn. However, several recent reports demonstrate that microinjection of morphine in the ventrolateral periaqueductal gray inhibits nociceptive responses to noxious heating of the tail by activating descending neuronal systems that are different from those that inhibit the nociceptive responses to noxious heating of the feet. More specifically, alpha2-adrenoceptors appear to mediate the antinociception produced by morphine using the tail-flick test, but not that using the foot-withdrawal or hot-plate tests. The present study extended these findings and determined the role of alpha1-adrenoceptors in mediating the antinociceptive effects of morphine microinjected into the ventrolateral periaqueductal gray using both the foot-withdrawal and the tail-flick responses to noxious radiant heating in lightly anesthetized rats. Intrathecal injection of selective antagonists was used to determine whether the antinociceptive effects of morphine were modulated by alpha1-adrenoceptors. Injection of the selective alpha1-adrenoceptor antagonists prazosin or WB4101 potentiated the increase in the foot-withdrawal response latency produced by microinjection of morphine in the ventrolateral periaqueductal gray. In contrast, either prazosin or WB4101 partially reversed the increase in the tail-flick response latency produced by morphine. These results indicate that microinjection of morphine in the ventrolateral periaqueductal gray modulates nociceptive responses to noxious heating of the feet by activating descending neuronal systems that are different from those that inhibit the nociceptive responses to noxious heating of the tail. More specifically, alpha1-adrenoceptors mediate a pro-nociceptive action of morphine using the foot-withdrawal response, but in contrast, alpha1-adrenoceptors appear to mediate part of the antinociceptive effect of morphine determined using the tail-flick test.

Adrenergic alpha-Antagonists↗

PubMed2003

Quantitative microinjection of trehalose into mouse oocytes and zygotes, and its effect on development.

Sugars such as trehalose are effectively used by various organisms as protective agents to undergo anhydrobiosis and cryobiosis. The objective of this study was first to establish a method for quantitative delivery of trehalose as a model sugar into oocytes, and then to evaluate its effect on development of mouse zygotes. To this end, a quantitative microinjection technique was developed using volumetric response of microdroplets suspended in dimethylpolysilaxene. To verify accuracy of this technique, both microdroplets and oocytes were microinjected with fluorophore-labeled dextran. Thereafter, injection volumes were calculated from fluorescence intensity, and volumetric responses of both microdroplets and oocytes. Comparison of calculated injection volumes revealed that this technique reflects microinjection into oocytes with pL-accuracy. The next series of experiments focused on toxicity of injection buffers (i.e., 10mM Tris and 15mM Hepes) and trehalose. Microinjection of Hepes and Tris buffer in the presence of 0.1M trehalose resulted in blastocyst rates of 86 and 72%, respectively, without a significant difference when compared to controls (86%). In subsequent experiments, Hepes was used as the injection buffer, and embryonic development of zygotes was studied as a function of intracellular trehalose concentrations. Microinjection of trehalose up to 0.15M resulted in development to blastocyst stage similar to controls (85 and 87%, respectively) while the blastocyst rate was significantly decreased (43%) in the presence of 0.20M intracellular trehalose. When transferred to foster mothers, trehalose-injected zygotes (0.1M) implanted and developed to day 16 fetuses similar to controls, healthy pups were born. The findings of this study suggest that trehalose at effective intracellular concentrations does not impair development of mouse zygotes.

Animals↗

PubMed2000

Bradycardic responses to microinjection of N-methyl-D-aspartate into the nucleus tractus solitarius are inhibited by local activation of 5-HT(3) receptors.

Previous reports have described that glutamate ionotropic receptors in the nucleus tractus solitarius (NTS) are involved in the reflex control of heart rate, and that such a control can be inhibited by NTS-5-HT(3) receptor stimulation. In the present study, we examined in urethane anaesthetized rats the effects of intra-NTS microinjection of 1-(m-chlorophenyl)-biguanide (CPBG), a potent and selective 5-HT(3) receptor agonist, on the cardiovascular responses to local administration of glutamate ionotropic receptor agonists. Intra-NTS microinjection of CPBG reduced the atropine-sensitive bradycardia elicited by local microinjection of NMDA without affecting the cardiovascular responses to intra-NTS microinjections of AMPA or kainic acid. The reduction by CPBG of the NMDA-evoked cardiac response was blocked by prior intra-NTS microinjection of granisetron, a 5-HT(3) receptor antagonist, as well as bicuculline, a GABA(A) receptor antagonist. These results suggest that the stimulation of NTS 5-HT(3) receptors specifically reduces, via a GABA-dependent mechanism, the cardiac response to local NMDA administration.

Animals↗

PubMed1999

The effects of microinjection of d-amphetamine into the n. accumbens during the late maintenance phase of an ethanol consumption bout.

The microinjection of d-amphetamine into the n. accumbens of rats, prior to the start of an operant ethanol self-administration session, increases operant behavior and the amounts of ethanol presented as the reinforcer. Although this effect could result by blocking termination processes regulating a consummatory bout, it could also be a result of enhancing the stimulus control regulating the maintenance of a drinking bout. To explore this issue, rats were trained to self-administer 10% ethanol in an operant situation. Following establishment of stable behavior, they were surgically instrumented so that the n. accumbens could be microinjected with d-amphetamine during a drinking bout, without having to handle the animal. The microinjection of d-amphetamine in the rats self-administering ethanol at the late phase of the drinking bout resulted in a prolonged bout and increased self-administration. During extinction testing, a reinstatement of responding was found following the amphetamine microinjection. The data suggest the most likely action of the amphetamine microinjection was to alter stimulus control factors, which normally regulate the maintenance of drinking, thereby prolonging the bout and increasing intake.

Alcohol Drinking↗

PubMed1997

Microinjection of a serotonin3 receptor agonist into the NTS of unanesthetized rats inhibits the bradycardia evoked by activation of the baro- and chemoreflexes.

In the present study we investigated the effects of microinjection into the commissural nucleus tractus solitarius (NTS) of unanesthetized rats of 2-methylserotonin (2-methyl-5-HT), a 5-HT3 receptor agonist, on the cardiac component of the baro- and chemoreflexes. The study was performed in conscious freely moving rats in order to avoid the possible effects of anesthetics on the cardiovascular responses to microinjection of neuroactive substances into the NTS. The baroreflex (phenylephrine, 0.5-2.0 micrograms/kg, i.v.) and the chemoreflex (potassium cyanide, 40 micrograms/rat, i.v) were activated in different groups of rats before and after bilateral microinjection of 2-methyl-5-HT into the NTS. Microinjections of 2-methyl-5-HT (5 nmol/50 nl) into the NTS produced a significant increase in basal mean arterial pressure (101 +/- 3 versus 125 +/- 8 mmHg), no changes in basal HR and a significant reduction in the reflex bradycardia triggered by baroreflex activation at 3 (-28 +/- 7 bpm), 10 (-35 +/- 4 bpm) and 20 min (-34 +/- 5 bpm) in comparison with the control value (-68 +/- 9 bpm). A similar reduction in the bradycardic response to chemoreflex activation was observed at 3 (-94 +/- 35 bpm), 10 (-98 +/- 38 bpm) and 20 min (-110 +/- 29 bpm) after 2-methyl-5-HT in comparison with the control value (-178 +/- 19 bpm). The effect of 2-methyl-5-HT on the basal mean arterial pressure and on the bradycardia evoked by stimulation of the baro- and chemoreflexes was blocked by pretreatment with granisetron bilaterally microinjected (500 pmol/50 nl) into the NTS. The data show that the stimulation of 5-HT3 receptors in the NTS of unanesthetized rats elicits a significant increase in basal mean arterial pressure and decreases the bradycardic response to baro- or chemoreflex activation.

Animals↗

PubMed1997

Regional differentiation of blood flow responses to microinjection of sodium nitroprusside into the nucleus tractus solitarius of anesthetized rats.

This study was undertaken to examine the effects of the activation of the neurons in the nucleus tractus solitarius (NTS) via microinjection of sodium nitroprusside (SNP), which spontaneously releases nitric oxide (NO), on the blood flows of the spleen, kidney, liver, brain and spinal cord and to investigate the regional differentiation of the blood flow changes between those organs. Employing urethane-anesthetized (1.5 g kg-1, i.p.), paralyzed and artificially ventilated rats, regional blood flows of those organs were determined simultaneously using radiolabeled microspheres (109Cd, 51Cr and 85Sr) Unilateral microinjection of SNP into the NTS (n = 9) decreased brain blood flow from 71 +/- 8 (mean +/- S.E.) to 54 +/- 6 (P < 0.01) and spinal cord blood flow from 58 +/- 8 to 43 +/- 5 ml min-1 (100 g)-1 (P < 0.05) and increased brain vascular resistance from 1.18 +/- 0.13 to 1.48 +/- 0.15 (P < 0.01) and spinal cord vascular resistance from 1.46 +/- 0.17 to 1.80 +/- 0.16 (P < 0.05) mmHg per [ml min-1 (100 g)-1]. Whereas the microinjection of SNP into the NTS increased splenic blood flow from 127 +/- 25 to 188 +/- 27 (P < 0.01) and renal blood flow from 346 +/- 28 to 371 +/- 26 ml min-1 (100 g) (P < 0.05) and decreased splenic vascular resistance from 0.77 +/- 0.13 to 0.44 +/- 0.06 (P < 0.01) and renal vascular resistance from 0.24 +/- 0.02 to 0.21 +/- 0.01 mmHg per [ml min-1 (100 g)-1] (P < 0.05). The blood flow of the liver was not significantly altered. Unilateral microinjection of NG-monomethyl-L-arginine, an inhibitor of the formation of NO from L-arginine, into the NTS (n = 10) did not significantly change the blood flows of all organs examined except for an increase in blood flow of the kidney. Unilateral microinjections of SNP into the area adjacent to the NTS (n = 9), of artificial cerebrospinal fluid into the NTS (n = 7) and of light-inactivated SNP into the NTS (n = 6) did not significantly alter the blood flows of all organs examined. These results suggest than the neurons in the NTS have a vasoconstrictor effect on the brain and spinal cord circulation and a vasodilator effect on the splenic and renal circulation. There is a regional qualitative differentiation of the blood flow responses between these organs during activation of the neurons in the NTS.

Anesthesia↗

PubMed1999

Modulation of sympathetic nerve activity by microinjection of the 5-HT1A receptor agonist 8-OH-DPAT into the rostroventrolateral medulla.

In the present study, renal sympathetic nerve activity was recorded simultaneously with sympathetic nerve activity to skeletal muscle vasculature to determine if the sympatho-inhibition evoked by microinjection of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)teralin (8-OH-DPAT) into the rostroventrolateral medulla (RVLM) was uniform or regional. Three patterns of sympatho-inhibition were observed in these sympathetic outflows and the type of response depended upon location of microinjection within the subretrofacial nucleus (SRF). Inhibition of renal nerve activity only was elicited by microinjections at rostral sites at the caudal pole of the facial nucleus. In contrast, inhibition of muscle sympathetic nerve activity was evoked from more caudal injections at the rostral pole of the inferior olives. Microinjection in the area between these two regions produced inhibition of both sympathetic outflows. This study demonstrates that differential inhibition of regional sympathetic outflows can be elicited by microinjection of the 5-HT1A receptor agonist 8-OH-DPAT into the RVLM. These data suggests that this modulation is due to differences in anatomical arrangement of the medullary neurons rather than differences in neuron sensitivity to the serotonergic agonist.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2001

Tolerance to repeated microinjection of morphine into the periaqueductal gray is associated with changes in the behavior of off- and on-cells in the rostral ventromedial medulla of rats.

Although the administration of opioids is the most effective treatment for pain, their efficacy is limited by the development of tolerance. The midbrain periaqueductal gray matter (PAG) participates in opioid analgesia and tolerance. Microinjection of morphine into PAG produces antinociception, probably through neurons in the rostral ventromedial medulla (RVM), namely through the activation of off-cells, which inhibit nociception, and the inhibition of on-cells, which facilitate nociception. After its repeated microinjection into the PAG morphine loses effectiveness. The present study sought to determine whether tolerance to PAG morphine administration is associated with changes in the behavior of RVM neurons. Morphine (0.5 microg/0.4 microl) or saline (0.4 microl) was microinjected into the ventrolateral PAG twice daily. Initially morphine caused a latency increase in the hot plate test (antinociception) but this effect disappeared by day 3 (tolerance). On day 4, each rat was anesthetized with halothane and recordings were made from off- and on-cells in the RVM, i.e. from neurons that decrease or increase their firing, respectively, just before a heat-elicited tail flick. In contrast to saline-pretreated rats, PAG microinjection of morphine in tolerant animals did not change the baseline activity of off- or on-cells, did not prevent the off-cell pause or the on-cell activation upon tail heating, and did not lengthen the tail flick latency. However, microinjection of kainic acid into the PAG (1) caused off-cells to become continuously active and on-cells to become silent, and (2) prevented the tail flick, i.e. exactly what morphine did before tolerance developed. These results demonstrate a correspondence between neuronal and behavioral measures of tolerance to PAG opioid administration, and suggest that tolerance is mediated by a change in opioid-sensitive neurons within the PAG.

Analgesics, Opioid↗