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PubMed1986

A microinjected monoclonal antibody against human DNA polymerase-alpha inhibits DNA replication in human, hamster, and mouse cell lines.

We have examined the effect that microinjection of a monoclonal antibody directed against human DNA polymerase-alpha (SJK-287) has on DNA synthesis in exponentially growing human, mouse, and hamster cell lines. We show that the SJK-287 antibody, when microinjected directly into the nuclei of cells is capable of inhibiting DNA synthesis in all three cell lines tested. Moreover, the effectiveness with which this antibody can inhibit ongoing DNA synthesis by the microinjection assay is closely correlated with the ability of the antibody to neutralize DNA polymerase-alpha activity fractionated from each cell line in vitro. Two other monoclonal antibodies of the same class, one directed against the cellular p53 protein (PAb122), and one directed against the c-myc protein (PM-8) were also tested for their ability to inhibit ongoing DNA synthesis by direct microinjection and in lysolecithin permeabilized cells. Both monoclonal antibodies failed to inhibit ongoing DNA synthesis in exponentially growing cells by these assays.

Animals↗

PubMed1983

Restoration of LPS responsiveness of C3H/HeJ mouse lymphocytes by microinjection of cytoplasmic factor(s) from LPS-stimulated normal lymphocytes.

Cytosol fractions of lymphocytes from LPS-responder mice (C3H/HeN) were prepared and injected into B lymphocytes of LPS-nonresponder mice (C3H/HeJ) by a microinjection technique utilizing polyethyleneglycol-mediated cell fusion. The B lymphocytes of C3H/HeJ mice microinjected with cytosol prepared from LPS-stimulated C3H/HeN cells became normally responsive to LPS. Microinjection of cytosol itself did not stimulate C3H/HeJ cells to proliferate or differentiate into immunoglobulin-producing cells, and the cells injected with cytosol had to be restimulated with LPS in order to proliferate and differentiate. These data suggested that C3H/HeJ B cells acquired LPS responsiveness by microinjection of cytoplasmic factor(s) from LPS-stimulated C3H/HeN cells and that these factor(s) may be one of the components involved in normal signal transmission from cell surface to nucleus in the early stages of the LPS response. The apparent m.w. of the cytoplasmic factor(s) is 100,000 by gel filtration. Chromatofocusing analysis suggested that these factors may consist of two components with the same m.w.

Animals↗

PubMedDate not supplied

Intratubular microinjection study of gentamicin transport in the rat.

The intratubular microinjection technique was used to determine the absorptive flux of radioactive gentamicin the rat. Microinjection into the early tubule and late proximal tubule resulted in recoveries of proximal 66.6 +/- 3.6% and 80.4 +/- 3.4%, respectively. Recoveries after microinjection into the distal convoluted tubule averaged 101.0 +/- 4.3%. The addition of tobramycin, phospholipase A, spermine or probenecid to the microinjection solution inhibited gentamicin absorption. These studies indicate that an absorptive flux of gentamicin is present in the superficial proximal tubule and at a nephron site or sites between the superficial proximal and distal tubules. Gentamicin absorption is mediated by a phospholipid carrier with specificity for polyamines and other aminoglycosides. The presence of probenecid in the perfusion solution inhibited the tubular absorption of gentamicin.

Absorption↗

PubMed1995

[Effect of microinjection of sodium giutamate and glycine into ventrolateral nucleus of tractus solitarius on the evoked potentials of arcuatus nucleus in rabbits].

Experiments were performed on 66 anaesthetized, vagotomized, paralyzed and artificially ventilated rabbits. The effects of microinjection sodium glutamate and glycine into ventrolateral nucleus of tractus solitarius (VLNTS) on hypothalamic arcuatus nucleus evoked potentials were observed. The main results obtained were as follows: (1) Phrenic nerve discharges were increased and the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials were decreased by microinjection of sodium glutamate into VLNTS. Phrenic nerve discharges were decreased and the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials were increased by microinjection of glycine into VLNTS. (2) After intravenous injection of naloxone, the phrenic nerve discharges could still be excited by microinjection of sodium glutamate as before, but the effects on the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials, unlike that of sodium glutamate, were reversed. The results suggest that the excitatory action of respiratory neurons in the VILTS may affect on the sensory function of arcuatus nucleus. The mechanism involved was discussed.

Animals↗

PubMed1993

[Effects of bromocriptine microinjection into VTA on the DOPAC level in nucleus accumbens].

The experiment was performed in sodium pentobarbital anesthetized male SD rats. In vivo differential pulse voltammetry (DPV) was used to monitor a metabolite of dopamine-3,4-dihydroxyphenylacetic acid (DOPAC) level in the ipsilateral nucleus accumbens following microinjection of bromocriptine (2.5 micrograms/0.5 microliters, n = 5) into left ventral tegmental area (VTA). The results indicated that after microinjection the amplitude of DOPAC peak increased gradually and reached to 128% and 143% compared to the control at the 50th and 80th min respectively (P < 0.01). The duration of the effect was about two hours. One hundred and eighty min after injection, the amplitude of DOPAC decreased to 111% of control (P > 0.05). SCH23390 (2 nmol/0.5 microliters, n = 4), a selective D1 antagonist was given into left VTA 40 min prior to microinjection of bromocriptine. In this group, the above-mentioned effect of bromocriptine was blocked, the amplitude of DOPAC peak showed no increase. The results suggest that the microinjection of bromocriptine into VTA induces an increase of activity of mesolimbic dopaminergic neurons probably mediated by D1 receptor.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

[Analgesic action of microinjection of neurokinin A into the lateral reticular nucleus and nucleus raphe magnus in rats].

Using the microinjection technique, the analgesic effect of neurokinin A (NKA) microinjected into the lateral reticular nucleus (LRN) and nucleus raphe magnus (NRM) was investigated in lightly pentobarbital-anesthetized rats using tail flick latency (TFL) as an index. Microinjection of NKA (0.5 microgram/0.5 microliter) into LRN significantly increased TFL lasting for 10 min (n = 12, P < 0.001). Microinjection of the same amount of NKA into NRM also produced evident increase in TFL for 5 min (n = 13, P < 0.001). The results indicate that NKA modulates pain reaction in both LRN and NRM in rats.

Acupuncture Analgesia↗

PubMed1997

Modulation of nociception by microinjection of delta-1 and delta-2 opioid receptor ligands in the ventromedial medulla of the rat.

In this study, we characterized the role of delta-1 and delta-2 opioid receptors in the ventromedial medulla (VMM) in the modulation of thermal nociception. Male Sprague-Dawley rats were prepared with an intracerebral guide cannula aimed at the nucleus raphe magnus or nucleus reticularis gigantocellularis pars alpha. Microinjection of the delta-1 opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) or the delta-2 opioid receptor agonist [D-Ala2, Glu4]deltorphin (DELT) in the VMM increased response latency in the radiant heat tail-flick test with respective ED50 values (95% CL) of 0.66 (0.07-1.5) nmol and 0.1 (0.03-0.21) nmol. In the 55 degrees C hot-plate test, DELT produced a modest, transient increase in response latency and DPDPE was ineffective. The antinociception produced by DPDPE was antagonized by microinjection at the same site of 1.5 pmol of the delta-1 opioid receptor antagonist 7-benzylidenenaltrexone (BNTX) but not by 0.15 nmol of the delta-2 opioid receptor antagonist naltriben (NTB). Conversely, the antinociception produced by DELT was antagonized by microinjection at the same site of 0.15 nmol of NTB but not by 1.5 pmol of BNTX. These doses of BNTX or NTB alone did not alter either tail-flick or hot-plate latency when microinjected in the VMM. However, at 10-fold higher doses, BNTX lost its selectivity for the delta-1 opioid receptor, and NTB by itself increased tail-flick and hot-plate latencies. These results collectively implicate both delta-1 and delta-2 opioid receptors in the VMM in the modulation of nociception. They also indicate that the antinociceptive effects of DPDPE and DELT can be distinguished by BNTX and NTB, providing additional support for the existence of delta-1 and delta-2 opioid receptor subtypes at supraspinal loci. Finally, the failure of effective doses of either BNTX or NTB to alter nociceptive threshold suggests that neurons in the VMM do not receive a tonic, inhibitory enkephalinergic input mediated by delta-1 or delta-2 receptors.

Analgesics, Opioid↗

PubMed1996

Apoptosis induced in cultured rat embryos by intra-amniotically microinjected sodium nitroprusside.

Previously, we reported that massive cell death was induced in the mesencephalic area of cultured rat embryos after embryos of gestational day 10.5 were intra-amniotically microinjected with sodium nitroprusside (SNP, 800 microM) and cultured for 24 hr at 37 degrees C. The massive cell death apparently was the result of NO-mediated embryotoxicity. Damage was concentration dependent and tissue specific. In follow-up studies, we now report evidence that NO generated from SNP induces apoptosis in organogenesis stage cultured rat embryos. Nile blue sulfate (NBS) staining suggested that microinjections of 400 microM SNP induced apoptosis in the mesencephalic area. Since we observed no massive cell death ("white caps") at this concentration, it appeared that early stages of apoptosis preceded "white cap" formation. At 800 microM SNP, total disintegration of cell bodies was evident and may have resulted from later stages of aoptosis or necrosis, or both. The "white caps" per se, an accumulation of disintegrated cell bodies, did not stain with NBS, probably due to total loss of cell integrity and resultant coagulation. The majority of the coagulated dead cells in the "white caps" were heavily stained with 3,3'-diaminobenzidine via in situ 3' end-labeling with terminal transferase. However, it is now known that NO can damage DNA directly and that in situ 3' end-labeling by terminal transferase detects not only apoptosis but also random DNA breakage. Increased 3' end-labeling and a "DNA ladder" were detectable within 5-10 hr after exposure of day 10.5 embryos to 400 or 800 microM of microinjected SNP. Some smear background was also observed in the "ladder." Rostral aspects of embryos exhibited more prominent indices of apoptosis than caudal regions. The results suggested that microinjections of SNP into the amniotic fluid of day 10.5 cultured rat embryos induces NO-mediated cell death in the mesencephalic and rhombencephalic regions by the process of apoptosis or of both apoptosis and necrosis, depending on the timing, concentration, and stage of gestation.

Animals↗

PubMed2002

Arrest of cell cycle progression during first interphase in murine zygotes microinjected with anti-PCM-1 antibodies.

To investigate the function of the centrosome protein PCM-1, antibodies against PCM-1 were microinjected into either germinal vesicle stage meiotic oocytes or fertilized mouse eggs, and cell cycle progression events (i.e., microtubule assembly, chromosome and centrosome organization, meiotic maturation) were assayed. These studies determined that microinjected PCM-1 antibodies arrested cell cycle progression, with anti-PCM-1 arresting fertilized eggs at the pronucleate stage when injected during G1. Analysis of the injected eggs determined that centrosome disruption and microtubule cytaster disorganization accompanied the cell cycle arrest. Anti-PCM-1 blocked neither pronuclear centration, completion of mitosis when microinjected into zygotes at G2, nor meiotic maturation when microinjected into immature oocytes. These results identify a novel role for PCM- 1 in cell cycle regulation, and indicate that PCM-1 must fulfill an essential function for cells to complete interphase.

Animals↗

PubMed1987

Fusion-mediated microinjection of active amine and diamine oxidases into cultured cells: effect on protein and DNA synthesis in chick embryo fibroblasts and in glioma cells.

Serum amine oxidase and/or porcine kidney diamine oxidase were trapped within reconstituted Sendai virus envelopes, and retained their activity. The trapped enzymes that were detected by radioimmunoblots were microinjected into cultured cells by fusion. When diamine oxidase was microinjected into cultured fibroblasts of chick or rat embryos, a temporary arrest in protein and DNA synthesis was observed. The inhibitory effect was more significant when both serum amine oxidase and kidney diamine oxidase were microinjected into those cultured cells. Fibroblasts of either chick or rat embryos transformed by Rous sarcoma virus were more susceptible to the injected enzymes than the normal cultures, showing a complete arrest in protein and DNA synthesis within 4 hours. Similar results were obtained by microinjecting diamine oxidase into cultured glioma cells. The injected enzyme catalyzed the oxidation of intracellular polyamines. The resulting oxidation product (hydrogen peroxide and aminoaldehydes) apparently caused the arrest in the synthesis of macromolecules.

Amine Oxidase (Copper-Containing)↗

PubMed1984

Cloning of the rat endogenous helper leukemia virus DNA sequence and expression of the helper activity encoded by the cloned DNA sequence in normal rat kidney cells by microinjection.

By the use of recombinant DNA technology and microinjection in cultured cells, the molecular genetic elements involved in the evolution of a retrovirus with the multipotential to infect, transform and replicate in host cell, have been critically examined in this investigation. Recently we have identified and purified the integrated and proviral DNA sequences specific for two rat endogenous helper leukemia viruses, WR- RaLV , originated from a chemically induced wild rat fibrosarcoma, and RHHV , isolated from a chemically induced rat hepatoma, HTC-H1 (1). By using a multidisciplinary approach combining restriction endonuclease analysis, reverse phase V-column chromatography, agarose gel electrophoresis, Southern blot transfer and filter nucleic acid hybridization, we were able to demonstrate that the rat helper leukemia viral DNA sequence was approximately 8.4-8.8 kb. The 8.8 kb RHHV DNA was molecularly cloned via the EK-1 certified vector pBR 322 plasmid into E. coli RRI cells. A successful recombinant clone, 8/32, that carried one entire RHHV 8.8 kb DNA sequence was mapped by restriction endonuclease analyses. Restricted DNA fragments of various sizes throughout the complete RHHV genome were isolated and purified for intranuclear microinjection into normal rat kidney cells. Release of type C infectious helper virus in these microinjected cells was investigated by superinfection on K-NRK, Kirsten sarcoma transformed non-producer cells. Recombination of the helper viral DNA sequence, en toto or of subgenomic sizes, carried in microinjected cells, with the sarcomagenic DNA sequence, carried in K-NRK cells, was also studied by genome-rescue and cell-transformation experiments. Our observations led to the conclusion that all critical genetic elements including the 5' LTR helper DNA sequence, gag, pol, and env genes, encoded for the biological activity of the type C helper virus resided within the 6.0 kb proximal to the 5' terminus of the endogenous rat type C helper virus DNA. They proved vitally essential for the recombination with the Src sequence during the evolution of an infectious, transforming and replication-competent retrovirus.

Animals↗

PubMed1979

Role of the nucleus raphe magnus in opiate analgesia as studied by the microinjection technique in the rat.

The analgesic effects of morphine (5 microgram, 0.2 microliter) microinjected into the nucleus raphé magnus (NRM) and the surrounding reticular formation of the rat were tested using vocalization after electric shock to the tail as the test for analgesia. Only sites in the NRM produced powerful analgesic effects, strongest analgesia being equivalent to 3 mg/kg i.v. morphine. The analgesia produced by the microinjection was reversed by systemic naloxone. Pretreatment with systemic cinanserin, a blocker of serotonergic receptors, led to a pronounced diminution of the analgesic effects of the morphine. The effects of microinjections of naloxone (5 microgram 0.2 microliter) were studied for their effect on analgesia produced by systemic morphine. The analgesia following 3 mg/kg i.v. morphine was diminished by the microinjection of naloxone but the naloxone almost completely reversed the analgesic effects of 1.5 mg/kg i.v. morphine. These results further substantiate the role of the NRM in analgesic mechanisms.

Animals↗

PubMed1980

Depressant and excitant effects of intraspinal microinjections of morphine and methionine-enkephalin in the cat.

The effects of intraspinal microinjectins of morphine (10 microgram) and methionine-enkephalin (Met-enkephalin) (5 microgram) on the C-fiber and polysynaptic reflexes in the acute decerebrate low spinal cat were investigated. Microinjected into the dorsal horn, morphine and Met-enkephalin depressed the nociceptive C-fiber reflex (CFR) without altering the short latency polysynaptic reflex. Microinjected into the ventral horn, morphine and Met-enkephalin facilitated the C-fiber and polysynaptic reflexes. Pretreatment of the cats with intravenous naltrexone (2 mg/kg) antagonized the depressant effects produced by dorsal horn intraspinal microinjections of morphine and Met-enkephalin. The excitant effects of ventral horn microinjections of morphine were not antagonized by naltrexone (2 mg/kg). These results support a hypothesis that the analgesic effects of morphine at the spinal cord level are due to interactions with opiate receptors in the dorsal horn.

Animals↗

PubMed1984

Comparison of the effects of ventral medullary lesions on systemic and microinjection morphine analgesia.

The effects of electrolytic lesions of the nucleus raphe magnus (NRM), nucleus reticularis paragigantocellularis (PGC) and nucleus raphe alatus (NRA) on analgesia elicited in the rat from systemic morphine and morphine microinjection into the periaqueductal gray (PAG) were evaluated using the tail flick test. No consistent change in baseline pain sensitivity was observed following lesions of the NRM, PGC or NRA. To determine the effect of ventral medullary lesions on systemic morphine analgesia, pain sensitivity was assessed prior to and 40 min after 6 mg/kg morphine administration (i.p.) at 2 days preceding lesioning and 5, 12 and 19 days post-lesion. NRM and PGC lesions produced only slight reductions in analgesia at 5 days after surgery. It was observed that large NRM, large PGC, and NRA lesions significantly attenuated analgesia evaluated at 12 days post-lesion. Smaller lesions confined within the NRM or PGC were reliably less effective than the larger lesions in reducing analgesia. In a subsequent study, 5 micrograms morphine in 0.5 microliter saline was microinjected into the ventral PAG at the level of the dorsal raphe. Identical testing procedures were used and the analgesia was assessed at 2 days before lesioning and 5 and 12 days post-lesion. In contrast to the previous study, large NRM lesions abolished analgesia as early as 5 days following lesioning. Small NRM lesions were less effective and PGC lesions were generally ineffective in attenuating analgesia induced by morphine microinjection. We conclude that the NRA may act as a functional unit in the mediation of systemic morphine analgesia. In contrast, analgesia elicited from intracerebral (PAG) morphine microinjection is mediated via the NRM.

Analgesia↗

PubMed1986

Effect of catecholamines on the swallowing reflex after pressure microinjections into the lateral solitary complex of the medulla oblongata.

The present study was carried out to elucidate the influence of catecholamines on swallowing, a polysynaptic reflex organized by an interneuronal network localized mainly within the lateral solitary complex (LSC) of the medulla oblongata. The effects of catecholaminergic agents were investigated in the rat, on rhythmic swallowing elicited by repetitive stimulation of the superior laryngeal nerve (SLN). Catecholaminergic agents were microinjected by pressure application, through multibarrelled glass micropipettes, into the LSC including the tractus solitarius, the swallowing region of the nucleus of the solitary tract and the adjacent reticular formation. Microinjections of noradrenaline (NA, 0.1-5 nmol, 50 nl) induced a significant decrease of the number and the amplitude of the rhythmic swallows elicited by stimulation of the ipsilateral SLN. This inhibitory effect was dose-related. Microinjections of clonidine (2.5 nmol, 50 nl), dopamine (0.25-2.5 nmol, 50 nl) and apomorphine (0.5 nmol, 50 nl), also inhibited swallowing. No significant modification of swallowing was induced by control injections of the vehicle (50 nl) within the active sites. Moreover the NA-induced inhibition of swallowing, was significantly antagonized by pretreatment with the alpha-adrenergic blocker phentolamine applied locally in the LSC. Furthermore neither blood pressure, nor respiratory rhythm were consistently modified by the catecholaminergic microinjections, indicating that the catecholamine-induced inhibition of swallowing was not a secondary side effect originating from alteration of these functions. It can therefore be concluded that the present results demonstrate the existence within the LSC of a catecholaminergic inhibition of the swallowing reflex. This inhibitory effect likely arises from activation of specific catecholaminergic receptors and affects the swallowing structures localized within the LSC, i.e., the laryngeal swallowing afferents running in the solitary tract and/or the swallowing interneurons within the nucleus of the solitary tract.

Animals↗

PubMed1995

Respiratory effects produced by microinjection of L-glutamate and an uptake inhibitor of L-glutamate into the caudal subretrofacial area of the medulla.

The purposes of our study were to determine the type of respiratory changes that would occur when either an excitatory amino acid receptor agonist or an uptake inhibitor was administered into the caudal subretrofacial area. This was done by microinjecting either L-glutamate or L-pyrrolidine-2,4-dicarboxylate (L-trans-2,4-PDC) into the caudal subretrofacial area while monitoring tidal volume, respiratory rate, mean arterial blood pressure and heart rate. Bilateral microinjection of 2.5 nmol of L-glutamate into the caudal subretrofacial area produced apnea in eight of eight animals tested, and the duration of apnea was 27 +/- 2 s. To determine the type of L-glutamate receptor responsible for mediating the apneic response, antagonists of the N-methyl-D-aspartate (NMDA) and non-NMDA receptor, namely, 3-[(RS)-carboxypiperazin-4-yl]-propyl-phosphonic acid (CPP), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), respectively, were tested. Neither antagonist in doses that blocked NMDA (in the case of CPP) and amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) (in the case of CNQX) blocked apnea elicited by L-glutamate. In addition, kynurenic acid, an antagonist of NMDA and non-NMDA ionotropic receptors, failed to block the effect of L-glutamate. Microinjection of the metabotropic receptor agonist drug, trans-L-1-amino-1,3-cyclopentone-dicarboxylic acid (L-trans-ACPD), into the caudal subretrofacial area failed to have any effect on respiratory activity. Because of the inability to block the effect of L-glutamate in the caudal subretrofacial area, and the lack of effect of L-trans-ACPD, the data suggest that the apneic response produced by L-glutamate is mediated by an as yet undefined receptor. Microinjection of the L-glutamate uptake inhibitor, L-trans-2,4-PDC, was found to produce apnea. Using the dose of 0.5 nmol of L-trans-2,4-PDC, we examined the type of excitatory amino acid receptor that mediated the response. Neither pretreatment with the NMDA receptor antagonist, CPP, nor the non-NMDA receptor antagonist, CNQX, affected L-trans-2,4-PDC-induced apnea. However, combined use of these two antagonists prevented L-trans-2,4-PDC-induced apnea. These data suggest that the effect of synaptically released exitatory amino acid at the caudal subretrofacial area on breathing is apnea, and that this effect is mediated by simultaneous activation of both NMDA and non-NMDA ionotropic receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1989

Effects of site-specific CNS microinjection of cholecystokinin on lordosis behavior in the male rat.

We have previously demonstrated that intracerebroventricular injections of sulphated cholecystokinin octapeptide (sCCK-8) had a dramatic facilitatory effect on lordosis behavior in the gonadectomized, estrogen-primed male rat. In the female, sCCK-8 facilitates or inhibits lordosis when microinjected into the medial preoptic nucleus (MPN) or ventromedial nucleus of the hypothalamus (VMH), respectively. In order to identify sCCK-8 responsive sites that modulate lordosis behavior in gonadectomized males, sCCK-8 was microinjected into the MPN or VMH. Sulphated CCK-8 significantly increased lordosis behavior when microinjected into the MPN of estrogen-primed males, but had no significant effects when microinjected into the VMH. These results imply that CCK-sensitive neural substrates within the MPN may act to disinhibit lordosis in the gonadectomized, estrogen-primed male rat. The lack of an effect of VMH injection of sCCK-8 on lordosis in males is discussed in terms of possible sex differences in sCCK-8-sensitive lordosis-modulating circuits.

Animals↗

PubMed1982

Locomotor activity of rats in open field after microinjection of procaine into superior colliculus or underlying reticular formation.

Whereas large lesions of the superior colliculus in rats increase locomotor activity in the open field, bilateral collicular microinjections of muscimol (an agonist of the inhibitory neurotransmitter GABA) have been reported to reduce open-field activity. This difference might be due to muscimol's acting on a subpopulation of collicular neurones, or to some feature of the microinjection technique. The issue was investigated by observing open-field behavior after reversible lesions produced by bilateral microinjections of the local anaesthetic procaine (10-300 micrograms in 0.5 microliter) into midbrain sites. Injections of procaine into the superior colliculus produced effects similar to those reported after muscimol injections: both locomotor activity and other exploratory responses were suppressed, with the rats spending much of their time motionless in an alert posture. In contrast, animals with injections of procaine into the mesencephalic reticular formation (MRF) ventral to the superior colliculus resembled rats given large collicular lesions: they showed very striking increases in locomotor activity, while their rearing and exploratory head movements were reduced. It is suggested that in some experiments large collicular lesions may have increased locomotor activity in the open field because they invaded underlying MRF. However, it is also possible that in rodents the acute effects of collicular inactivation, as assessed by microinjection of muscimol or procaine, are different from the chronic effects that are observed in experiments with electrolytic or radiofrequency lesions.

Animals↗