SEARCH · PubMed Health

Results for “Microinjection”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

PubMed1992

Morphological changes of cultured endothelial cells after microinjection of toxins that act on the cytoskeleton.

Clostridium novyi alpha-toxin and C. difficile toxins A and B (all 200 to 300 kDa) and C. botulinum C2-I toxin (50 kDa) caused a delayed and persistent retraction and rounding of microinjected cells. Microinjected phalloidin acted fast and reversibly. Unlike C2-I toxin, phalloidin passed through the intercellular junctions. Specific antitoxin applied to the medium did not prevent the action of microinjected C. novyi or C. difficile toxin B. Microinjected antitoxin protected against the toxins applied with the medium or injected into the same cells.

Bacterial Proteins↗

PubMed1985

Phosphorylation and protein synthetic events in Xenopus laevis oocytes microinjected with pp60v-src.

Microinjection of purified pp60v-src, the transforming protein of Rous sarcoma virus, into Xenopus laevis oocytes accelerated the rate of progesterone- or insulin-induced meiotic maturation. This acceleration was abolished by incubating the oocytes with cycloheximide or puromycin during a 2-h interval between pp60v-src microinjection and progesterone addition. In contrast, exposure to actinomycin D did not alter the acceleration of maturation by microinjected pp60v-src. Associated with progesterone treatment and pp60v-src microinjection were a number of qualitative changes in phosphoproteins; a few of these changes are common to both stimuli. These results indicate that the action of pp60v-src in oocytes involves both phosphorylation and protein synthetic events that affect oocyte maturation.

Animals↗

PubMed1990

Cardiovascular effects of microinjection of ANF and brain natriuretic peptide into ventrolateral medulla.

Cardiovascular effects of microinjection of atrial natriuretic factor (ANF) into 77 sites of the ventrolateral medulla (VLM) were investigated in urethan-anesthetized rats. Changes in mean arterial pressure (MAP) and heart rate (HR) in response to injections of glutamate into these sites were used to determine that they contained cardiovascular neurons. ANF (20 nl of 10(-7) M) decreased MAP [-8.9 +/- 1.5 (SE) mmHg] and HR [-9.0 +/- 2.8 (SE) beats/min] in 5 of 36 vasopressor sites identified by glutamate located in the more rostral and lateral aspect of the rostral VLM (RVLM); no effect was elicited in the other 31 RVLM sites. ANF decreased MAP (-10.4 +/- 2.4 mmHg) and HR (-9.8 +/- 3.0 beats/min) in 25 of 41 depressor sites distributed throughout the caudal VLM (CVLM); no response was observed in the other 16 CVLM sites. Brain natriuretic peptide (BNP) was microinjected (20 nl of 10(-7) M) in 21 VLM sites, before or after microinjection of ANF. BNP and ANF elicited similar results in 17 sites, a decline in MAP and HR in 10 sites, and no effect in 7 sites. In the remaining four cases ANF caused a decline in MAP and in HR, whereas BNP had minimal or no effect. Cardiovascular responses to ANF microinjection into the RVLM and CVLM support the hypothesis that ANF is involved in the transmission of baroreceptor information from the nucleus tractus solitarii to these medullary regions. The similarity of the results obtained with BNP and ANF suggests that these peptides may serve similar roles in medullary pathways involved in the control of the cardiovascular system.

Animals↗

PubMed1991

Neuronal and cardiovascular responses to ANF microinjected into nucleus ambiguous.

Effects of microinjection of atrial natriuretic factor (ANF) into cardioinhibitory sites in the nucleus ambiguous (NA) or on single vagal cardioinhibitory neurons (VCN) were investigated in urethan-anesthetized rats. Sites containing cardioinhibitory neurons were identified by observing a marked and reproducible bradycardia in response to microiontophoretically applied (20-40 nA) or microinjected (20 nl) 0.1 M L-glutamate. In 35 of the 40 (87.5%) cardioinhibitory sites identified by microinjection of glutamate, ANF (20 nl of 10(-7) M) decreased heart rate (HR; -47.1 +/- 2.5 beats/min). No responses were elicited in the other five sites. In animals paralyzed and artificially ventilated, the HR effects of ANF were not significantly different before and after muscle paralysis. Microinjections of 10 nl of 10(-7) M ANF caused excitation of 19 of 21 VCN (90%), which was followed by a decrease in HR (-20.8 +/- 2.3 beats/min); no neuronal or cardiovascular responses were elicited by ANF in the remaining two VCN. Bilateral vagotomy or atropine sulfate (1 mg/kg iv) abolished cardiac slowing without affecting neuronal activation, whereas propranolol (2 mg/kg iv) did not affect either response to ANF. These results suggest that ANF is a neuromediator involved in the excitation of cardioinhibitory neurons in the NA.

Animals↗

PubMed1995

Hypothalamic sites mediating cardiovascular effects of microinjected bicuculline and EAAs in rats.

Microinjection of gamma-aminobutyric acidA receptor antagonist bicuculline methiodide (BMI) into either the dorsomedial hypothalamic nucleus (DMH) or the nearby paraventricular hypothalamic nucleus (PVN) has been reported to evoke marked tachycardia and modest pressor effects. We compared the effects of microinjecting BMI and excitatory amino acids (EAAs) into 1) the DMH, 2) the PVN, and 3) an intermediate area between the two nuclei. In conscious rats, microinjection of (in pmol) 10 BMI, 0.5 kainic acid, or 5 N-methyl-D-aspartate into the DMH markedly increased heart rate and slightly elevated arterial pressure, whereas injections into other regions provoked changes that progressively declined in magnitude with increasing distance from the nucleus. A similar pattern was evident in urethan-anesthetized rats, where the shortest latency to onset of BMI-induced increases in heart rate was seen after injection into the DMH. These findings demonstrate that the cardiovascular changes seen after microinjection of BMI or EAAs into the medial hypothalamus result from an action in the DMH and not from spread to the PVN.

Anesthesia↗

PubMed2000

Receptor subtypes mediating depressor responses to microinjections of nicotine into medial NTS of the rat.

Microinjections (50 nl) of nicotine (0.01-10 microM) into the nucleus of the solitary tract (NTS) of adult, urethan-anesthetized, artificially ventilated, male Wistar rats, elicited decreases in blood pressure and heart rate. Prior microinjections of alpha-bungarotoxin (alpha-BT) and alpha-conotoxin ImI (specific toxins for nicotinic receptors containing alpha7 subunits) elicited a 20-38% reduction in nicotine responses. Similarly, prior microinjections of hexamethonium, mecamylamine, and alpha-conotoxin AuIB (specific blockers or toxin for nicotinic receptors containing alpha3beta4 subunits) elicited a 47-79% reduction in nicotine responses. Nicotine responses were completely blocked by prior sequential microinjections of alpha-BT and mecamylamine into the NTS. Complete blockade of excitatory amino acid receptors (EAARs) in the NTS did not attenuate the responses to nicotine. It was concluded that 1) the predominant type of nicotinic receptor in the NTS contains alpha3beta4 subunits, 2) a smaller proportion contains alpha7 subunits, 3) the presynaptic nicotinic receptors in the NTS do not contribute to nicotine-induced responses, and 4) EAARs in the NTS are not involved in mediating responses to nicotine.

Anesthesia↗

PubMed2001

Microinjection of glutamate into the pedunculopontine tegmentum induces REM sleep and wakefulness in the rat.

The aim of this study was to test the hypothesis that the cells in the brain stem pedunculopontine tegmentum (PPT) are critically involved in the normal regulation of wakefulness and rapid eye movement (REM) sleep. To test this hypothesis, one of four different doses of the excitatory amino acid L-glutamate (15, 30, 60, and 90 ng) or saline (control vehicle) was microinjected unilaterally into the PPT while the effects on wakefulness and sleep were quantified in freely moving chronically instrumented rats. All microinjections were made during wakefulness and were followed by 6 h of polygraphic recording. Microinjection of 15- ng (0.08 nmol) and 30-ng (0.16 nmol) doses of L-glutamate into the PPT increased the total amount of REM sleep. Both doses of L-glutamate increased REM sleep at the expense of slow-wave sleep (SWS) but not wakefulness. Interestingly, the 60-ng (0.32 nmol) dose of L-glutamate increased both REM sleep and wakefulness. The total increase in REM sleep after the 60-ng dose of L-glutamate was significantly less than the increase from the 30-ng dose. The 90-ng (0.48 nmol) dose of L-glutamate kept animals awake for 2-3 h by eliminating both SWS and REM sleep. These results show that the L-glutamate microinjection into the PPT can increase wakefulness and/or REM sleep depending on the dosage. These findings support the hypothesis that excitation of the PPT cells is causal to the generation of wakefulness and REM sleep in the rat. In addition, the results of this study led to the identification of the PPT dosage of L-glutamate that optimally induces wakefulness and REM sleep. The knowledge of this optimal dose will be useful in future studies investigating the second messenger systems involved in the regulation of wakefulness and REM sleep.

Animals↗

PubMed2006

Microinjection of DLH into the region of the caudal ventral respiratory column in the cat: evidence for an endogenous cough-suppressant mechanism.

The caudal ventral respiratory column (cVRC) contains premotor expiratory neurons that play an important role in cough-related expiratory activity of chest wall and abdominal muscles. Microinjection of d,l-homocysteic acid (DLH) was used to test the hypothesis that local activation of cVRC neurons can suppress the cough reflex. DLH (20-50 mM, 10-30 nl) was injected into the region of cVRC in nine anesthetized spontaneously breathing cats. Repetitive coughing was elicited by mechanical stimulation of the intrathoracic airways. Electromyograms (EMG) were recorded bilaterally from inspiratory parasternal and expiratory transversus abdominis (ABD) and unilaterally from laryngeal posterior cricoarytenoid and thyroarytenoid muscles. Unilateral microinjection of DLH (1-1.5 nmol) elicited bilateral increases in tonic and phasic respiratory ABD EMG activity, and it altered the respiratory pattern and laryngeal motor activities. However, DLH also decreased cough frequency by 51 +/- 7% compared with control (P < 0.001) and the amplitude of the contralateral (-35 +/- 3%; P < 0.001) and ipsilateral (-34 +/- 5%; P < 0.001) ABD EMGs during postinjection coughs compared with control. The cough alterations were much less pronounced after microinjection of a lower dose of DLH (0.34-0.8 nmol). No cough depression was observed after microinjections of vehicle. These results suggest that an endogenous cough suppressant neuronal network in the region of the cVRC may exist, and this network may be involved in the control of cough reflex excitability.

Animals↗

PubMed2001

Increased and decreased muscle tone with orexin (hypocretin) microinjections in the locus coeruleus and pontine inhibitory area.

Orexin-A (OX-A) and orexin-B (OX-B) (hypocretin 1 and hypocretin 2) are synthesized in neurons of the perifornical, dorsomedial, lateral, and posterior hypothalamus. The locus coeruleus (LC) receives the densest extrahypothalamic projections of the orexin (OX) system. Recent evidence suggests that descending projections of the LC have a facilitatory role in the regulation of muscle tone. The pontine inhibitory area (PIA), located ventral to LC, receives a moderate OX projection and participates in the suppression of muscle tone in rapid-eye-movement sleep. We have examined the role of OX-A and -B in muscle-tone control using microinjections (0.1 microM to 1 mM, 0.2 microl) into the LC and PIA in decerebrate rats. OX-A and -B microinjections into the LC produced ipsi- or bilateral hindlimb muscle-tone facilitation. The activity of LC units was correlated with the extent of hindlimb muscle-tone facilitation after OX microinjections (100 microM, 1 microl) into fourth ventricle. Microinjections of OX-A and -B into the PIA produced muscle-tone inhibition. We did not observe any significant difference in the effect of OX-A and -B on muscle tone at either site. Our data suggest that OX release activates LC units and increases noradrenergic tonus in the CNS. Moreover, OX-A and -B may also regulate the activity of pontine cholinoceptive and cholinergic neurons participating in muscle-tone suppression. Loss of OX function may therefore disturb both facilitatory and inhibitory motor processes.

Animals↗

PubMed1998

Dopamine release in the nucleus accumbens and latent inhibition in the rat following microinjections of a 5-HT1B agonist into the dorsal subiculum: implications for schizophrenia.

Microinjection of a serotonergic 5-HT1B agonist (S-CM-GTNH2, 3 microg/l) into the dorsal subiculum (DS) induced long-lasting increases in dopamine (DA; +58%), dihydroxyphenylacetic acid (DOPAC; +15%) and homovanillic acid (HVA; +31%), without changing extracellular levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), measured by microdialysis in freely moving rats in the shell area of the nucleus accumbens (n. acc). Perfusion of a glutamate-N-methyl-D-aspartate (NMDA) receptor antagonist (MK 801, dizocilpine, 10 microM) through the dialysis probe in the n. acc induced similar long-lasting increases in DA and DOPAC, whereas the glutamate-quisqualate/kainate receptor antagonist (CNQX, 50 microM) had no effect. In the presence of dizocilpine in the n. acc, microinjection of S-CM-GTNH2 into the DS could still increase DOPAC and HVA, but DA levels were not further changed, whereas in the presence of CNQX, microinjection of S-CM-GTNH2 into the DS still increased not only DOPAC and HVA, but also DA levels in a way similar to that in the absence of glutamate antagonist. Therefore, activation of 5-HT1B receptors located in the DS increases the release of DA in the n. acc, presumably via the glutamatergic projection to this structure and acting through NMDA receptors in it. This implies either the suppression of a tonic indirect inhibitory influence and/or stimulation of a phasic excitatory effect of glutamate. Disruption of latent inhibition (LI) has been suggested as a model for a cognitive deficit in schizophrenia (hyperattention to irrelevant stimuli) and is usually associated with an increase in DA release in the n. acc. However, s.c. injection of RU 24 969 (0.5 mg/kg), a mixed 5-HT1A-5-HT1B agonist, which was previously shown to increase DA release in the n. acc, left LI unchanged. Moreover, bilateral microinjections of S-CM-GTNH2 into the rat DS tended to potentiate LI, in spite of the increase in DA in n. acc demonstrated here. It is concluded that not all increases in DA release in the n. acc are functionally equivalent. Sensitization of receptors or impulse-dependent increase in DA release might be necessary to disrupt LI. The possible role of altered serotonergic transmission, through h5-HT1B receptors (human homologue of the rat 5-HT1B receptors) located in the DS, in acute schizophrenia needs to be further investigated.

Animals↗

PubMed2005

Differential anaesthetic effects following microinjection of thiopentone and propofol into the pons of adult rats: a pilot study.

Identifying the central nervous system sites of action of anaesthetics is important for understanding the link between their molecular actions and clinical effects. The aim of the present pilot study was to compare the anaesthetic effect of bilateral microinjections of propofol and thiopentone (both 200 microg/microl, in Intralipid and 0.9% saline respectively) into a recently discovered anaesthetic-sensitive region in the rat brainstem, the "mesopontine tegmental anaesthetic area" (MPTA). Microinjections (1 microl per side) were made into the MPTA of fifteen male Sprague-Dawley rats. The effect of each agent on spontaneous behaviour, postural control and nociceptive responsiveness was subjectively assessed according to established criteria. The main finding was that thiopentone induced an "anaesthesia-like" state, including complete atonia and loss of righting ability, in 20% of the subjects. Overall, thiopentone significantly reduced postural control and had a moderate antinociceptive effect compared to saline microinjections (P < 0.01 and 0.05, respectively, Wilcoxon test). In contrast, propofol did not induce "anaesthesia" in any animal tested, although a similar antinociceptive effect to that of thiopentone was observed (P < 0.05, Wilcoxon test). In summary, propofol and thiopentone have different effects when microinjected into the MPTA. While both agents reduced reflex withdrawal to a nociceptive stimulus, only thiopentone induced an "anaesthesia-like" state.

Anesthesia↗

PubMed2004

Preclinical evaluation of a novel intracerebral microinjection instrument permitting electrophysiologically guided delivery of therapeutics.

OBJECTIVE: This series of studies was designed to evaluate the function of a new neurosurgical instrument for precision injection of therapeutics within the central nervous system. METHODS: An intracerebral microinjection instrument was designed to 1) allow multiple injections to be placed in three-dimensional space within a target structure from a single proximal brain penetration, 2) incur minimal injury at the site of injection, 3) enable accurate microvolume injections, and 4) permit electrophysiological recording during the injection procedure. Rats received injections of fluorescent microspheres or suspensions of labeled cells to test instrument function and level of induced trauma. A rodent model of stroke was used to test the instrument's ability to record electrocorticograms or somatosensory evoked potentials from normal and damaged tissue. RESULTS: Microliter volumes of fluorescent microspheres were accurately placed at predetermined sites within the rat striatum. Reactive gliosis was markedly reduced using the intracerebral microinjection instrument when compared with standard cannulas. In a stroke model, electrophysiological recording with the instrument allowed discrimination between viable and nonviable ischemic tissue, and function of pathways or circuits was assessed using evoked potentials. Embryonic stem cells grafted immediately after electrophysiological recordings demonstrated robust long-term survival. CONCLUSION: The intracerebral microinjection instrument enables electrophysiologically guided microinjection of therapeutics to target areas with exquisite accuracy while incurring minimal local trauma and reactive gliosis at the injection site. The instrument also permits minimally invasive, multiple injections to be disseminated in three-dimensional space within the target region from a single proximal penetration of the brain.

Animals↗

PubMed1996

Incorporation of proteins into (Xenopus) oocytes by proteoliposome microinjection: functional characterization of a novel aquaporin.

Xenopus laevis oocytes are widely used as an expression system for plasma membrane proteins, achieved by cytoplasmic microinjection of messenger RNA. In the present study, we propose an alternative system allowing functional insertion of exogenous proteins into the plasma membrane of Xenopus oocytes. We microinjected proteoliposome suspensions into the cytoplasm and then analyzed membrane protein function. The proteins used in this work were members of the MIP family: the human erythrocyte water channel aquaporin 1 (AQP1), the major intrinsic protein (MIP26) from bovine eye lens and a 25 kDa polypeptide (P25) from a water shunting complex found in the digestive tract of an homopteran sap-sucking insect (Cicadella viridis). Proteoliposomes containing either AQP1, MIP26, or P25 were injected into Xenopus oocytes. The subsequent insertion of these proteins into the plasma membrane of oocytes was demonstrated by immunocytochemistry. Oocytes microinjected with either AQP1 or P25-proteoliposomes exhibited significantly increased osmotic membrane water permeabilities (Pf = 3.16 +/- 026 and 4.03 +/- 0.26 x 10(-3) cm/second, respectively) compared to those measured for oocytes injected with liposomes alone or with MIP26-proteoliposomes (Pf = 1.39 +/- 0.07 and 1.44 +/- 0.10 x 10(-3) cm/second, respectively). These effects were inhibited by HgCl2 in a reversible manner. Arrhenius activation energies of water transfer were low when AQP1 or P25 were present in oocyte plasma membranes (Ea = 2.29 and 3.01 kcal/mol, respectively, versus Ea = 11.75 kcal/mol for liposome injected oocytes). The properties observed here for AQP1 are identical to those widely reported following AQP1 cRNA expression in oocytes. From the present study, we conclude that: (1) exogenous plasma membrane proteins incorporated into liposomes and microinjected into the cytoplasm of Xenopus oocytes are subsequently found in the plasma membrane of the oocytes in a functional state; and (2) in this system, the P25 polypeptide from the MIP family found in the digestive tract of Cicadella viridis exhibits properties similar to those described for the archetype of water channels AQP1, and thus is a new member of the aquaporin family.

Animals↗

PubMed1991

Propagation of transient Ca2+ increase in sea urchin eggs upon fertilization and its regulation by microinjecting EGTA solution.

Upon fertilization, the concentration of intracellular Ca2+ (Cai) in sea urchin eggs increased up to 3 microM when measured with fura-2, a fluorescent Ca indicator and the increase in Cai traversed from the sperm entry point as a wave over the entire egg at the mean propagation velocities of 5.0 microns/sec in C. japonicus egg and 5.3 microns/sec in H. pulcherrimus egg. However, the velocity was not uniform; i.e., it was rapid in the vicinity of the sperm entry point and the opposite point, but slow in the central region of the egg. Microinjecting a Ca-EGTA buffer and an IP3 solution into the C. japonicus egg induced the transient Cai increase more rapidly than that upon fertilization, due perhaps to the diffusion of the injectates. In order to investigate Ca2+ release during Cai increase upon fertilization, EGTA solutions were microinjected into unfertilized or fertilizing eggs. Microinjecting 100 mM EGTA (final concentration of 1 mM) not only suppressed the transient Cai increase, but also reduced the increased Cai rapidly, and never induced egg activation after insemination, whereas 10 mM EGTA (final concentration of 0.1 mM) did not significantly affect the Cai increase or the activation. Ca2+ released upon fertilization was estimated to be 150-170 microM in the egg cytoplasm from the amount of microinjected EGTA and fura-2. It was concluded that although more than 150 microM of Ca2+ was released intracellularly upon fertilization, Cai increased to only a few microM because most of the released Ca2+ was sequestered by intracellular Ca2+ binding substances.

Animals↗

PubMed2002

[Coughing model by microinjection of citric acid into the larynx in guinea pig].

Many studies of cough were performed under the restrained or anesthetized condition, and coughs were evoked by inhalation of capsaicin or citric acid. Inhalation of irritants induced by "diving response" with apnea and coughs, and these responses induced a change of tidal volume. As a result, respiratory responses are dependent on the inhalation volume. Therefore we developed a new coughing model, and coughs were evoked by microinjection of citric acid into the larynx in the unanesthetized unrestrained guinea pig. Microinjection of 7.5% citric acid (2 microliters/30 s, 5 min) induced coughs (27.03 +/- 4.03 coughs/10 min), and citric acid-induced responses were stable independent of the inhalation volume. In the inhalation studies, animals were exposed to citric acid only once because induced-responses were remarkably decreased by repeated administration at an interval of 24 h. However in our coughing model it was possible to repeatedly challenge the animals by microinjection of citric acid at intervals of 24 h. Microinjection of citric acid into the larynx induced coughs in Sprague-Dawley rats, but inhalation of citric acid did not induce cough. These results indicate that this coughing model is highly sensitive and correctly assessed cough responses.

Animals↗

PubMed1987

Antidiuretic effects of morphine microinjected into the hypothalamic supraoptic and paraventricular nuclei in a water-loaded and ethanol-anesthetized rat.

Effects of morphine microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, which contain neurons producing and releasing antidiuretic hormone (vasopressin), on the outflow and the osmotic pressure of urine and other visceral functions were investigated in a rat which was loaded with water and anesthetized with ethanol. The opioid drug, having predominantly mu-agonist activity, when microinjected into the SON or PVN induced potent antidiuretic effects in dose-dependent and time-dependent manners with no significant effects on the other visceral functions. The approx. ED50 values for morphine were 19 and 9 nmol when it was microinjected into the SON and PVN, respectively. The antidiuretic effects showed slow onset and long duration, with a minimal outflow at approx. 50 min after microinjection and a return to approx. 50% of the initial control value by 1.5 hr. The morphine-induced effects were inhibited by pretreatment with naloxone or atropine, but not inhibited by pretreatment with alpha- or beta-adrenoceptor antagonists, suggesting that the antidiuretic effects were mediated through an opioid receptor having low sensitivity to naloxone and also possibly mediated through a muscarinic receptor which was stimulated probably by the ACh released by morphine.

Anesthesia↗

PubMed1989

Effect of vasopressin antagonist on antidiuresis by oxotremorine microinjected into the hypothalamic supraoptic and paraventricular nuclei in a water-loaded and ethanol-anesthetized rat.

Microinjection of the muscarinic agonist oxotremorine into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei which contain cell bodies of vasopressinergic neurons induced potent antidiuretic effects in water-loaded and ethanol-anesthetized rats. The effects included both decreases in urine outflow and increases in urine osmotic pressure. However, no significant changes in various visceral functions other than antidiuresis such as mean blood pressure, heart rate, respiration rate and rectal temperature were observed when oxotremorine was microinjected into the SON. Only a slight change in mean blood pressure (approx. 10 mmHg decrease) was observed by the microinjection into the PVN. Intravenous preinjection of a vasopressin (AVP) V1 V2 antagonist that has one of the most potent V2 (antidiuretic)-antagonist activities, d(CH2)5-D-Tyr(Et)VAVP, inhibited nearly completely the antidiuretic effects induced by the microinjection of oxotremorine. The results demonstrated that oxotremorine stimulated muscarinic receptors in the hypothalamic SON and PVN, released AVP and induced an antidiuretic effect through AVP-receptors in the kidney.

Anesthesia↗

PubMed2003

Cardiovascular responses to microinjections of GABA or anesthetics into the rostral ventrolateral medulla of conscious and anesthetized rats.

The rostral ventrolateral medulla (RVLM) contains neurons involved in tonic and reflex control of arterial pressure. We describe the effects of gamma-aminobutyric acid (GABA) and anesthetics injected into the RVLM of conscious and urethane (1.2 g/kg, iv) anesthetized Wistar rats (300-350 g). In conscious rats, bilateral microinjection of GABA (50 nmol/200 nl) induced a small but significant decrease in blood pressure (from 130 +/- 3.6 to 110 +/- 5.6 mmHg, N = 7). A similar response was observed with sodium pentobarbital microinjection (24 nmol/200 nl). However, in the same animals, the fall in blood pressure induced by GABA (from 121 +/- 8.9 to 76 +/- 8.8 mmHg, N = 7) or pentobarbital (from 118 +/- 4.5 to 57 +/- 11.3 mmHg, N = 6) was significantly increased after urethane anesthesia. In contrast, there was no difference between conscious (from 117 +/- 4.1 to 92 +/- 5.9 mmHg, N = 7) and anesthetized rats (from 123 +/- 6.9 to 87 +/- 8.7 mmHg, N = 7) when lidocaine (34 nmol/200 nl) was microinjected into the RVLM. The heart rate variations were not consistent and only eventually reached significance in conscious or anesthetized rats. The right position of pipettes was confirmed by histology and glutamate microinjection into the RVLM. These findings suggest that in conscious animals the RVLM, in association with the other sympathetic premotor neurons, is responsible for the maintenance of sympathetic vasomotor tone during bilateral RVLM inhibition. Activity of one or more of these premotor neurons outside the RVLM can compensate for the effects of RVLM inhibition. In addition, the effects of lidocaine suggest that fibers passing through the RVLM are involved in the maintenance of blood pressure in conscious animals during RVLM inhibition.

Anesthetics, Intravenous↗