Ventricle Injection Research Articles

Stress-Induced Secretion ofα-Melanocyte-Stimulating Hormone and Its Physiological Role in Modulating the Secretion of Prolactin and Luteinizing Hormone in the Female Rat

The pattern of alpha MSH release during immobilization stress in ovariectomized rats was determined and correlated with that of plasma PRL and LH. Stress induced a marked elevation in plasma immunoreactive alpha MSH, with a time course identical to that of plasma PRL. The increment in plasma PRL was greater than that in plasma alpha MSH. Plasma LH was markedly lowered by stress. Analysis of pituitary and hypothalamic alpha MSH indicated a significant (P less than 0.05) increase in the neurointermediate lobe and anterior lobe content of alpha MSH. The alpha MSH content in the hypothalamus was lowered by stress when expressed as tissue content (P less than 0.025), although no significant differences in content in this area were detected when the results were expressed in terms of tissue protein. Stress induced a marked increase (P less than 0.01) in the median eminence levels of alpha MSH. Intraventricular (third ventricle) injection of the gamma-globulin fraction of a specific antiserum raised against alpha MSH increased basal PRL levels (P less than 0.025) and prevented the decline in plasma PRL that occurred 60 min after the onset of stress in the normal rabbit serum-injected rats. The stress-induced suppression of plasma LH was attenuated and delayed by the administration of alpha MSH antibodies. In conclusion, alpha MSH of brain origin is released during stress and is involved in lowering plasma PRL to basal levels and producing a partial suppression of plasma LH.

The rat urinary bladder: A novel preparation for the investigation of central opioid activity in vivo

A novel method, which utilized spontaneous, volume-induced contractions of the urinary bladder in the anesthetized rat, was developed to assess the central activity of substances with opioid properties. It was discovered that intracerebroventricular (i.c.v.) injections made directly into the lateral ventricle or intrathecal (i.t.) injections made into the spinal subarachnoid space inhibited bladder contractions in a dose-dependent manner. The methods for spinal and supraspinal drug administrations are described as is the estimation of the spread of drug as determined by i.c.v. and i.t. dye injections. The pharmacology of the i.c.v. and i.t. effects of opioids was determined by use of selective opioid agonists (μ-agonists: morphine, DAGO; δ-agonists: DADLE, DPDPE; k-agonist: U-50, 488H) and antagonists (μ-antagonist, naloxone; δ-antagonist, ICI 174,864). It was concluded that the i.c.v. and i.t. effects were mediated by μ- and δ-opioid receptors and not by k-receptors. A number of other agents such as pentobarbital, haloperidol, and desipramine also inhibited bladder activity following i.c.v. and i.t. administration, but their actions were insensitive to naloxone. This in vivo model was considered useful in the detection and evaluation of the central actions of substances with opioid properties.

Comparative Effects of Urapidil, Prazosin, and Clonidine on Ligand Binding to Central Nervous System Receptors, Arterial Pressure, and Heart Rate in Experimental Animals

We studied the effects of urapidil, clonidine, and prazosin on ligand binding to central nervous system receptors in rats and on arterial pressure and heart rate in chloralose-anesthetized cats. Ligand binding studies indicated that urapidil had 90 times greater affinity for alpha 1 than for alpha 2 adrenergic receptors. Administration of urapidil (129 micrograms) into the cerebroventricles of cats revealed no effect after lateral ventricle injection, a decrease of 9.7 +/- 3.0 mm Hg after fourth ventricle injection, and an increase of 10.8 +/- 2.2 mm Hg after restriction of the drug in the forebrain ventricles. Clonidine (30 micrograms) produced hypotension and bradycardia after injection into the lateral ventricle. Prazosin was ineffective after cerebroventricular injection. Intravenous administration of 0.22, 0.67, and 2.00 mg/kg urapidil produced dose-dependent decreases in arterial pressure that were associated with blockade of alpha 1 adrenergic receptors. Intravenous administration of prazosin elicited the same response. Clonidine (10 micrograms/kg, intravenously produced an initial increase in arterial pressure that was unaffected by pretreatment with urapidil or prazosin. These results suggest that urapidil produces hypotension by an action on the peripheral vasculature and in the hindbrain. The peripheral effect involves blockade of alpha 1 adrenoceptors.

Influences of norepinephrine and α-adrenergic mechanisms on gonadotropin secretion in female goldfish, Carassius auratus

Intraperitoneal or intraventricular (3rd cranial ventricle) injection of norepinephrine (NE) caused an increase in serum gonadotropin (GtH) concentrations in female goldfish at times of the year when the ovaries were regressed or at early stages of recrudescence, but had no influence at other stages of the ovarian cycle. In a previous report it was shown that clonidine (α-agonist) increased serum GtH levels in fish at early or mid-ovarian recrudescence [ J. P. Chang, A. F. Cook, and R. E. Peter (1983) Gen. Comp. Endocrinol. 49, 22–31]; however, intraperitoneal injection of clonidine had no effect on circulating GtH levels when tested in fish at late ovarian recrudescence. In fish at early stages of ovarian recrudescence, intraperitoneal injection of phentolamine (α-blocker) did not alter GtH levels, but it blocked the NE-induced increase in serum GtH levels when injected simultaneously with NE. These results suggest that NE stimulates GtH release by α-adrenergic mechanisms at the brain and/or pituitary level in female goldfish in a sexually regressed or early ovarian recrudescence condition.

Cardiovascular effects produced by injections of thyrotropin-releasing hormone in specific preoptic and hypothalamic nuclei in the rat

Microinjection of 1.4 pmol TRH (0.5 ng; 50–150 nl) into both the preoptic suprachiasmatic nucleus (pos) and the A6800–7000 region of the medial preoptic nucleus (pom) produced increases in blood pressure and heart rate of 7% and 19%, respectively; heart rate responses in these two areas were higher than those occurring in other areas tested. TRH induced a significant increase in blood pressure and heart rate in the posterior hypothalamic nucleus (nhp) and increased heart rate only in the anterior (nha) and dorsomedial (ndm) hypothalamic nuclei. A small decrease in both blood pressure and heart rate resulted with TRH injections in the A7050–7400 region of the pom. No changes in respiratory rate or rectal temperature were observed at any site with this dose of TRH. Preliminary studies into the mechanism of the cardiovascular actions of TRH suggested that inhibition of the parasympathetic nerves to the heart make a partial contribution to the TRH-induced heart rate increase in the pos and that adrenal catecholamine release mediates the TRH response in the nhp. Neither methylatropine pretreatment nor adrenalectomy prevented the response to TRH injected into the nha, suggesting that activation of the cardiac sympathetic nerves may mediate TRH actions in this region. In the ndm, neither methylatropine nor adrenalectomy prevented the response to TRH; however, there was a tendency for the response to be less after methylatropine. Therefore, both inhibition of the parasympathetic and activation of the sympathetic nervous systems may contribute to the response observed, but no adrenal involvement could be demonstrated. Discrete injections of 0.8 nmol TRH produced increases in heart rate and blood pressure in all preoptic and hypothalamic nuclei tested with accompanying changes in respiratory rate and rectal temperature in some areas. Lateral cerebral ventricle injections of as little as 2.8 pmol TRH produced increases in blood pressure and heart rate; cardiovascular responses to higher doses (0.8–22 nmol) in the ventricle were often accompanied by arousal, piloerection, “wet dog” shakes and changes in respiratory rate and rectal temperature. Previous immunohistochemical demonstration of nerve cells and fibers in the preoptic-hypothalamic area and the present finding of specific sites responsive to low dose TRH injections (1.4 pmol) both support a physiological role for this peptide in central control of the cardiovascular system.

Chlorpromazine methiodide acts at the vestibular nuclear complex to induce barrel rotation in the rat

Barrel rotation is a unique motor response observed in rats in which, following an intracerebral injection, the animal develops a twist about the long axis and rolls laterally repeatedly. The response was first described following injection of somatostatin. We have previously shown that 'experimental dystonia' in rats induced by intraventricular chlorpromazine methiodide (CPZMI) is identical to barrel rotation, and that it is due to an antimuscarinic effect. The purpose of the present study was to investigate the neuroanatomical basis of CPZMI-induced rotation. We injected CPZMI in 3 microliters into right lateral and IVth ventricle and found that IVth ventricle injections were significantly more likely to induce rotation. Nuclear groups adjacent to the IVth ventricle, which are rich in muscarinic cholinergic receptors, include locus coeruleus and vestibular nuclear complex (VNC). We found that only VNC injections induced rotation. Only certain control compounds injected into VNC elicited the response. We conclude that barrel rotation has a specific neuroanatomical basis, involving central vestibular mechanisms, and that it has a specific pharmacologic basis.

Involvement of hypothalamic somatostatin in glucagon-induced suppression of growth hormone secretion in conscious rats

The role of central glucagon in regulating GH secretion was studied in conscious male rats with chronic indwelling intra-atrial and intracerebro-ventricular (ICV) cannulae. Repeated blood sampling every 20 min from 1000 hr to 1700 hr showed two major GH bursts occurring at regular intervals ( 3.6±0.1 hr ) around 1200 hr and 1540 hr. The ICV (lateral ventricle) injection of glucagon (10 μg/rat) at 1100 hr inhibited spontaneous GH secretion, and the mean (±SE) plasma GH levels from 1120 hr to 1700 hr were lower than those in controls injected ICV with the vehicle solution only ( 31.9±7.8 ng/ml vs. 157.1±13.4 ng/ml , p<0.01). The GH bursts did not appear until 5 hr after the injection. The intravenous (IV) injection of glucagon (10 μg/rat) did not change plasma GH levels or the occurrence of spontaneous GH bursts. The glucagon-induced suppression of GH release was attenuated when anti-somatostatin serum (ASS), but not normal rabbit serum (NRS), was given IV in a volume of 0.25 ml immediately before the ICV injection of glucagon (10 μg/rat) (mean GH levels at 1120–1700 hr: ASS+glucagon, 133.6±26.7 ng/ml vs. NRS+glucagon, 30.5±7.4 ng/ml , p<0.01). These findings suggest that central glucagon may play an inhibitory role in regulating GH secretion by stimulating SRIF release from the hypothalamus in the rat.

Respiratory depression produced by centrally administered taurine in the cat

The effects of taurine (0.8–64.8 umol) were studied on respiratory activity following intracisternal (cisterna magna) and intracerebroventicular (lateral ventricle) injections in cats anesthetized with alpha-chloralose. Respiratory activity was measured by using a Fleisch pneumotachograph and monitoring trachael airflow. The flow signal was integrated to obtain tidal volume (V T) and respiratory rate (f) was obtained by counting the number of V T excursions over one minute. Inspiratory (T I), expiratory (T E) and total (T TOT) cycle durations were also determined during this time period. In addition, end-tidal CO 2 was continuously monitored. Associated changes in arterial pressure (femoral artery cannula) and heart rate were also determined. After injections into the cisterna magna, taurine caused dose-related decreases in minute ventilation (V̇ E). The maximal decrease in V̇ E was from 495 ± 59 to 64 ± 14 ml/min (p < 0.05), and was due to both decreases in V T (from 27 ± 3 to 5 ± 1 ml; p < 0.05) and f (from 18 ± 1 to 12 ± 2 breaths/min; p < 0.05). T E and T TOT were increased from 2.4 ± 0.4 to 4.5 ± 0.6 sec (p < 0.05) and from 3.7 ± 0.4 to 6.4 ± 0.8 sec (p < 0.05), respectively. Mean inspiratory flow (V T/T I), a measure of inspiratory drive, was decreased from 21 ± 4 to 4 ± 2 ml/sec (p < 0.05). Apnea occurred in 5 of 6 animals after the 64.8 umol dose. This respiratory depression occurred without any significant change in arterial pressure. After lateral ventricle injections, taurine also caused dose-related, but not as pronounced, decreases in respiratory activity. In addition, taurine caused significant decreases (p< 0.05) in arterial pressure in doses that decreased V̇ E. Taurine administered intravenously had no significant cardiorespiratory depressant effects. These data indicate that centrally administered taurine produces respiratory depression and, depending on the route of CNS administration, also produces hypotension.

Possible Control by Oxytocin of Periodical and Synchronous Neurosecretory Bursts of Oxytocin Cells

Publisher Summary This chapter presents some experimental data, obtained in vivo and in vitro , to determine more precisely the central excitatory effect of oxytocin on its own release and explains that oxytocin may be involved in the control of its own release. Injection into the 3rd ventricle of an oxytocin antagonist, d(CH 2 ) 5 OVT, inhibits the milk-ejection reflex in the rat, decreasing both the frequency and amplitude of neurosecretory bursts and milk-ejection. Moreover, this antagonist prevents the facilitatory effect of intraventricular injection of oxytocin on the milk-ejection reflex. Oxytocin injections into the 4th ventricle are not sufficient to activate the milk-ejection reflex, and the effects observed after lateral ventricle injections are inferior to those obtained after 3rd ventricle injections. Oxytocin is released by axon collaterals or dendrites into the extracellular spaces of the magnocellular nuclei, as is dopamine in the substantia nigra. Such an increase of the endogenous oxytocin concentration during suckling could control the frequency and amplitude of the periodic activation of oxytocin cells. Although no experimental data is available in favor of such an hypothesis, oxytocin could be a synchronizing factor of the bursting activation of oxytocin cells in the magnocellular nuclei.

Antidromic indentification of hypothalamic neurosecretory cells in rats

Characteristics of antidromic action potentials of neurons of the paraventricular and supraoptic nuclei of the rat hypothalamus were studied during stimulation of the hypothalamo-hypophyseal tract by stimuli of varied amplitude and frequency. Step-like changes were found in spike latency in response to an increase in strength (up to 1.5–2.5 thresholds) or frequency (over 100 Hz) of stimulation, as well as cases with variation of the degree of division of the peak into A and B components. Injection of leu-enkephalin analog into the third ventricle or intravenous injection of NaCl solution (1 M) caused reversible changes in the level of excitability of antidromically activated neurons: leu-enkephalin mainly increased the latent period and threshold of action potential generation and reduced the reproducible frequency of stimulation to 10 Hz, whereas NaCl had the opposite effect. The results indicate that when the adopted criteria of antidromic identification of neurosecretory cells are used the level of their excitability must be taken into account.

Terminal degeneration demonstrated by the Fink-Heimer method following lateral ventricular injection of 6-hydroxydopamine

Degenerating terminals were mapped by the Fink-Heimer method after lateral or fourth ventricular administration of 6-hydroxydopamine (60OHDA). This method marks dopaminergic terminals and has the advantage that noradrenergic terminals are not stained. Fink-Heimer stained degeneratig terminals were seen bilaterally in specific patterns in many nuclei known to have a dopaminergic innervation: neostriatum, nucleus accumbens, olfactory tubercle, the dorsolateral and ventral parts of the bed nucleus of the stria terminalis, laterla septal nucleus, amygdala, and layers II-III of anterior cingulate cortex. Detailed maps are provided of the dopaminergic innervation in the bed nucleus of the atria terminalis in relatin to the cytoarchitectural subdivisions of this nucleus. A Fink-Heimer stained field was discovered in the lateral parabrachial nucleus, suggesting the presence of a previously unreported dopaminergic innervation of this nucleus. It was also noted that nonspecific degeneration near the injection site was much worse after lateral ventricle than after fourth ventricle injection.

On acute hypotensive effects of pindolol and propranolol in conscious rats

1. 1. An acute hypotensive effect of pindolol or propranolol have been identified in conscious normotensive and experimental hypertensive rats. 2. 2. The hypotensive effect induced with pindolol (0.1 mg/kg i.p.) was slightly inhibited by lateral ventricle injection of 6-hydroxydopamine (6-OHDA), but that induced with propranolol (5 mg/kg i.p.) was not. 3. 3. These hypotensive effects were abolished by systemic administration of 6-OHDA (50 mg/kg i.v.) or by pretreatment with indomethacin (1 mg/kg i.p.).

H1- and H2-histamine receptor antagonists and induced release of prolactin in male rats.

The effects of 3rd ventricle injection of metiamide, an H2-histamine receptor antagonist and pyrilamine, an H1-histamine receptor antagonist, on the increase of plasma prolactin induced by two doses of histamine in normal male rats were studied. Metiamide did prevent the stimulating action of histamine whereas pyrilamine was not effective. Histamine-induced prolactin release was also blocked by low doses of the 2 antihistamines given in combination. Metiamide per se has no effect but high doses of pyrilamine increased plasma prolactin levels and augmented the hormone response to histamine. The results suggest mediation of H2-receptors in the facilitatory action of histamine on prolactin release.

Involvement of 5-hydroxytryptamine in the central control of respiration, blood pressure and heart rate in the anaesthetized rat

5-Hydroxytryptamine (5-HT, 1 ng-25 μg) injected into the cerebral ventricles of urethananaesthetized rats produced a rise in blood pressure, a biphasic change in heart rate and a decrease in ventilation. Responses were largest after injections into the 3rd ventricle. Lateral ventricle injections produced smaller responses while 4th ventricle injections produced the least response. The cardiovascular responses were prevented or reduced by prior intraventricular injection of bromolysergic acid diethylamide. The pressor response was not blocked by hexamethonium (10 mg/kg i.v.) and was only partly reduced by pretreatment with either 6-hydroxydopamine (3 × 100 mg/kg i.v.) or atropine methonitrate (10 mg/kg i.v.). The pressor response was prevented by spinal transection at C1 or C3 but only slightly reduced by transection at C5 or C7. In animals curarized and artificially respired with air, the blood pressure response was reduced. It is conjectured that the rise in blood pressure may involve a direct effect of hypoxia or hypercapnia resulting from a decrease in respiratory activity which is in turn mediated by a direct action of 5-HT on structures lining the 3rd ventricles. There appears to be little or no involvement of the autonomic nervous system in the response. The fall in heart rate is mediated sympathetically.

Effects of third ventricle injection of prostaglandins on gonadotropin secretion in goldfish, Carassius auratus

The effects of injection of prostaglandin (PG) E 1, PGE 2, and PGF 2α into the third ventricle on serum gonadotropin (GTH) concentrations in the goldfish were tested. Blood samples were taken at 30 min postinjection for radioimmunoassay of serum GTH. PG dosages of 0.5 and 1.0 μg were ineffective. However, PGE 2 and PGF 2α at the 2.0-μg dosage significantly suppressed serum GTH. PGE 1 at a 2.0-μg dosage had no effect. There were no effects on serum GTH when 2.0 μg of PGE 1, PGE 2, or PGF 2α were injected intraperitoneally. The results indicate that PGE 2 and PGF 2α suppress gonadotropin secretion by some action, presumably on the hypothalamus. However, action of PGE 2 and PGF 2α by diffusion from the site of injection to some other brain site or the pituitary cannot be eliminated in the present study.

Increased Intraocular Pressure After Third Ventricle Injections of Prostaglandin E1 and Arachidonic Acid

Prostaglandin E1 administered into the third ventricle of rabbits produced increased intraocular pressure and body temperature. Similar responses were observed after third ventricle instillation of arachidonic acid, a precursor of prostaglandin E2. Increase of body temperature occurred with lower doses of prostaglandin E1 and arachidonic acid while the intraocular pressure response required larger amounts of these drugs. Pretreatment with aspirin rectal suppositories had no effect on the third ventricle responses induced by prostaglandin E1. Aspirin pretreatment before third ventricle instillation of arachidonic acid blocked the increases of intraocular pressure and temperature.

Effects of clonidine on the baroreceptor-heart rate reflex and on single aortic baroreceptor fibre discharge

The effects of clonidine (Catapres ®) on the baroreceptor-heart rate reflex were studied in unanaesthetized rabbits, and its action on single aortic baroreceptor fibre discharge was examined under anaesthesia. Intravenous clonidine (bolus 2.5 to 10 μg/kg + infusion of 0.25 to 1.5 μg/kg/min) altered the mean arterial pressure (MAP) — heart period (HP; pulse interval) curve, reducing median blood pressure and increasing the gain and heart period range (HPR). At low dose increased HPR by enhancing both vagal excitation and sympathetic inhibition of HP during a rise in MAP, compared with control conditions. At high i.v. dose of drug sympathetic inhibition was complete even at low MAP, and HPR increased due to a rise in vagal output to 4–6 times control. Lateral ventricle injections of 0.5 to 1.5 μg/kg of clonidine altered MAP - HP curve parameters in a similar manner as i.v. infusion. High dose of clonidine i.v. enhanced single aortic baroreceptor fibre discharge at a given MAP in anaesthetized animals, but there was no effect at low dose. Clonidine alters heart rate mainly through its direct central action on the baroreceptor pathways; at high dose these effects are reinforced by peripheral baroreceptor resetting. Clonidine has only slight effects on cardiac motoneurones not receiving baroreceptor projections.

Alteration of Intraocular Pressure After Third Ventricle Injections of Osmotic Agents

Alteration of Intraocular Pressure After Third Ventricle Injections of Osmotic Agents

Slow potential changes due to osmotic stimuli in supraoptic nucleus of the rabbit.

ARTICLESSlow potential changes due to osmotic stimuli in supraoptic nucleus of the rabbitRM Durham, and D NovinRM Durham, and D NovinPublished Online:01 Aug 1970https://doi.org/10.1152/ajplegacy.1970.219.2.293MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByRenal Regulation of Extracellular Volume and OsmolalityResponses of lateral preoptic neurons in the rat to hypertonic sucrose and NaClElectroencephalography and Clinical Neurophysiology, Vol. 46, No. 4Equipotency of hypertonic solutions of mannitol and sodium chloride in eliciting thirst in the dogPflügers Archiv European Journal of Physiology, Vol. 358, No. 3Alteration of Intraocular Pressure After Third Ventricle Injections of Osmotic AgentsAmerican Journal of Ophthalmology, Vol. 76, No. 6Orthodromic and antidromic activation of the paraventricular nucleus of the hypothalamus in the rabbitExperimental Neurology, Vol. 41, No. 2 More from this issue > Volume 219Issue 2August 1970Pages 293-298 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.2.293PubMed5448056History Published online 1 August 1970 Published in print 1 August 1970 Metrics

Effect of Ventricular Injections of Ribonuclease on Learned Discrimination and Avoidance Tasks in the Rat

Behavioral studies relating ribonucleic acid (RNA) to performance dependent on memory have involved humans and lower animals. It has been reasoned that introduction of ribonuclease, an enzyme which breaks down RNA, would modify this RNA structure and the long-term memory which it stores. However, evidence is contradictory regarding its effect on intact tissue and regenerating tissue. Corning and John (1961) from their work on transected conditioned planarians reported that only the regenerating tissue appeared to be affected by the ribonuclease. This contrasts with unpublished observations by E. R. John, B. Wenzel, and R. Tschirigi (personal communication, 1963; cf. Corning & John, 1961) of a decrease in performance on pattern discrimination for food but no decrease in the conditioned avoidance response to visual or auditory cues when a ribonuclease solution had been injected into the lateral ventricle of cats. The purpose of the present study was to assess the effect of such lateral ventricle injections of ribonuclease on avoidance and/or discrimination tasks in the rat. In an effort to replicate the study of John, er al. using rats, parallel procedures were designed. Eight rats were trained to discriminate visual patterns and obtain food by pushing open a door in the pattern and to avoid shock upon the presentation of visual and auditory stimuli. Cannulas were then permanently implanted into the lateral ventricles of the brain and injections of the ribonuclease solution introduced through the cannulas. Analysis indicated that there were no significant differences in number of correct discriminations, number of avoidance failures, or avoidance latencies following ribonuclease injections. The fact that a high concentration of ribonuclease in combination with a volume of solution which approached the maximum for one injection, led to no significant decreases in either a learned pattern discrimination task or avoidance task suggests that such single injections of ribonuclease into the ventricular system do not cause losses in retention in rats within a short time span. Thus, our results do nor replicate those of John, et al., in which the effect was noted within a shorr rime after the injection, precluding the assumption that the ribonuclease interfered only with transmission to newly formed brain tissue. Our results with rats constitute negative evidence for such modification of RNA within intact tissue.