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PubMed1985

Microinjection of morphine into nucleus reticularis paragigantocellularis of the rat: suppression of noxious-evoked activity of nucleus raphe magnus neurons.

Microinjection of 1 microgram of morphine into nucleus reticularis paragigantocellularis (Pgc) of anesthetized rats depressed both noxious-evoked and spontaneous activity of nociresponsive neurons in the nucleus raphe magnus (NRM). This effect was naloxone-reversible, and was not observed after control injections dorsal to Pgc. The percent change in spontaneous firing was significantly greater than the percent change in pinch-evoked firing. This reduction in NRM neuronal discharge may contribute to the antinociceptive effects produced by microinjection of morphine into Pgc.

Animals↗

PubMed1986

Susceptibility to seizures produced by pilocarpine in rats after microinjection of isoniazid or gamma-vinyl-GABA into the substantia nigra.

Pilocarpine, given intraperitoneally to rats, reproduces the neuropathological sequelae of temporal lobe epilepsy and provides a relevant animal model for studying mechanisms of buildup of convulsive activity and pathways operative in the generalization and propagation of seizures within the forebrain. In the present study, the effects of manipulating the activity of the gamma-aminobutyric acid (GABA)-mediated synaptic inhibition within the substantia nigra on seizures produced by pilocarpine in rats, were investigated. In animals pretreated with microinjections of isoniazid, 150 micrograms, an inhibitor of activity of the GABA-synthesizing enzyme, L-glutamic acid decarboxylase, into the substantia nigra pars reticulata (SNR), bilaterally, non-convulsant doses of pilocarpine, 100 and 200 mg/kg, resulted in severe motor limbic seizures and status epilepticus. Electroencephalographic and behavioral monitoring revealed a profound reduction of the threshold for pilocarpine-induced convulsions. Morphological analysis of frontal forebrain sections with light microscopy revealed seizure-related damage to the hippocampal formation, thalamus, amygdala, olfactory cortex, substantia nigra and neocortex, which is typically observed with pilocarpine in doses exceeding 350 mg/kg. Bilateral intrastriatal injections of isoniazid did not augment seizures produced by pilocarpine, 200 mg/kg. Application of an irreversible inhibitor of GABA transaminase, gamma-vinyl-GABA (D,L-4-amino-hex-5-enoic acid), 5 micrograms, into the SNR, bilaterally, suppressed the appearance of electrographic and behavioral seizures produced by pilocarpine, 380 mg/kg. This treatment was also sufficient to protect animals from the occurrence of brain damage. Microinjections of gamma-vinyl-GABA, 5 micrograms, into the dorsal striatum, bilaterally, failed to prevent the development of convulsions produced by pilocarpine, 380 mg/kg. The results demonstrate that the threshold for pilocarpine-induced seizures in rats is subjected to the regulation of the GABA-mediated synaptic inhibition within the substantia nigra.

Aminocaproates↗

PubMed1988

Microinjection of muscimol into entopeduncular nucleus suppresses pilocarpine but not maximal electroshock seizures in rats.

Microinjection of muscimol (406 pmol) into the rat entopeduncular nucleus, the analogue of the primate globus pallidus pars interna, significantly suppressed pilocarpine but not maximal electroshock seizures in a spatially specific manner. In contrast to its lack of efficacy in the entopeduncular nucleus, microinjection of muscimol into the substantia nigra suppressed maximal electroshock seizures. These findings suggest that the neural networks and/or the neurotransmitters that subserve the propagation of pilocarpine and maximal electroshock seizures differ with regard to the entopeduncular nucleus. The data also underscore the powerful regulatory role of the substantia nigra in diverse models of seizures.

Animals↗

PubMed1988

Microinjection of carbachol into the pontine area is unable to modify insomnia induced by p-cholorophenylalanine (PCPA).

It has previously been shown that cholinergic drugs administered into the pontine area (field tegmental gigantocellular, FTG) are capable of inducing significant increases of rapid eye movement (REM) sleep periods in normal cats. The purpose of this study was to determine whether such cholinergic stimulation is capable of inducing similar effects in p-chlorophenylalanine (PCPA) insomniac cats. Four groups (n = 6) of cats were used in this study. The first two groups received a microinjection of either, saline (1 microliter) or carbachol (8 micrograms/1 microliter). The last two groups, prior to the microinjection, received PCPA (400 mg/kg) pre-treatment. Histological analysis showed that the tips of the cannulae were located in the caudal FTG, at the level of the ponto-medullary union. Results showed that carbachol significantly increased REM sleep in normal cats as compared to saline, whereas, carbachol was unable to modify the insomnia induced by PCPA. These findings suggest that cholinergic effects on REM sleep require a serotoninergic system. The results are discussed in terms of acetylcholine/serotonin interaction in the control of REM sleep.

Animals↗

PubMed1988

Integrated defence reaction elicited by excitatory amino acid microinjection in the midbrain periaqueductal grey region of the unrestrained cat.

Unilateral microinjections (0.20 microliter) of the excitatory amino acids (EAA), L-aspartate (ASP), D,L-homocysteate (DLH) or kainate (KA) were made into the midbrain of freely moving cats. Injections of DLH (20 nmol) or ASP (200 nmol) made within the midbrain periaqueductal grey matter (PAG) consistently elicited a threat display characteristic of defensive behaviour (i.e., pupillary dilatation, piloerection, retraction of the ears, sideways backing, arching of the back, hissing, howling, growling), whereas injections of DLH or ASP made in the tegmentum bordering the PAG did not elicit such behaviour. Injections of KA (940 pmol) made within the PAG, but not the tegmentum, elicited not only a threat display but also directed attack (striking with unsheathed claws and biting). As injections of EAA depolarize cell bodies, but not axons, the results suggest that a population of neurones whose excitation elicits all of the behavioural signs of defence, including directed attack, is found within the PAG. Histology indicated that the region of the PAG from which the defence reaction was elicited was not confined to any PAG subnucleus. Rather, the 'defence region' of the PAG formed a cylindrical column lateral to the midbrain aqueduct, approximately 1.5 mm in diameter and 5.0 mm in length, the rostral end of which lay dorsal to the caudal end. Further, it was found that EAA microinjections made in different portions of the defence region of the PAG elicited defence reactions characterised by different patterns of vocalization and differing intensities of display. It was also observed following unilateral injection of KA into the PAG that defence reactions, including attack, were elicited by approach in the visual hemifield or touch of the body contralateral, but not ipsilateral, to the injection site. The asymmetry of the defence reaction was not due to any obvious ipsilateral motor impairment and thus suggests that the PAG mediation of the defence reaction, in addition to controlling the outflow to the somatic and autonomic motor systems, also affects sensory processing.

Animals↗

PubMed1988

Microinjection of cis-flupenthixol, a dopamine antagonist, into the medial preoptic area impairs sexual behavior of male rats.

Systemically administered dopamine agonists have been shown to facilitate copulation in male rats. Microinjection of the dopamine agonist apomorphine into the medial preoptic area has also been reported to facilitate sexual behavior. The present experiments investigated the effects of medial preoptic microinjections of the dopamine antagonist cis-flupenthixol on male rat copulatory behavior. Fewer males initiated copulation and fewer ejaculated following flupenthixol administration. Those males that did ejaculate following flupenthixol injections had fewer ejaculations and longer interintromission intervals. Flupenthixol also antagonized the facilitative effects of apomorphine injections into the medial preoptic area. Flupenthixol and apomorphine produced only minor alterations in noncopulatory behaviors. The results suggest that dopamine receptors within the medial preoptic area are important in the regulation of masculine sexual behavior in the rat.

Animals↗

PubMed1989

Respiratory effects of 5'-ethylcarboxamidoadenosine, an analog of adenosine, following microinjections into the nucleus tractus solitarius of rats.

Microinjections of 5'-ethylcarboxamidoadenosine (NECA), an adenosine analog, were made into respiratory-related regions of the nucleus tractus solitarius (NTS) of spontaneously breathing rats and cardiorespiratory parameters were recorded during a 60-min test period. Microinjections of NECA, in the dose range of 0.35-350 picomol per rat, produced significant dose-related reductions in respiratory rate which were accompanied by correlative increases in tidal volume. At the end of the 60-min test period following the administration of NECA, the respiratory rate remained profoundly depressed, whereas blood pressure and heart rate were not significantly affected compared to preinjection control values. The data from this study suggest that adenosine may exert modulatory influences in brainstem respiratory control regions.

Adenosine↗

PubMed1989

Regional neuroleptic microinjections indicate a role for nucleus accumbens in lateral hypothalamic self-stimulation reward.

Bilateral microinjections of the neuroleptic, cis-flupenthixol, were made into 56 forebrain targets distributed across various dopamine (DA) terminal fields in the forebrain. Drug effects on medial forebrain bundle (MFB) stimulation-produced reward were assessed with a rate-frequency procedure implemented in a runway paradigm in a discrete-trial fashion. This method generated independent measures of drug-induced changes in the MFB stimulation reward and operant motor/performance capacity. Control experiments were run with the inactive isomer, trans-flupenthixol. Results indicate a major role for accumbens DA in MFB reward, but not for the DA in caudate and medial frontal cortex. Few drug-induced motor/performance deficits were found at any site. In 14 selected subjects, 6-OHDA-induced chronic DA lesions were made at the same site as neuroleptic microinjection. These results confirmed the reward effects of acute DA receptor blockade, but produced a greater associated motor/performance impairment. Both behavioral effects of the lesion recovered within 2 weeks in many, but not all subjects.

Animals↗

PubMed1990

Alpha-adrenergic receptor agonists, but not antagonists, alter the tail-flick latency when microinjected into the rostral ventromedial medulla of the lightly anesthetized rat.

The present experiments, part of an ongoing study designed to characterise the role of norepinephrine (NE) in regulating the activity of putative nociceptive modulatory neurons in the rostral ventromedial medulla (RVM), assessed the effects of alpha-adrenergic receptor-selective agents on the nociceptive threshold (as measured by the tail-flick withdrawal response on noxious heat). These microinjection studies were carried out in the barbiturate-anesthetized rat, a preparation which is favourable for acute neurophysiological studies. The data obtained demonstrate that, as observed by others in the awake animal, activation of alpha 2-adrenergic receptors in the RVM produces hypoalgesia. However, unlike in the awake animal, when antagonists selective for either the alpha 1- or alpha 2-adrenergic receptor are microinjected alone into the RVM there is no change in the nociceptive threshold. These data suggest that the alpha 2-adrenergic receptor has a postsynaptic location and that barbiturate anaesthesia suppresses a tonically active or noxious stimulus-activated noradrenergic input to the RVM that is present in the awake animal.

Adrenergic alpha-Agonists↗

PubMed1991

Microinjections of norepinephrine into the intermediolateral cell column of the spinal cord exert excitatory as well as inhibitory effects on the cardiac function.

Cardiac responses to microinjections of norepinephrine (NE) into the intermediolateral column of the spinal cord (IML) at T2 level were studied in pentobarbital-anesthetized, immobilized and artificially ventilated, male Wistar rats. For describing the effects of NE conveniently, the doses of NE were divided into two ranges. The small dose-range consisted of 20 nl volumes of 50, 75 and 100 micromolar (microM) solutions (i.e. 1, 1.5 and 2 pmole in 20 nl, respectively). The larger dose-range consisted of 20 nl volumes of 2.5, 25, 40 and 50 millimolar (mM) solutions (i.e. 0.05, 0.5, 0.8 and 1 nmole in 20 nl, respectively). Injections of small doses of NE (1-2 pmole) into the IML increased heart rate (HR); intravenous injections of these doses did not alter either blood pressure (BP) or HR. Larger doses of NE (0.05-1 nmole) elicited a decrease in HR; intravenous injections of these doses increased HR and BP. Maximum increase in HR was produced by injections of 1.5 pmole of NE into the IML; this effect was blocked by prior injections of prazosin (an alpha 1 adrenergic receptor antagonist; 50 pmole) but not idazoxan (an alpha 2 adrenergic receptor blocker; 10 pmole) into the IML. Maximum decrease in HR was elicited by injections of 0.8 nmole of NE into the IML; this effect was blocked by idazoxan (10 pmole) but not prazosin (50 pmole). Microinjections of idazoxan (10 pmole) alone increased HR while prazosin (50 pmole) alone was ineffective. Intravenous injections of chlorisondamine (a ganglion blocker) blocked the increase in HR elicited by injections of 1.5 pmole of NE into the IML.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1991

Microinjections of calcitonin gene-related peptide within the trigeminal subnucleus caudalis of the cat affects adrenal and autonomic function.

To assess the role of calcitonin gene-related peptide (CGRP) within the trigeminal subnucleus caudalis (Vc) on adrenal and autonomic function, microinjections were directed at different laminae of Vc in chloralose-anesthetized cats. Microinjections of CGRP (5 pmol, 100 nl) into laminae I-II increased significantly the adrenal secretion of epinephrine, adrenal blood flow, adrenal vascular conductance, mean arterial pressure and heart rate. Injections of CGRP into laminae V-VI decreased significantly the adrenal secretion of epinephrine, however, other measured variables were not affected. To examine if CGRP interacts with substance P within Vc to modify adrenal and autonomic function, subthreshold doses of each peptide were injected alone and simultaneously. Combined subthreshold doses of CGRP and substance P injected into laminae V-VI, but not into laminae I-II or III-IV, evoked increases in arterial pressure and in heart rate that exceeded the responses seen after injection of either peptide alone. The adrenal secretion of catecholamines was not affected by individual or combined subthreshold doses of either peptide, regardless of the laminar site of injection. These data suggest that release of CGRP within laminae I-II of Vc alters adrenal and autonomic function via mechanisms separate from those that mediate substance P-evoked responses. In contrast, CGRP and substance P may act, at least in part, through a common neural substrate within the deeper laminae of Vc to modify arterial pressure and heart rate. Thus, multiple subpopulations of peptide-responsive neurons in the medullary dorsal horn likely contribute to the reflex adrenal and autonomic responses that often accompany nociception.

Adrenal Glands↗

PubMed1991

Ventral pallidal microinjections of receptor-selective opioid agonists produce differential effects on circling and locomotor activity in rats.

Locomotor activity was investigated following microinjections of receptor-selective opioid agonists into the ventral pallidum (VP) of rats. In Expt. 1, male Long-Evans rats were treated with unilateral microinjections of the mu agonist [D-Ala2-MePhe4, Gly-ol5]-enkephalin (DAGO), the delta agonist [D-Pen2, D-Pen5]-enkephalin (DPDPE) or the kappa agonist U50,488H, and the rate and duration of circling behaviour were measured. DAGO (0.01, 0.1, 1.0 nmol) produced a dose-dependent increase in contralateral circling; pretreatment with 1.0 mg/kg naltrexone blocked the circling induced by the highest dose. The behavioral effect was largest when injections were targeted at the VP rather than structures dorsal to the VP. In contast to DAGO, intrapallidal DPDPE (0.01, 0.1, 1.0, 10.0 nmol) produced a slight increase in contralateral circling only at the highest dose and U50, 488H (0.01, 0.1, 1.0, 10.0 nmol) produced no effect. In Expt. 2, the effects of bilateral injections of DAGO, DPDPE and U50,488H were tested in photocell activity boxes. DAGO produced a dose-dependent increase in locomotor activity and this increase was decreased by 1.0 mg/kg naltrexone. A slight increase in activity was observed with the highest dose of DPDPE, and a slight decrease was observed with the highest dose of U50,488H. These findings confirm that opiate actions in the VP contribute to opiate-induced locomotion and suggest that mu and to some extent delta receptors are involved in this behavior.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1991

Microinjections of norepinephrine within the superficial laminae of trigeminal subnucleus caudalis evoke increases in plasma adrenocorticotropin in the rat.

To determine if local release of norepinephrine within the medullary dorsal horn influences autonomic responses often associated with nociception, microinjections of norepinephrine or of specific adrenergic receptor agonists were directed at the trigeminal subnucleus caudalis (Vc) in pentobarbital-anesthetized rats. Norepinephrine (20 nmol, 100 nl) evoked a significant increase (+ 233.8 +/- 89.5 pg/ml, P less than 0.01) in plasma concentrations of adrenocorticotropin (ACTH) after injections within the superficial laminae (I-II) of Vc, whereas mean arterial pressure or heart rate were not affected. Methoxamine (20 nmol), an alpha 1-adrenoceptor agonist, injections into laminae I-II also increased plasma ACTH (+ 90.6 +/- 32 pg/ml, P less than 0.025) without affecting arterial pressure or heart rate. Norepinephrine injections into the deeper laminae (III-V) of Vc caused a variable increase in plasma ACTH (+ 203.5 +/- 146.5 pg/ml, P less than 0.01) that was not mimicked by injections of methoxamine. Microinjections of alpha 2-(clonidine) or beta-(isoproterenol) adrenergic receptor agonists into Vc had no effect on plasma ACTH regardless of the laminar site of injection. The results suggest that norepinephrine acts within Vc to alter selected autonomic responses often associated with nociception. The involvement of an alpha 1-adrenergic receptor subtype within the superficial laminae of the medullary dorsal horn suggests a neural mechanism for norepinephrine-evoked increase in plasma ACTH that is distinct from the well known alpha 2-adrenergic receptor-mediated antinociceptive effects of norepinephrine.

Adrenocorticotropic Hormone↗

PubMed1992

Microinjection of arginine-vasopressin into the periaqueductal gray stimulates flank marking in Syrian hamsters (Mesocricetus auratus).

Syrian hamsters can communicate using a distinctive form of scent marking called flank marking. Vasopressin-sensitive neurons within the medial preoptic-anterior hypothalamic continuum (MPOA-AH) play a critical role in the control of this form of olfactory communication. Extrahypothalamic regions may also mediate hamster flank marking. Since the MPOA-AH and the periaqueductal gray (PAG) are reciprocally connected, the present study investigated whether PAG neurons are involved in the control of flank marking. The first study found that microinjection of vasopressin, but not oxytocin or saline, into the PAG induced high levels of flank marking in male (n = 8) and female (n = 5) hamsters (P less than 0.01). The second study demonstrated that microinjection of vasopressin into the PAG stimulated flank marking in a dose-dependent manner in both male (n = 7) and female (n = 11) hamsters (P less than 0.01). These data suggest that vasopressin-responsive neurons within the periaqueductal gray participate in the control of hamster flank marking.

Animal Communication↗

PubMed1992

Microinjection of opioid antagonists into the substantia nigra reduces stress-induced eating in rats.

Stress produced by pinching the tail has been shown to cause satiated animals to eat and to display oral stereotypies. Endogenous opioids and central dopamine systems have been implicated in the mediation of these effects. In order to test the possibility that the substantia nigra (SN) might be involved, the amount of food intake and gnawing produced by mild tail pinch were assessed following bilateral microinjections of opioid antagonists into the SN. Evaluations of nociceptive thresholds were also conducted using tail flick and hot plate tests. Eating induced by tail pinch was reduced by microinjections of the non-selective opioid antagonist naloxone (3, 10, 20 and 30 nmol) and by the mu-selective antagonist Cys2, Tyr3, Orn5, Pen7 Amide (CTOP) (1, 3 and 10 nmol). These effects on eating occurred in the absence of effects on gnawing. kappa- and delta-antagonists (10 nmol) had no effect on eating or gnawing. Naloxone did not alter either tail flick or hot-plate response latencies. The highest dose of CTOP increased response latency on the hot-plate test only. The results are interpreted as suggesting that the SN may be an important central site of action for opioid antagonists in reducing stress-induced eating. The possibility that the SN may be a central site mediating the effects of dopamine on this phenomenon is also discussed.

Animals↗

PubMed1994

Antinociceptive effects of carbachol microinjected into different portions of the mesencephalic periaqueductal gray matter of the rat.

The changes in tail-flick latency (TFL) to noxious heating of the skin produced by the microinjection of carbachol (CCh) into the dorsal (dPAG), lateral (lPAG), and ventral (vPAG) portions of the mesencephalic periaqueductal gray matter (PAG) were studied in the rat. A significant increase in TFL was produced by CCh (0.2 microgram/0.5 microliter) microinjected into sites widely distributed within the PAG. The effect of CCh was stronger in the most caudal portion of the DPAG. Smaller effects were obtained after injection of CCh into the aqueduct, indicating that drug diffusion from the injection sites to the aqueduct lumen is unlikely to cause the antinociceptive effect of CCh. Dimethyl-phenyl-piperazinium (0.35 microgram/0.5 microliter), but not bethanechol (0.22 and 0.44 microgram/0.5 microliter), produced effects similar to CCh (0.2 microgram/0.5 microliter), when injected into the dPAG. The effects of CCh were inhibited by the previous administration of mecamylamine (1 microgram/0.5 microliter), but not atropine (1 microgram/0.5 microliter) or naloxone (1 microgram/0.5 microliter), into the dPAG. These results are indicative that antinociception produced by CCh from the dPAG depends on nicotinic, but not muscarinic or opioid mechanisms within the dPAG. The intraperitoneal administration of phenoxybenzamine (1 mg/kg) or mecamylamine (1 mg/kg), but not naloxone (1 mg/kg), methysergide (1 mg/kg), or atropine (1 mg/kg), inhibited the effects of CCh injected into the dPAG. In contrast, a higher dose of intraperitoneal phenoxybenzamine (5 mg/kg) was ineffective against the antinociception evoked by CCh when injected into the vPAG. Therefore, the effects of CCh from the dPAG may depend on the activation of centrifugal pathways involving both nicotinic and alpha-adrenergic mechanisms. In addition, the results indicate that different cholinergic substrates in the PAG may mediate both alpha-adrenergic and non-alpha-adrenergic descending pain mechanisms activated by the dPAG and vPAG, respectively.

Analgesics↗

PubMed1995

Bicuculline blocks neuropeptide Y-induced phase advances when microinjected in the suprachiasmatic nucleus of Syrian hamsters.

Microinjection of neuropeptide Y (NPY) into the suprachiasmatic nucleus of the hypothalamus (SCN) during the middle of the subjective day (i.e. circadian time 6) causes large phase advances in circadian rhythms. The present study demonstrates that microinjection of the gamma-aminobutyric acid (GABA) antagonist, bicuculline, completely blocks NPY-induced phase advances. These data indicate that GABAA activity within the SCN may mediate the phase shifting effects of some stimuli on the circadian pacemaker.

Animals↗

PubMed1995

Effects of the dopamine D-1 antagonist SCH 23390 microinjected into the accumbens, amygdala or striatum on cocaine self-administration in the rat.

This study tested the hypothesis that blockade of D-1 dopamine receptors in the nucleus accumbens shell, central nucleus of the amygdala or dorsal striatum by intracerebral microinjection of the dopamine antagonist SCH 23390 produces an attenuation of the effects of self-administered cocaine. Microinjection of SCH 23390 (0-4.0 micrograms total dose) into any of the three brain regions dose-dependently increased the rate of cocaine self-administration, consistent with a partial attenuation of the effects of cocaine under these conditions (0.25 mg cocaine i.v.; fixed-ratio 5 timeout 20 s). The regional rank order potency of SCH 23390 was accumbens > amygdala > striatum, striatal injections being equipotent with subcutaneous administration. Moreover, SCH 23390 produced rapid effects on cocaine self-administration only when injected into the accumbens or amygdala. The time course of this regional selectivity was consistent with the rate of diffusion of SCH 23390 from the site of injection as measured by quantitative autoradiography, demonstrating that the regional selectivity of intracerebral injections of SCH 23390 is time-dependent. These results support a role for D-1 dopamine receptors in the nucleus accumbens and amygdala in the effects of self-administered cocaine, and suggest that D-1 receptors in certain portions of the 'extended amygdala' may be an important substrate for the reinforcing actions of cocaine.

Amygdala↗