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At least 1,225 records · Page 68Linked to original sources
PubMed1987

Cardiovascular effects of substance P and capsaicin microinjected into the nucleus tractus solitarii of the rat.

This report deals with the effect of substance P (SP) and capsaicin on blood pressure and heart rate after administration into different sites of the nucleus tractus solitarii (NTS) of urethane-anesthetized rats. Microinjection of SP at 6 different coordinates throughout the NTS showed 3 sites where SP administration evoked changes in blood pressure and heart rate. The most sensitive sites where application of SP into the NTS evoked dose-dependent hypotension and bradycardia were at the level of the posterior tip of the area postrema (zero level) and at the level of the obex. Capsaicin evoked dose-dependent hypotension and bradycardia at the same sites. These results further support the possibility that SP may be a neurotransmitter or neuromodulator of baroreceptor afferents in the NTS.

Animals↗
PubMed1987

Microinjections of the gamma-aminobutyrate antagonist, bicuculline methiodide, into the caudate-putamen prevent amygdala-kindled seizures in rats.

We used amygdala-kindled seizures in rats to study the function of striatal gamma-aminobutyrate (GABA) in the regulation of the seizure threshold of the limbic forebrain. Microinjections of the GABAA antagonist, bicuculline methiodide, 1 pmol, into the caudate-putamen protected rats against amygdala-kindled seizures. This result shows that striatal GABA differentially modulates the threshold for limbic seizures.

Amygdala↗
PubMed1987

Stimulation of vasopressin by calcium microinjections in the area of the paraventricular nucleus of the hypothalamus.

The present experiments were designed to investigate the effect of local calcium application on the paraventricular nucleus (PVN) on arginine-vasopressin (AVP) release and blood pressure. A microinjection of 2 microliter of calcium gluconate 10% in the PVN elevated AVP levels to 71.6 +/- 8.7 pg/ml compared to 3.3 +/- 0.6 pg/ml in control rats receiving iso-osmolar solution of dextrose 11% (P less than 0.001), whereas peripheral plasma epinephrine and norepinephrine were normal. Despite the increase of plasma AVP levels, blood pressure and heart rate remained unchanged indicating that other unknown mechanisms counteract AVP's pressor effect. These data suggest that locally applied Ca2+ in the vasopressinergic neurons of the hypothalamus strongly stimulates the release of AVP.

Animals↗
PubMed1987

Tolerance to morphine microinjections in the periaqueductal gray (PAG) induces tolerance to systemic, but not intrathecal morphine.

The acquisition and retention of tolerance to the antinociceptive effect of supraspinal morphine on the tail withdrawal reflex was assessed in rats implanted with unilateral cannulae in the periaqueductal gray (PAG). Development of tolerance to daily microinjections of morphine was indicated by the return of the tail flick response within 4 days, followed by the recovery of analgesic sensitivity one week later. After tolerance had developed, the effect of an acute systemic (1.5-4.5 mg/kg) or intrathecal (5-15 micrograms) morphine injection was determined. 'Cross-tolerance' was observed between systemic and supraspinal morphine but not between intrathecal and supraspinal morphine. The data indicate that tolerance to chronic intracerebral morphine produces the same behavioral consequences as tolerance to systemic morphine.

Animals↗
PubMed1987

Excitatory and inhibitory effects on respiration of L-glutamate microinjected superficially into the ventral aspects of the medulla oblongata in cat.

L-Glutamate (4-40 nmol) was microinjected at superficial depths beneath the ventral surface of the medulla oblongata in cats. Injections (100-300 microns beneath the surface) made rostromedial to the hypoglossal nerve, less than 1.5 mm lateral to the pyramidal tract, caused stimulation of phrenic nerve activity. Injections (100-500 microns beneath the surface) up to 1 mm further lateral caused a marked increase in arterial pressure and depression of phrenic nerve activity. These findings support the existence of two cell groups in the ventral medulla that are involved in regulation of respiration; when activated, one (medial group) causes facilitation and the other (lateral group) inhibition of respiration.

Animals↗
PubMed1988

Testosterone alters the behavioral response of the medial preoptic-anterior hypothalamus to microinjection of arginine vasopressin in the hamster.

The medial preoptic-anterior hypothalamus (MPOA-AH) is necessary for expression of several testosterone-dependent behaviors including a form of hamster scent marking, called flank marking. Since arginine vasopressin (AVP) plays a critical role in the control of flank marking by the MPOA-AH the present study examined whether testosterone can influence the amount of flank marking produced by AVP microinjected into the MPOA-AH. The dose-dependent induction of flank marking by AVP was found to be reduced by approximately 50% in castrated male hamsters when compared to intact or testosterone-treated castrates. These data demonstrate that testosterone influences the amount of flank marking produced by AVP within the MPOA-AH.

Animals↗
PubMed1988

Differential enhancement of rapid eye movement sleep signs in the cat: a comparison of microinjection of the cholinergic agonist carbachol and the beta-adrenergic antagonist propranolol on pontogeniculo-occipital wave clusters.

The cholinergic agonist carbachol and the beta-adrenergic antagonist propranolol were microinjected at the same pontine sites and their effects on polygraphic rapid eye movement (REM) sleep, especially pontogeniculo-occipital (PGO) waves, were measured. While both propranolol and carbachol enhanced PGO wave activity and polygraphic REM sleep, the carbachol-correlated enhancement was more impressive. The increases in REM sleep signs elicited by carbachol were 5-fold over baseline and lasted throughout the 4-h recording period. Propranolol elicited 2.5-fold increases that were significant in the first 2 h only. Yet, the increase in PGO wave activity evoked by propranolol was equal to that of carbachol during non-REM sleep and wakefulness. The results indicate that while propranolol is less potent in activating the distributed neuronal network responsible for REM sleep generation, it selectively facilities that part of the network responsible for PGO waves.

Adrenergic Fibers↗
PubMed1988

Effects of D-Ala2-Met5-enkephalinamide microinjections placed into the bed nucleus of the stria terminalis upon affective defense behavior in the cat.

This study examined the effects of intracerebral injections of D-Ala2-Met5-enkephalinamide (DAME) upon hypothalamically elicited hissing behavior in the cat. The bed nucleus of the stria terminalis (BNST) was selected for investigation because of its anatomical connections with the medial hypothalamus, its relatively high concentrations of enkephalins and opiate receptors and its demonstrated ability to modulate hypothalamically elicited aggressive reactions in the cat. DAME microinjected into the BNST in 1.0 or 10.0 micrograms/0.5 microliter quantities resulted in significant dose dependent increases in mean latencies for elicitation of the hissing response. Suppression of hissing following the 1.0 microgram dose of DAME was selectively diminished by prior administration of naloxone. These findings suggest that the opiate receptors within the BNST play a role in the regulation of the hissing component of hypothalamically elicited affective defense behavior.

Amygdala↗
PubMed1988

Dopamine-independent motor behavior following microinjection of rimorphin in the substantia nigra.

The motor-activating effects of rimorphin, an opioid peptide derived from prodynorphin, were examined in the substantia nigra pars reticulata of rats. Unilateral microinjections of rimorphin produced dose-dependent contralateral rotational behavior that was antagonized by naloxone, suggesting that these effects were mediated by opiate receptors. Lesions of midbrain dopamine cells with 6-hydroxydopamine (6-OHDA) produced a 95% or greater depletion of tyrosine hydroxylase in the striatum ipsilateral to the lesion, but failed to reduce the number of circles made by the rats. In addition to an overall preservation of rimorphin-induced circling in animals with 6-OHDA lesions, 50% of these rats exhibited circling that was at least 2 standard deviations above the mean of animals without lesions. The motor activating effects of rimorphin, thus, appear to occur independently of the nigrostriatal dopamine system; these effects may instead be mediated by GABAergic efferents in the pars reticulata.

Animals↗
PubMed1988

Awaking effect of PGE2 microinjected into the preoptic area of rats.

We examined the effect of prostaglandin (PG)E2 on the sleep-wake activity and on body temperature by microinjecting PGE2 into the preoptic area of rats that had been chronically implanted with guide cannulae and electrodes for the recordings of electroencephalogram and electromyogram. PGE2 at doses of 2.5 X 10(-13), 2.5 X 10(-11), and 2.5 X 10(-9) mol reduced the time of slow wave sleep (SWS) to 75%, 61%, and 59% and that of paradoxical sleep (PS) to 73%, 50%, and 25% of the controls, respectively. The SWS and PS reductions were mainly due to the shortening of the SWS episode and the less frequent occurrence of PS episodes. The sleep reduction was accompanied by increased behavioral movement. The maximum increases of rectal temperature at doses of 2.5 X 10(-11) and 2.5 X 10(-9) mol of PGE2 were 1.3 degrees C and 2.7 degrees C, respectively. At a dose of 2.5 X 10(-13) mol of PGE2, the time of SWS and that of total sleep (sum of SWS and PS) decreased significantly, but the change in body temperature was negligible. This may imply that the effect of PGE2 on the sleep-wake activity is not caused by the hyperthermia produced by PGE2. Injections of PGE2 at a dose of 2.5 X 10(-15) mol and saline control induced alteration in neither sleep-wake activity nor body temperature. PGD2 at a dose of 2.5 X 10(-9) mol slightly elevated the rectal temperature (0.5 degree C), but did not produce any change in the sleep-wake activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Role of mu 1-opiate receptors in supraspinal opiate analgesia: a microinjection study.

Microinjection of opiates into either the periaqueductual gray, locus coeruleus, nucleus raphe magnus, or nucleus reticularis gigantocellularis elicits a profound naloxone-sensitive analgesia. mu-Opioid receptors have been implicated in supraspinal analgesia and studies from our laboratory have demonstrated the importance of the mu 1-receptor subtype. In an effort to examine the receptor subtypes responsible for opioid analgesia in specific brain regions, we examined dose-response relationships and naloxonazine sensitivity of morphine and two enkephalin derivatives in the above 4 brain regions. Both morphine and [D-Ser2,Leu5]enkephalin-Thr6 (DSLET) were effective analgesics in all regions examined. The poor affinity of DSLET for mu 2-receptors and of morphine for delta-receptors, combined with their similar, high affinity for mu 1-receptors, implied a mu 1-mechanism of action. The mu 1-selective antagonist naloxonazine effectively blocked the analgesic responses of both compounds in all regions. [D-Pen2,D-Pen5]enkephalin (DPDPE), a potent delta-ligand which does not interact with mu 1-receptors, did not elicit analgesia in either the periaqueductal gray or locus coeruleus at any dose tested. These results suggest that opiates and opioid peptides produce analgesia in these 4 brain regions through mu 1-receptors. The inactivity of DPDPE argues against a role for delta-receptors and the similar analgesic potencies of morphine and DSLET makes a significant role for mu 2-receptors unlikely.

Analgesia↗
PubMed1989

Kindling of full limbic seizures by repeated microinjections of excitatory amino acids into the rat amygdala.

Fully developed limbic seizures were kindled by repeated (every second day) microinjections of an L-glutamate plus L-aspartate (Glu/Asp) mixture (1:3 ratio; 1.5 mumol total dose). Glu alone (1.5 mumol) or Asp alone (1.5 mumol), into the rat amygdala. This excitatory amino acid (EAA)-induced kindling was durable, persisting for at least several months, and showed strong positive transfer to electrical kindling. Fully EAA kindled seizures were inhibited by focally applied NMDA-receptor antagonists. EAA kindling and electrical kindling are shown to have many similar properties. This strongly suggests that they may also have neurochemical mechanisms in common. These results further highlight the important role of EAAs in basic mechanisms involved in the generation and expression of epilepsy.

Amygdala↗
PubMed1989

Characterization of pretentorial periaqueductal gray matter neurons mediating intraspecific defensive behaviors in the rat by microinjections of kainic acid.

Unilateral microinjections of 40 pmol of kainic acid (KA; in 0.2 microliter) within the periaqueductal gray matter (PAG) evoked intraspecific defensive postures (defensive uprights, defensive alterting, defensive sideways, backing) in rats confronted with a conspecific. These reactions, which lasted for up to 30 min, were seemingly identical to the rat's natural defensive reaction to attacks by a conspecific although they were evoked by the investigatory approach, rather than the attack, of another rat. Histological analysis revealed that the strongest defensive reactions were evoked from sites within a restricted part of the pretentorial periaqueductal gray matter. Lower doses of KA induced fewer (20 pmol) or non-significant increases (4 pmol) in defensive reactions. Higher doses (100 and 200 pmol) increased the percentage of defensive behavior and also induced oriented jumps out of the test cage. In tests with a conspecific, defensive reactions were elicited most frequently when investigation by the partner was localized to the side of the body contralateral to the injection site. This was confirmed in a sensory reactivity test in which tactile stimulation by the experimenter elicited most defensive reactions when applied on the side of the body contralateral to the injection side. This test also revealed a somatotopic gradient in the animal's reaction: tactile stimulation of the contralateral head and the forelimb evoked the strongest reactions, whereas no responses were observed upon tactile stimulation of the contralateral flank or hindlimb. Measurement of electroencephalographic activity at the cortical, hippocampal, amygdala and PAG levels indicated that the evoked defensive reactions were not secondary to epileptogenic effects. Finally, quantitative analysis of an autoradiographic study found that [3H]KA diffused within a diameter of 1.0-1.2 mm around the cannula tip. Taken together, these results indicate the existence of a population of neurons within a restricted part of the pretentorial PAG of the rat, the excitation of which produces defensive responses and demonstrate that these defensive reactions have a socially adaptive value.

Animals↗
PubMed1990

Morphine and dynorphin(1-13) microinjected into the medial preoptic area and nucleus accumbens: effects on sexual behavior in male rats.

The effects on sexual behavior of opiate receptor stimulation within A10 and A14 terminal areas were examined in the following experiments. Morphine (0.01-6 nmol) and dynorphin(1-13) (0.01-3 pmol) were microinjected into the medial preoptic area (MPOA). Morphine (10-100 pmol) and dynorphin (10-100 fmol) injected into the MPOA reduced both the latency to ejaculate and the number of intromissions triggering ejaculation. Morphine (6 nmol) produced a failure to resume copulating following the second ejaculation. Morphine (1-10 nmol) injected into the nucleus accumbens (ACC) shortened the latency to the first intromission and lengthened the second postejaculatory interval. Naloxone (3 mg/kg i.p.) reversed the effects of morphine on intromission latency and attenuated the lowering of ejaculatory threshold.

Animals↗
PubMed1990

Insulin co-injection suppresses the thermogenic response to glutamate microinjection into the VMH in rats.

Selective stimulation of ventromedial hypothalamic nucleus (VMH) neurons by microinjection of the excitatory amino acid glutamate sharply increased interscapular brown adipose tissue (IBAT) and core temperatures in urethane-anaesthetized rats. This effect was blocked by co-injection of insulin (0.1-1 microgram) though not an inactive insulin analog, TNB3 insulin. Injection of insulin (1 microgram) into the contralateral VMH or systemic administration of insulin (1 microgram) had no effect on the thermogenic response to intra-VMH glutamate. These results complement those showing that intra-VMH insulin suppresses the basal firing rate of sympathetic nerves to IBAT and diminishes cold-induced nonshivering thermogenesis in BAT and add support to the view that insulin functions as an inhibitory signal on VMH neurons controlling thermogenesis in BAT.

Adipose Tissue, Brown↗
PubMed1990

Bombesin microinjected into the dorsal vagal complex inhibits TRH-stimulated gastric contractility in rats.

The effects of centrally injected bombesin on central and peripheral stimulated gastric contractility were investigated in fasted urethane-anesthetized rats. Miniature strain gauge force transducers were acutely implanted on the corpus of the stomach and gastric contractility was analyzed by computer. Intracisternal injection of the stable thyrotropin-releasing hormone (TRH)-analog RX 77368 (77 pmol) induced a stimulation of gastric contractility for 40 min. Intracisternal injection of bombesin (62-620 pmol) followed 30 min later by that of RX 77368 resulted in a dose-related inhibition of the TRH-analog-induced gastric contractility. Intracisternal injection of bombesin (620 pmol) did not modify gastric contractility stimulated by intravenous carbachol. Stimulation of gastric contractility induced by TRH-analog microinjected into the dorsal vagal complex (DVC) was dose-related suppressed by concomitant injections of bombesin (6.2-620 pmol). Neither bombesin alone (6.2 pmol) nor vehicle modified basal gastric contractility. These results demonstrate that bombesin acts within the brain to inhibit vagally stimulated gastric contractility and that the DVC is a sensitive site for bombesin inhibitory action. These findings suggest a possible interaction between TRH and bombesin in the central vagal regulation of gastric contractility.

Animals↗
PubMed1990

Neurotensin and cholecystokinin microinjected into the ventral tegmental area modulate microdialysate concentrations of dopamine and metabolites in the posterior nucleus accumbens.

Neurotensin and cholecystokinin, neuropeptides which coexist with dopamine in many ventral tegmental neurons, were microinjected into the ventral tegmental area during in vivo microdialysis in the posterior nucleus accumbens. Neurotensin significantly elevated concentrations of dopamine and its metabolites at doses of 10 pmol, 1 nmol, and 10 nmol, while cholecystokinin significantly elevated dopamine metabolite concentrations only at a dose of 10 nmol. These data suggest that neurotensin potently mediates the release of dopamine from the mesolimbic pathway via direct actions on the cell body.

3,4-Dihydroxyphenylacetic Acid↗