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At least 487 records · Page 27Linked to original sources

PubMed2006

Microinjection of the L-type calcium channel antagonist diltiazem into the ventral nucleus accumbens shell facilitates cocaine-induced conditioned place preferences.

BACKGROUND: Calcium (Ca2+) influx within the nucleus accumbens shell (NASh) can influence brain reward processes. We found previously that rats self-administer NMDA receptor antagonists (which block Ca2+ influx through NMDA receptors) into the NASh. We also found that manipulations which increase expression of Ca2+-permeable AMPA receptors within this region make cocaine aversive. Here we examined if Ca2+ influx via L-type Ca2+ channels within the NASh would influence cocaine reward. METHODS: Rats received bilateral microinjections of the L-type Ca2+ channel antagonist diltiazem into the ventral NASh prior to place conditioning with systemic cocaine. RESULTS: Microinjections of diltiazem (10 nmol/hemisphere) into the ventral NASh facilitated the ability of a sub-threshold dose of cocaine (5.0 mg/kg) to establish place preferences, but did not affect place conditioning on their own (5.0-40 nmol/hemisphere). Microinjections into more dorsal regions had no effects. CONCLUSIONS: Blockade of Ca2+ influx through L-type channels Ca2+ within the ventral NASh increases cocaine reward.

Anesthetics, Local↗

PubMed2004

Aging and SB-269970-A, a selective 5-HT7 receptor antagonist, attenuate circadian phase advances induced by microinjections of serotonergic drugs in the hamster dorsal raphe nucleus.

Aging leads to many changes in the circadian timekeeping system, including reduced sensitivity to phase-resetting signals such as systemic administration of the serotonergic agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). In previous studies, we observed an age-related decrease in 5-HT7 receptor binding sites, one of the receptor subtypes that is activated by 8-OH-DPAT, in the dorsal raphe nucleus. In this study, we tested the hypotheses that (1) aging reduces circadian phase shifts induced by local administration of 8-OH-DPAT (30 microM, i.e., 1.97 ng) or 5-carboxamidotryptamine (5-CT, 100 nM, i.e., 6.39 pg), another serotonin agonist, into the dorsal raphe and (2) 5-HT7 receptors mediate the phase shifts induced by administration of 5-CT and 8-OH-DPAT into the dorsal raphe. Young (3-5 months), middle-aged (12-13 months) and old hamsters (17-19 months) were surgically implanted with chronic guide cannulae aimed at the dorsal raphe, and were housed in cages equipped with running wheels. Aging significantly inhibited (P<0.01) the phase advances in running-wheel rhythms induced by 8-OH-DPAT microinjected during the midsubjective day. 5-CT induced phase advances tended to decrease with aging, but this effect was not significant (P<0.12). Microinjection of the selective 5-HT7 receptor antagonist, SB-269970-A (50-5000 nM, i.e., 0.39-390 pg), 15 min before microinjection of 5-CT or 8-OH-DPAT into the dorsal raphe of young hamsters, significantly inhibited phase shifts. In conjunction with our previous study, these findings indicate that an age-related reduction in 5-HT7 receptors in the dorsal raphe nucleus is an important neurochemical mechanism leading to aging deficits in the circadian timekeeping system.

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

PubMed2005

Effects of microinjections of neurotoxin AvTx8, isolated from the social wasp Agelaia vicina (Hymenoptera, Vespidae) venom, on GABAergic nigrotectal pathways.

Several investigations have provided information that defensive behaviors evoked by stimulation of deep layers of the superior colliculus (dlSC) are subjected to inhibitory nigral modulation. This inhibition is made mainly through GABAergic neurons from substantia nigra, pars reticulata (SNpr), that sends outputs toward neural networks of the deep layers of the superior colliculus and dorsal periaqueductal gray matter involved with the organization of fear-like responses. In this work, we compared the effects of two GABAergic agonists, muscimol and baclofen, with the effect of neurotoxin AvTx8 (1567 Da), isolated from the venom of the social wasp Agelaia vicina, microinjected into SNpr of Rattus norvegicus (Wistar rats) prior to dlSC saline or bicuculline microinjections, considering that wasp venom has some influence on the uptake of GABA and/or glutamate neurotransmitters. GABA(A) receptor blockade in the dlSC evoked a vigorous escape behavior, expressed by rapid running, jumps and turns, as compared to control. These defensive reactions were maximized after the intranigral GABA(A) agonism with muscimol, but not after in situ GABA(B) agonism. Nigral microinjection of AvTx8 induced similar effects to those of baclofen, decreasing the intensity of behavioral defensive reactions caused by GABA(A) receptor blockade in the dorsal mesencephalon. These findings suggest that AvTx8 has some effects on GABAergic neurotransmission, increasing the activity of the inhibitory nigro-collicular pathways, causing an anti-panic (antiaversive) effect. Therefore, our work suggests AvTx8 as a novel pharmacological tool to study differences between the two types of GABAergic receptors and excitatory amino acid-mediated mechanisms in the brain and brainstem networks.

Animals↗

PubMed2005

Microinjection of neostigmine into the pontine reticular formation of the mouse: further evaluation of a proposed REM sleep enhancement technique.

Microinjections of cholinergic agonists into the pontine reticular formation (PRF) powerfully induce rapid eye movement sleep (REMS) in cats but have comparatively weaker effects in rats. Recently, the cholinomimetic neostigmine has been reported to strongly enhance REMS following microinjection into the PRF of the mouse. That study used behavioral assessments of locomotion in lieu of electrophysiological measures of muscle tone to identify REMS. We sought to confirm that the behavioral state induced in mice by PRF injections of neostigmine meets standard electroencephalogram (EEG) and electromyogram (EMG) criteria for defining REMS. Cortical EEG, nuchal muscle EMG, and PGO waves were recorded from male C57BL/6N mice with chronic indwelling cannulae for the delivery of neostigmine to the PRF. Recordings were made during midday following injections of neostigmine (8.8 mM, 50 nl), 2 h after lights on (LD 12:12). Neostigmine induced a behavioral state characterized by low amplitude, highly desynchronized cortical EEG with little theta, no PGO waves, and a sustained high muscle tone. Behavioral states meeting standard criteria for slow-wave sleep (SWS) and REMS were significantly suppressed compared to baseline recordings, and REMS onset was delayed by 3 h. Consistent with earlier reports, neostigmine did strongly suppress locomotor activity in open field tests and in the home cage. Due to the failure to meet criteria for defining REMS, we conclude that neostigmine microinjection into the PRF of the mouse induces an abnormal waking state rather than REMS.

Animals↗

PubMed2006

Cardiovascular effects of adrenocorticotropin microinjections into the rostral ventrolateral medullary pressor area of the rat.

The presence of adrenocorticotropic hormone (ACTH)-immunoreactive cells and melanocortin (MC) receptors (MC4 and to a lesser extent MC3) has been demonstrated in the medullary reticular formation in the general area where rostral ventrolateral medullary pressor area (RVLM) is located. The importance of RVLM in the regulation of cardiovascular function is well established. Based on these reports, it was hypothesized that ACTH may play a role in the regulation of cardiovascular function. To test this hypothesis, experiments were carried out on artificially ventilated, adult male, urethane-anesthetized and unanesthetized mid-collicular decerebrate rats. The RVLM was identified by microinjections (100 nl) of L-glutamate (L-Glu). Microinjections (100 nl) of ACTH (0.5, 1 and 2 mmol/l) into the RVLM elicited increases in MAP and HR; tachycardic responses were relatively inconsistent. The effects of ACTH were blocked by SHU9119 and agouti-related protein (AGRP). SHU9119 (a synthetic compound) and AGRP (an endogenous peptide) are antagonists for MC4, and to a lesser extent MC3, receptors. The specificity of these antagonists for MC receptors was indicated by their lack of effect on l-Glu responses. Microinjection of ACTH into the RVLM increased the efferent discharge in the greater splanchnic nerve. It was concluded that (1) ACTH exerts excitatory effects on RVLM neurons resulting in pressor and tachycardic responses, (2) these responses were mediated via MC4 and to a lesser extent MC3 receptors in the RVLM, and (3) the pressor effects of ACTH were mediated via sympathetic activation. This is the first report showing central cardiovascular actions of ACTH.

Adrenocorticotropic Hormone↗

PubMed2006

Microinjecting recombinant rainbow trout Ea4-peptide of pro-IGF-I into zebrafish embryos causes abnormal development in heart, red blood cells, and vasculature.

E-peptides and mature insulin-like growth factors (IGFs) are produced from pre-pro-IGFs during post-translational processing and co-secreted into the circulation. Previously, we reported that introduction of a transgene encoding the secreted form of rainbow trout (rt) Ea4-peptide or human (h) Eb-peptide into newly fertilized eggs of medaka (Oryzias latipes) and zebrafish (Danio rerio) resulted in developmental defects in heart, red blood cells and vasculature. In addition to vasculature and red blood cell developmental defects, multiple phenocopies of heart developmental defects categorized by developmental arrest at cardiomyocyte, heart tube and heart looping stages were also observed. These results raise a question of whether rtEa4- or hEb-peptide exerts pleiotropic inhibitory effects on heart, vasculature and red blood cell development in fish embryos. To answer this question, various amounts of recombinant rtEa4-peptide were microinjected into zebrafish eggs at 1.5, 2.5 and 5.5 h post-fertilization (hpf). Although a dose-dependent developmental defect in heart, vasculature and red blood cells was observed in embryos microinjected with rtEa4-peptide at 1.5 and 2.5 hpf, the heart development in all of the microinjected embryos was arrested at the cardiomyocyte stage. Furthermore, the mRNA levels of Nkx2.5, GATA5, VEGF, GATA1 and GATA2 genes in defective embryos were significantly reduced by rtEa4-peptide. These results confirm our previous findings that rtEa4- or hEb-peptide exhibits pleiotropic effects in inhibiting heart, vasculature and red blood cell development in zebrafish embryos.

Animals↗

PubMed2006

The effects of microinjection of morphine into thalamic nucleus submedius on formalin-evoked nociceptive responses of neurons in the rat spinal dorsal horn.

Previous studies have indicated that the thalamic nucleus submedius (Sm), as an ascending component, is involved in an endogenous analgesic system consisting of spinal cord-Sm-ventrolateral orbital cortex (VLO)-periaqueductal gray (PAG)-spinal cord loop. To investigate the action of opioid in this antinociception pathway, the effects of microinjection of morphine and naloxone into the Sm on the formalin-induced nociceptive responses of neurons in the spinal dorsal horn were determined in the anesthetized rat. Formalin (5%, 50 microl) subcutaneously injected into unilateral hindpaw produced a biphasic nociceptive response which was similar to that obtained from assessing the nociceptive behavior either in the relative magnitude of response or the time course. A unilateral microinjection of morphine (5 microg, 0.5 microl) into the Sm 15 min after formalin injection significantly depressed the second phasic responses of neurons induced by formalin, and this effect was significantly attenuated by pre-microinjection of opioid receptor antagonist naloxone (1 microg, 0.5 microl) into the same site. The results suggest that the Sm is involved in opioid receptor-mediated antinociceptive effect on the persistent nociception through depression of the nociceptive transmission at the spinal cord level.

Action Potentials↗

PubMed2005

Teratogenic effects of azaspiracid-1 identified by microinjection of Japanese medaka (Oryzias latipes) embryos.

Azaspiracid-1 (AZA-1) is a newly identified phycotoxin that accumulates in commercially important bivalve molluscs harvested in several European countries and causes severe human intoxications. Molluscan shellfish are known vectors for accumulation and subsequent transfer of phycotoxins such as brevetoxin and domoic acid through various trophic levels within food webs. Finfish can also accumulate phycotoxins, both directly from toxic algae or from consumption of contaminated shellfish and smaller intoxicated fish. To evaluate the teratogenic potential of AZA-1 and its relevancy to toxin accumulation in finfish, we have utilized a microinjection technique to mimic the maternal-egg toxin transfer of an AZA-1 reference standard and a shellfish extract containing azaspiracids in an embryonic Japanese medaka (Oryzias latipes) fish model. Microinjection of purified AZA-1 caused dose-dependent effects on heart rate, developmental rate, hatching success, and viability in medaka embryos. Within 4 days of exposure to doses > or = 40 pg AZA-1/egg, substantial retardation in development was observed as reduced somatic growth and yolk absorption, and delayed onset of blood circulation and pigmentation. Embryos treated to > or =40 pg AZA-1/egg had slower heart rates (bradycardia) for the 9 days in ovo period, followed by reduced hatching success. Microinjection of a contaminated mussel (Mytilus edulis) extract containing AZAs (AZA-1, -2, and -3), okadaic acid, and dinophysistoxin-2 resulted in similar responses from the fish embryos at equivalent doses. These studies demonstrate that AZA-1 is a potent teratogen to finfish. This work will complement future investigations on AZA-1 accumulation in marine food webs and provide a basis for understanding its toxicity at different trophic levels.

Animals↗

PubMed2002

Intracerebral microinjections of delta 9-tetrahydrocannabinol: search for the impairment of spatial memory in the eight-arm radial maze in rats.

The purpose of this study was to identify brain sites that contribute to the delta(9)-tetrahydrocannabinol (delta(9)-THC)-induced impairment of spatial memory in rats. Rats were tested in the eight-arm radial maze after microinjections of delta(9)-THC into one of 14 different brain regions. The bilateral microinjection of delta(9)-THC (20 microg/side) impaired spatial memory when injected into the dorsal hippocampus (DH), ventral hippocampus (VH) or dorsomedial thalamus nucleus (DMT). However, rats treated with delta(9)-THC into DMT produced preseverative behavior which has not been observed by systemic administration of delta(9)-THC. On the other hand, spatial memory was unaffected by microinjections of delta(9)-THC into the other 11 areas examined: frontal (FC) and frontoparietal (FPC) cortex, central (ACE) and basolateral (ABL) amygdaloid nucleus, medial caudate putamen (CPM), lateral hypothalamus (LH), mammillary body (MB), basal forebrain (BF), medial septal nucleus (SEP) and dorsal (DR) and median (MR) raphe nucleus. These results suggest that DH and VH may be important brain sites for the delta(9)-THC-induced impairment of spatial memory.

Animals↗

PubMed2003

Cardiovascular responses to microinjections of nociceptin into a midline area in the commissural subnucleus of the nucleus tractus solitarius of the rat.

Immunoreactivity for nociceptin, an endogenous ligand for the ORL1 opioid receptors, has been reported in the nucleus tractus solitarius (nTS). A midline area in the commissural subnucleus (nCom) of nTS is the site of peripheral chemoreceptor projections. This investigation was carried out in urethane-anesthetized, artificially ventilated, adult male Wistar rats, to study the cardiovascular effects of the activation of ORL1 receptors in a midline area of the nCom. Microinjections (30 nl) of nociceptin (0.15-0.62 mM) into the nCom elicited depressor and bradycardic responses. Prior microinjections of [N-Phe(1)]-nociceptin-(1-13)-NH(2) (4.5 mM), a specific antagonist for ORL1 opioid receptors, into the nCom blocked the effects of nociceptin (0.31 mM, the maximally effective concentration), but not endomorphin-2 (0.6 mM; an endogenous ligand for micro -opioid receptors). On of other hand, naloxone (0.125 mM; an antagonist for classical opioid receptors) did not block the effects of nociceptin, while it did block the effects of endomorphin-2. The blockade of nociceptin effects by [N-Phe(1)]-nociceptin-(1-13)-NH(2) and endomorphin-2 by naloxone, was not due to some nonspecific effects because the responses to L-Glu (5 mM) remained unaltered after the microinjection of these antagonists. These results indicate that activation of ORL1 receptors in the nCom may play a role in the regulation of cardiovascular function.

Animals↗

PubMed1996

Effect of microinjection of muscimol into the dorsomedial or paraventricular hypothalamic nucleus on air stress-induced neuroendocrine and cardiovascular changes in rats.

The paraventricular nucleus (PVN) contains neurons that release corticotrophin-releasing factor (CRH) and thus provide the stimulus for the release of adrenocorticotrophic hormone (ACTH), the neuroendocrine hallmark of the response to stress. However, inhibition of neuronal activity in the nearby dorsomedial hypothalamic nucleus (DMH) by microinjection of the GABA(A) receptor agonist muscimol suppresses cardiovascular changes seen in air stress in conscious rats, while similar treatment in the PVN has no effect. Because the DMH projects to the PVN and also contains CRH neurons, we decided to investigate the role of neuronal activity in the DMH in the neuroendocrine response to stress. In control rats or after microinjection of saline vehicle into either the PVN or the DMH, air stress resulted in equivalent increases in plasma levels of ACTH, heart rate, and arterial pressure. Bilateral microinjection of muscimol 80 pmol/100 nl/side into either the PVN or the DMH prior to air stress reduced the associated increases in plasma ACTH (-37% and -71%, respectively), while only injection into the DMH attenuated the accompanying tachycardia (-62%) and pressor (-83%) effects. Thus, neurons in the DMH, but not in the PVN, play a role in both the cardiovascular and neuroendocrine response to air stress.

Adrenocorticotropic Hormone↗

PubMed1997

Role of spinal delta1 and delta2 opioid receptors in the antinociception produced by microinjection of L-glutamate in the ventromedial medulla of the rat.

This study examined the contribution of spinal delta1 and delta2 opioid receptors to the antinociception produced by microinjection of L-glutamate in either the nucleus raphe magnus (NRM) or the nucleus reticularis gigantocellularis pars alpha (NGCp alpha) of the rat. Intrathecal (i.t.) pretreatment with 1 microg of 7-benzylidinenaltrexone (BNTX), a delta1 opioid receptor antagonist, did not antagonize the increase in tail flick latency (TFL) produced by microinjection of L-glutamate in either the NRM or the NGCp alpha. In contrast, i.t. pretreatment with 3 microg of naltriben (NTB), a delta2 opioid receptor antagonist, completely antagonized the increase in TFL evoked by microinjection of L-glutamate in the NRM, but did not antagonize the increase in TFL evoked from the NGCp alpha. These results suggest that the antinociception produced by activation of these bulbospinal pathways is predominantly mediated by spinal delta2 opioid receptors and that there is little, if any, contribution by spinal delta1 opioid receptors.

Analgesics↗

PubMed1998

Microinjections of dopamine agonists and cocaine elevate plasma corticosterone: dissociation effects among the ventral and dorsal striatum and medial prefrontal cortex.

There is evidence suggesting the involvement of central dopamine (DA) systems in the regulation of plasma corticosterone (CORT). We examined whether or not microinjections of DA agonists and cocaine into three DA-rich terminal regions, the medial prefrontal cortex (MPC), ventral striatum (VStr) and dorsal striatum (DStr), would increase plasma CORT in Sprague-Dawley rats. The highest dose tested (18 nmol) of a mixture of the dopamine D1 receptor agonist SKF 38393 and the D2 agonist quinpirole (SKF/Quin) increased plasma CORT when injected into each of the three brain regions. Microinjections of the medium dose (i.e., 3 nmol) of SKF/Quin into the VStr also increased plasma CORT, while the injections into the MPC and DStr did not. Systemic pretreatment with haloperidol attenuated the elevated CORT induced by intra-VStr injections of SKF/Quin. Cocaine (25, 50, and 100 microg) also increased CORT when injected into the VStr, but not into the MPC or DStr. Microinjections of local anesthetics, lidocaine (100 microg) and procaine (100 microg), which have similar chemical structures to cocaine, into the VStr did not increase CORT. These results suggest that the VStr plays an important role in mediating the elevated plasma CORT induced by DA agonists and cocaine administration.

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

PubMed1999

Cardiovascular responses to microinjections of excitatory amino acids into the area postrema of the rat.

Although, area postrema (AP) as been implicated in the regulation of cardiovascular function, there is no consensus regarding the type of responses elicited by stimulation of this brain structure. Microinjections (50 nl) of smaller concentrations of excitatory amino acid receptor agonists (e.g., NMDA, KA and trans-ACPD, 10 microM each) into the AP elicited pressor and tachycardic responses in unanesthetized decerebrate as well as urethane-anesthetized rats. Microinjections of higher concentrations (e.g., 50 microM NMDA) of excitatory amino acids (EAAs) into the AP elicited an initial pressor and tachycardic response which was followed by a depressor and bradycardic response; when high concentrations of NMDA were microinjected into the AP, enough concentration may have reached the nucleus tractus solitarius (nTS) to elicit depressor and bradycardic responses. Alternatively, high concentrations of NMDA may excite known projections from AP to the nTS.

2-Amino-5-phosphonovalerate↗

PubMed1999

Pharmacological evidence for a periaqueductal gray-nucleus raphe magnus connection mediating the antinociception induced by microinjecting carbachol into the dorsal periaqueductal gray of rats.

A previous study demonstrated that microinjection of carbachol (CCh) into the dorsal periaqueductal gray matter (dPAG) of rats increases the latency for the tail flick reflex. Several other studies have implicated the raphe magnus (NRM) and the reticularis paragigantocellularis (NRPG) nuclei as relay stations through which descending pathways from the PAG project to the spinal cord via the dorsolateral funiculus (DLF). In the present study, the effects of microinjecting CCh into the dPAG on the tail flick test were examined in rats in which the ipsilateral DLF was previously lesioned, or saline or lidocaine (2%) was microinjected into the NRM or ipsilateral NRPG. The DLF lesion did not change the baseline threshold of the animals in the test, but abolished the CCh-induced increase in the tail flick latency from the dPAG. The neural block of the NRM or NRPG with lidocaine also did not change significantly the latency for the tail flick reflex. The increase in the tail flick latency produced by CCh from the dPAG was not changed by the neural block of the NRPG, but was significantly reduced by the neural block of the NRM. These results are interpreted as indicative that the central antinociceptive mechanisms activated by CCh from the dPAG depend on a descending pathway that projects to the spinal cord via DLF utilizing at least the NRM, but not the NRPG, as an intermediary relay station.

Anesthetics, Local↗

PubMed2000

The antinociceptive effect of PAG-microinjected dipyrone in rats is mediated by endogenous opioids of the rostral ventromedical medulla.

Microinjection of non-opioid analgesics, such as dipyrone (DIP), into the periaqueductal gray matter (PAG) in rats causes an inhibition of nociceptive circuits in the spinal cord. We have herein investigated whether this effect is mediated by opioidergic mechanisms in the rostral ventromedial medulla (RVM), which is an important relay between the PAG and the spinal cord. The responses of spinal wide-dynamic-range neurons to noxious stimulation of their receptive field (RF) were inhibited by microinjection of DIP (100 microg/0.5 microl) into PAG. Subsequent microinjection of naloxone (NAL; 0.5 microg/0.5 microl) into RVM reversed this inhibition. The present and previous results suggest that non-opioid analgesics, as well as opiates, inhibit nociception by activating descending opioidergic mechanisms in PAG and RVM.

Animals↗

PubMed2003

Effects of 5-HT1B receptor ligands microinjected into the ventral tegmental area on cocaine discrimination in rats.

Some recent data indicate a significant interaction between serotonin (5-hydroxytryptamine; 5-HT) and dopamine in mesolimbic brain structures (e.g. the ventral tegmental area) which modulate the behavioral effects of cocaine in rats. The present study investigated the role of 5-HT(1B) receptors in the ventral tegmental area in the discriminative stimulus effects of cocaine in rats. Male Wistar rats were trained to discriminate cocaine (10 mg/kg, intraperitoneally (i.p.)) from saline (i.p.) in a two-choice, water-reinforced fixed-ratio 20 procedure. After reaching the cocaine-saline discrimination criterion, the rats were stereotaxically implanted with bilateral cannulae in the ventral tegmental area and were then microinjected with selective 5-HT(1B) receptor ligands. In substitution studies, microinjections of the 5-HT(1B) receptor antagonist, 3-[3-(dimethylamino)propyl]-4-hydroxy-N-[4-(4-pyridinyl)phenyl]benzamide dihydrochloride (GR 55562; 0.1-1 microg/side), did not evoke cocaine-lever responding, whereas the 5-HT(1B) receptor agonist, 1,4-dihydro-3-(1,2,3,6-tetrahydro-4-pyridinyl)-5H-pyrrolo[3,2-b]pyridin-5-one (CP 93129; 0.3-1 microg/side), induced partial substitution for cocaine. Intra-tegmental microinjections with the 5-HT(1B) receptor antagonist, GR 55562 (0.1-1 microg/side), before cocaine (5 mg/kg), which alone produced 98% cocaine-lever responses, decreased in a dose-dependent manner the discriminative stimulus effects of the psychostimulant. On the other hand, combination tests using a fixed dose of CP 93129 (0.3 or 1 microg/side), given into the ventral tegmental area prior to low systemic doses of cocaine (1.25-2.5 mg/kg), increased cocaine discrimination. These results seem to indicate that tegmental 5-HT(1B) receptors are necessary to express the discriminative stimulus effects of cocaine.

Animals↗

PubMed1988

A preclinical evaluation of pronuclear formation by microinjection of human spermatozoa into human oocytes.

In vitro fertilization (IVF) is recognized as an accepted treatment for male infertility. However, the fertilization rate is significantly lower than the fertilization rate of other IVF patient groups. Some male factor infertility patients still have a basic semen quality too poor for treatment by IVF. Microinjection of a spermatozoon directly into ooplasm has been recommended to assist fertilization in this subfertile population. This study found that oocytes from 5 of 11 patients microinjected with human spermatozoa demonstrated successful pronuclear formation and correlated with the incidence of pregnancy in these patients transferred with same-source oocytes inseminated by standard protocols. This initial evidence promotes the supposition of clinical feasibility of assisted fertilization by sperm microinjection.

Female↗