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PubMed1990

Respiratory and cardiovascular effects of tetrodotoxin in urethane-anesthetized guinea pigs.

Cardiorespiratory effects of tetrodotoxin (TTX) (15 micrograms/kg, i.p.) were investigated in urethane-anesthetized guinea pigs acutely instrumented for the recording of medullary respiratory-related units (RRUs), diaphragm electromyogram (DEMG), electrocorticogram (ECoG), electrocardiogram (ECG), blood pressure (BP), endtidal CO2, and arterial O2 and CO2. Respiratory system responses showed a hyperventilatory profile during the initial stage of intoxication. This was followed by an abrupt onset of a progressive decrease in the respiratory frequency, and a respiratory rate depression-related respiratory failure. The average time to TTX-induced respiratory arrest and death was 10.3 +/- 4.2 min. Concurrently recorded inspiratory and expiratory RRU activities indicated that respiration invariably failed in an end-expiratory position as manifested by a sustained period of expiratory RRU discharge. The progressive rate depression prior to respiratory arrest was temporally correlated only to a concomitantly augmenting expiratory RRU discharge duration. Inspiratory RRU discharge duration, on the other hand, did not display any significant change throughout the course of intoxication. The asymmetry in RRU response patterns indicates either an expiratory network component's particular sensitivity to perturbation by TTX or a dissociative trend in some bulbar respiratory rhythmogenic mechanisms. Peripheral cardiorespiratory changes were also quite profound. These included a gradual and steadfast decline in BP, a steadily decreasing amplitude in DEMG oscillations, and a state of progressive hypercapnia and hypoxemia. Changes in heart rate and ECG waveform attributes prior to respiratory arrest were not appreciable. In conclusion, in addition to a variety of TTX-induced peripheral cardiorespiratory effects, findings from this study have revealed a central respiratory system component that appears to show an unusual sensitivity to perturbation by TTX. The significance of this unique phenomenon as it relates to the nature and extent of TTX-induced central respiratory depression is discussed.

Anesthesia, General↗
PubMed1992

Amygdala stimulation produces two types of hippocampal afterdischarges in the urethane-anesthetized rat.

How seizures spread during epileptiform events has been the subject of intensive investigation over the years. The present study explored the relationship between the amygdala and the hippocampus during afterdischarges. Stimulating electrodes were placed in the amygdala and CA3 regions on the left side in urethane-anesthetized rats. Recording microelectrodes were placed in the dentate gyrus on the left and the CA1 cell layer on the right. Afterdischarges were elicited by stimulus trains between 10 and 50 Hz to the amygdala. Most of the afterdischarges consisted of broad positive potentials in dentate gyrus and no shift of the DC potential. When the stimulus trains were repeated, the afterdischarge evolved, first by spreading to the contralateral side and then by the appearance of maximal dentate activation. The onset of maximal dentate activation was indicated by the appearance of bursts of large amplitude population spikes and a negative shift of the DC potential. These data demonstrate that two types of afterdischarges can be produced in the hippocampus of the anesthetized rat after amygdala stimulation. The observations support the hypothesis that maximal dentate activation represents synchronized reverberatory activity throughout the hippocampal-parahippocampal circuit and indicate that amygdala stimulation can access this circuit in the anesthetized animal.

Action Potentials↗
PubMed1993

NMDA receptors have a dominant role in population spike-paired pulse facilitation in the dentate gyrus of urethane-anesthetized rats.

Paired-pulse facilitation was studied at the perforant path-granule cell synapses in the dentate gyrus of urethane-anesthetized rats. Extracellular field potentials comprising excitatory postsynaptic potentials (EPSPs) and population spikes (PSs) were used to compare facilitation of both responses at interpulse intervals between 10 and 1000 ms. In this model system EPSPs, produced at stimulus intensities well below the PS threshold, exhibited paired-pulse facilitation (PPF) at intervals less than 40 ms. Between 40 and 100 ms both responses were of equal size and from 200 to 1000 ms the second response exhibited paired-pulse depression (PPD). With higher stimulus intensities, PSs exhibited early (10-30 ms) and late (400-1000 ms) PPD and intermediate interval (40-200 ms) PPF. The enhanced PS amplitude during facilitation was accompanied by a modest decrease in EPSP slope and increase in PS latencies to onset and to peak. If PS amplitude was increased to the same extent by simply increasing stimulus intensity, an increase in EPSP slope and decrease in PS latencies to onset and peak were observed. Current source-density analysis revealed that the current sink generated by synaptic activation of granule cell dendrites was indistinguishable between control and facilitated responses up to the onset of the PS. However, the facilitated response exhibited a marked increase in the duration and amplitude of current flowing into the dendrites during the late phase of the EPSP. PPF of the PS was attenuated or blocked by the administration of the known NMDA receptor-ion channel blockers, MK-801, dextromethorphan and ketamine. The depressant effects of these pharmacological agents on facilitation shared the same time course as facilitation itself, peaking at 60 ms and lasting approximately 200 ms. These data suggest that facilitation in this situation is due to postsynaptic rather than presynaptic modulations, and is based upon an increase in the NMDA-mediated component of the evoked response. No increase in transmitter release, per se, could be demonstrated.

Analysis of Variance↗
PubMed1993

Induction of c-fos immunoreactivity in tyrosine hydroxylase and phenylethanolamine-N-methyltransferase immunoreactive neurons of the medulla oblongata of the rat after phosphate-buffered saline load in the urethane-anaesthetized rat.

We have studied the induction of c-fos immunoreactivity (c-fos IR) in catecholaminergic and vasopressinergic immunoreactive neurons after repeated phosphate-buffered saline (PBS) loading or after repeated elicitation of the baroreceptor reflex via repeated infusion of the vasoconstrictor agent L-phenylephrine. About 75% and 30%, respectively, of the tyrosine-hydroxylase immunoreactive (IR) cell bodies of the ventral noradrenaline (NA) A1/adrenaline (A) C1 and dorsal NA A2/A C2 areas and 60% and 30%, respectively, of the phenylethanolamine N-methyltransferase IR nerve cells of the adrenaline C1 and C2 areas and 25% of the vasopressin (VP) IR neurons of the supraoptic (SO) nucleus developed nuclear c-fos IR after repeated PBS loading. This phenomenon remained unaltered by the repeated elicitation of the baroreceptor reflex. These results suggest that the activation of volume receptors promotes homeostatic responses via activation of early genes in subsets of central medullary noradrenaline and adrenaline neurons and SO VP neurons of the urethane-anaesthetized rat.

Amino Acid Sequence↗
PubMed1993

Hippocampal EEG responses induced by carbachol and atropine infusions into the septum and the hippocampus in the urethane-anaesthetized rat.

Infusion of 1 microgram of carbachol, a potent cholinergic agonist, into the lateral septum of the urethane-anaesthetized rat systematically caused the induction of clear-cut hippocampal theta (theta). However, infusion of an equivalent amount of the drug into the hippocampus, close to the recording electrode, failed to induce theta in 50% of the animals and produced a mixture of theta waves and desynchronized activity, resulting in atypical EEG patterns, in the remaining subjects. Both carbachol EEG effects were blocked by intraseptal infusion of the antimuscarinic agent, atropine. Our data demonstrate that muscarinic receptors in the septum are predominant sites for cholinergic agonist-antagonist action capable of generating or suppressing hippocampal theta in the rat. They also indicate that intraseptal cholinergic mechanisms play an important role in the initiation and generation of this rhythm.

Anesthesia↗
PubMed1994

Cardiovascular changes elicited by microinjection of glycine or GABA into the spinal intermediolateral nucleus in urethane-anesthetized rats.

Sympathetic preganglionic neurons (SPNs), located in the intermediolateral cell column (IML) of the thoracolumbar spinal cord, contribute to the maintenance of arterial pressure (AP) and heart rate (HR) within normal limits under different physiological conditions. The purpose of this study was to examine the effects of microinjecting the putative inhibitory transmitters glycine (GLY) or gamma-amino-butyric acid (GABA) into functionally identified cardioacceleratory and vasoconstrictor IML sites at T1-T3. Rats were anesthetized (1.4 g/kg urethane i.p.), paralysed with decamethonium bromide (3.3 mg/kg i.v.) and artificially ventilated. Glutamate (GLU) microinjection (10-20 nl, pH = 7.4, 0.15 M in phosphate-buffered saline (PBS)) was used to identify 29 vasoconstrictor sites, of which 23 were also cardioacceleratory, in the right side of the T2 segment. GLY microinjection (10-20 nl, pH = 7.4, 0.5 M in PBS) into these sites resulted in significant decreases in both AP (n = 18) and HR (n = 14). The AP and HR responses to GLY were brief in duration and were attenuated by the specific GLY antagonist strychnine (STR). Microinjection of GABA (10-20 nl, pH = 7.4, 0.15-0.84 M in PBS, n = 6) and its agonist muscimol (10-20 nl, pH = 7.4, 0.9 mM in PBS, n = 6) into GLU-identified sites in the IML caused no changes in AP or HR. However, after the application of either GABA or muscimol, the changes in AP or HR elicited by GLU were eliminated, suggesting that GABA and muscimol decrease the excitability of SPNs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Pentylenetetrazol elicits epileptiform activity in the dentate gyrus of the urethane anesthetized rat by activation of the entorhinal cortex.

Pentylenetetrazol is a chemical convulsant, often used to generate experimental seizures, that is thought to act as a GABA antagonist. In the urethane anesthetized rat, pentylenetetrazol produces a characteristic epileptiform discharge in the dentate gyrus. The hypothesis that this discharge is generated by activity in the entorhinal cortex was examined in this study. Recording electrodes were placed in the dentate gyrus bilaterally and neuronal activity was recorded after administration of pentylenetetrazol. A laminar analysis of the convulsant-induced activity was compared to responses evoked by angular bundle stimulation (n = 6). Both convulsant-induced and evoked activity were negative-going in the molecular layer of the dentate gyrus. In other animals tetrodotoxin (TTX) was injected into the right entorhinal cortex before the onset of epileptiform activity (n = 5). The TTX prevented epileptiform activity in the right dentate gyrus. Injection of TTX after the onset of epileptiform activity caused the epileptiform activity to cease on the side of injection (n = 5). These experiments support the hypothesis that pentylenetetrazol specifically activates the entorhinal cortex to produce the epileptiform activity recorded in the dentate gyrus. This selective activation suggests that the mechanism of action of pentylenetetrazol, as a convulsant, is not simply as an antagonist of GABA receptors.

Anesthesia↗
PubMed1994

Injections of excitatory amino acid antagonists into the median raphe nucleus produce hippocampal theta rhythm in the urethane-anesthetized rat.

The median raphe nucleus (MR) exerts a pronounced desynchronizing influence on the hippocampal EEG. MR stimulation disrupts theta, while MR lesions produce constant uninterrupted theta. The MR receives pronounced excitatory amino acid (EAA)-containing afferents that have been implicated in several MR-mediated behaviors. The present study examined the effects on the hippocampal EEG of MR injections of the following EAA antagonists in the urethane-anesthetized rat: 2-amino-7-phosphonoheptanoate (AP-7), dizocilpine maleate (MK-801), and gamma-glutamyl-aminomethylsulfonic acid (GAMS). MR injections of the competitive (AP-7) and non-competitive (MK-801) N-methyl-D-aspartic acid (NMDA) receptor antagonists produced theta at short latencies (2.86 min; 4.02 min, respectively) and for long durations (116.1 min; 66.8 min, respectively). It was further shown that the theta-eliciting effects of AP-7 injections could be reliably and temporarily reversed with MR injections of NMDA. MR injections of the kainate/quisqualate receptor antagonist (GAMS) also produced theta at relatively short latencies (6.5 min) and for long durations (60.5 min) indicating that EAA effects on the MR are not NMDA receptor specific. Injections of each of the foregoing EAA antagonists into regions of the brainstem adjacent to the MR including the dorsal raphe nucleus and the medullary or pontine reticular formation generated theta at very long latencies or were without effect. The present findings indicate EAA afferents to the MR normally exert an excitatory influence on the MR in its desynchronization of the hippocampal EEG, whereas the removal of EAA inputs to MR produces the opposite: a reduction of MR activity and hence the elicitation of theta.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1994

Interactions between glutamatergic and monoaminergic systems controlling the micturition reflex in the urethane-anesthetized rat.

The effects of MK-801 (0.001-3 mg/kg i.v.), a non-competitive NMDA glutamate receptor antagonist, on the micturition reflex were examined during continuous saline infusion (0.21 ml/min) cystometrograms (CMGs) in urethane-anesthetized (1.2 g/kg s.c.) rats pretreated with either reserpine (5 mg/kg i.p.), p-chlorophenylalanine (p-CPA; 150 mg/kg i.p., twice a day, 3 consecutive days), L-DOPA (200 mg/kg i.p. + carbidopa 100 mg/kg i.p.) or apomorphine (10 mg/kg i.v.). Pretreatment with reserpine 8-12 h prior to the CMG recording, antagonized the inhibitory effect of MK-801 on the amplitude of micturition contractions while pretreatment with vehicle had no effect. However, pretreatment with the same dose of reserpine 18-22 h prior to the experiment failed to antagonize the inhibitory effect of MK-801. Both reserpine pretreatments enhanced the amplitude of reflex bladder contractions. Pretreatment with p-CPA did not alter bladder activity or the inhibitory effect of MK-801 on amplitude of micturition contractions. When administered 15 min prior to the MK-801, L-DOPA or apomorphine reduced by 70% or 63%, respectively, the maximal inhibitory effect of MK-801 on the amplitude of reflex bladder contractions. These data suggest that there is an interaction between glutamatergic and monoaminergic mechanisms in the regulation of micturition reflex. Since reserpine which reduces both catecholamine and serotonin levels in the nervous system altered the depressant effect of MK-801 on bladder activity, but p-CPA, an agent which depletes serotonin stores, did not, it is concluded that catecholaminergic pathways are involved in this interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1995

Difference in LTP at basal and apical dendrites of CA1 pyramidal neurons in urethane-anesthetized rats.

In urethane-anesthetized rats, excitatory currents in hippocampal CA1 area following local stimulation were analyzed using the current source density technique. Systematic variation of stimulus depth revealed two dominant patterns of activation: basal versus apical dendritic excitation. The basal dendritic excitation (sink) was maximal after stimulation of stratum oriens; its onset latency was consistent with a monosynaptic excitation, and a late (presumed di- and polysynaptic) sink at the apical dendrites was observed. The apical dendritic excitation (sink) was maximal after stimulation of stratum radiatum; the early latency, presumed monosynaptic excitation was followed by a late, weak basal dendritic sink. Theta-frequency primed bursts of either high (400 microA) or low intensity (40-70 microA; 2 x threshold intensity) was delivered to either stratum oriens or radiatum, and long-term potentiation (LTP) was assessed. LTP was observed in both positive and negative components of the dipole field, as well as the (active) sink and (passive) source. Tetanus of stratum oriens resulted in a significant (P < 0.05) potentiation of the monosynaptic basal sink (at 2 ms from onset) following either high (135 + 11%, means +/- S.E.M., n = 7) or low intensity tetanus (178 +/- 21%, n = 7). Tetanus of stratum radiatum resulted in significant potentiation of the rise of the apical sink only for a high (173 +/- 51%, n = 6), but not for a low intensity tetanus (106 +/- 28%, n = 6). Significant LTP of the late apical sink was found following a high intensity tetanus of stratum oriens (155 +/- 15%, n = 7), but no significant change of the late basal sink was found following tetanization of stratum radiatum (118 +/- 20%, n = 6). UP of either the apical and basal sinks was blocked by intraventricular infusion of +/- 2-amino-5-phosphonovalerate, an N-methyl-D-aspartate antagonist. Thus, UP has a lower threshold at the basal than apical synapses of CA1 cells.

2-Amino-5-phosphonovalerate↗
PubMed1979

Hippocampal theta in rats under urethane: generators and phase relations.

Recordings were made from the directly visualized dorsal hippocampus of urethane-anesthetized rats with silver ball and tungsten microelectrodes. Theta of about 5 c/sec was elicited by reticular stimulation and was located in two broad strata in and subjacent to CA1. A superficial generator yielded 200-250 microV theta from the alveus, stratum oriens and stratum pyramidale; a null-theta and phase-reversal point was located in stratum radiatum; a deep generator yielded 300-500 microV theta in stratum lacunosum-moleculare of the hippocampus and distal stratum moleculare of the dentate gyrus, with maximum amplitude near the fissure. No theta was found in CA3. Cross-correlation analyses between generators yielded coefficients on the order of -0.80 while within a generator--especially the deep one--coefficients could reach +0.95. Phase analyses showed the two generators were about 180 degrees out of phase, with the deep generator leading. Septotemporal movement along the upper generator yielded no phase shifts; similar movement along the deep generator showed slight lead ing in septal portions. Subiculofimbrial movement in both generators showed a complex pattern of phase shifts: generally, subicular sites led fimbrial sites, but an inversion of 10 degrees-20 degrees occurred in the millimeter anterior to the center of the hippocampus. Anatomical, phase and other datal led to consideration of a possible retrohippocampal role in supplementing the well-known pacemaker in the medial septum.

Anesthesia, General↗
PubMed1988

Spontaneous EEG spikes in the normal hippocampus. V. Effects of ether, urethane, pentobarbital, atropine, diazepam and bicuculline.

Spontaneous EEG spikes (SPKs) were recorded from the CA1 region of the dorsal hippocampus in normal rats during behavioral states not accompanied by rhythmical slow activity (RSA) such as awake immobility and slow wave sleep. In the present study we examined the effects of various systemically administered drugs on hippocampal SPK activity. Three general anesthetics (ether, urethane and pentobarbital) all reduced SPK activity. At anesthetic doses both ether and pentobarbital completely abolished SPKs. This SPK abolition during anesthesia seemed qualitatively different from RSA-related SPK suppression in undrugged animals in that unlike the latter case RSA generation was not the cause of SPK abolition in the former case. Atropine (50-100 mg/kg, i.p.) did not change greatly SPK activity or its behavioral correlation. Diazepam (5-10 mg/kg, i.p.) increased amplitude and decreased frequency of hippocampal fast EEG activity, and reduced SPK activity. These effects may be based on the known action of diazepam to enhance GABA-mediated postsynaptic inhibition. At subepileptic doses (1-6 mg/kg, i.p.) the GABA antagonist bicuculline enhanced dramatically SPK-related activities. Particularly, SPK-concurrent population burst discharges in the pyramidal cell layer were greatly increased in amplitude and complexity after bicuculline. These results suggest that the SPK generation mechanism in the hippocampus is sensitive to the level of GABA-mediated inhibition.

Anesthetics↗
PubMed1985

Comparison of the effects of substance P and substance K on blood pressure, salivation and urinary bladder motility in urethane-anaesthetized rats.

The effects of substance P and substance K on blood pressure, salivation and urinary bladder motility were investigated in urethane-anaesthetized rats. On intravenous administration, both peptides produced dose-related reductions in blood pressure, substance P being 25-30 times more potent than substance K. Substance P induced a dose-dependent increase of salivation, while substance K was half as active and induced only 40% of the maximum effect of substance P. The two tachykinins induced contractions of the urinary bladder, substance K being about twice as effective as substance P. Substance K was more effective than substance P in activating micturition. These findings provide further evidence that multiple receptor types are involved in mediating the effects of tachykinins in peripheral organs.

Anesthesia↗
PubMed1987

Effects of diethyl ether, halothane, ketamine and urethane on sympathetic activity in the rat.

The present paper describes the effects of different general anaesthetics on plasma catecholamine (CA) concentrations taken as biochemical index of peripheral sympathetic activity. In chronically catheterized rats, diethyl ether, ketamine and urethane increased plasma adrenaline (A) and noradrenaline (NA) concentrations, indicating that these drugs stimulate both neurosympathetic and adrenomedullary functions. These effects appear to be centrally mediated, since ganglionic blockade or spinal transection completely counteracted the diethyl ether- and ketamine-induced increases in plasma CA levels. Halothane induced a transient decrease in circulating A and an increase in NA. These results support the concept that general anaesthetics may have different effects on sympathetic function. Arterial blood pressure and heart rate were also measured to look for possible correlations with peripheral sympathetic activity. The enhanced release of peripheral CAs seemed to be the determining factor for increasing blood pressure and heart rate with ketamine only. In the other instances the activation of the peripheral sympathetic system appeared to maintain homeostasis by counterbalancing the various depressive effects of anaesthetics on the cardiovascular system.

Anesthetics↗
PubMed1989

Modification of evoked hippocampal dentate inhibition by diazepam and three antagonists in urethane-anesthetized rats.

Urethane-anesthetized rats with perforant pathway stimulating electrodes and recording electrodes placed in the hippocampal dentate gyrus were exposed to increasing doses of either the benzodiazepine agonist diazepam or an antagonist (PK-11195, CGS-8216, and RO15-1788). Analysis of the monosynaptic evoked field potentials indicated that none of the four compounds altered the threshold for eliciting the excitatory postsynaptic potential (EPSP). Reductions in field population spike (PS) amplitudes were seen after exposure to RO15-1788, CGS-8216, and diazepam, but not PK-11195. Using a paired-pulse paradigm, diazepam significantly increased early gamma-aminobutyric acid (GA-BAA)-mediated recurrent inhibition. The antagonist RO15-1788, but not CGS-8216 or PK-11195, also significantly increased early GABAA-mediated inhibition. The increase in GABAA-mediated inhibition after diazepam was reversed by the subsequent administration of the central antagonists RO15-1788 or CGS-8216, but not the peripheral antagonist PK-11195. Pretreatment with CGS-8216 or RO15-1788 prevented diazepam-induced inhibition. These data support the important modulatory role of the central benzodiazepine receptor in early GABAA-mediated inhibition at this synapse. They also suggest that basal granule cell excitability is not importantly modulated by this benzodiazepine receptor.

Anesthesia↗
PubMed1985

The use of urethane sponge matrix to assess in vivo recovery of murine cellular immunity following syngeneic bone marrow transplantation.

A unique method for assessing the in vivo recovery of cellular immunity following sublethal irradiation and syngeneic bone marrow transplantation of CBA/J mice is described. This method employs the serial surgical implantation of a urethane sponge matrix followed by impregnation of the sponge matrix with alloantigen. Sponge matrices were harvested from each mouse subject at 2 weeks, 4 weeks, and 8 weeks post transplant with and without treatment with interleukin-2. Recovery of cellular immunity was assessed as a function of cytotoxic T lymphocyte activity via cell-mediated lympholysis using chromium labeled targets. Repetitive procedures of implantation and removal of the matrices from the same animal were surgically feasible and were exceptionally well tolerated by the animals with insignificant morbidity thereby permitting continuous monitoring of immunologic recovery. Although the results of treatment with interleukin-2 were inconclusive, this method provides a sensitive, technically manageable means by which to assess an antigenic response in vivo at predetermined time intervals utilizing the same mouse subject. The method additionally affords the potential of being applicable to the in vivo assessment and manipulation of other aspects of the immune response.

Animals↗
PubMed1993

Micronuclei in adult and foetal mice exposed in vivo to heliotrine, urethane, monocrotaline and benzidine.

The level of clastogenic damage in mice following in vivo adult and transplacental exposure to benzidine, heliotrine, monocrotaline and urethane was compared using the micronucleus (MN) assays of polychromatic erythrocytes (PCE) found in mouse adult bone marrow and foetal liver. Saline was used as a negative control. Swiss-albino mice (gestation 17-19 days) were given a single acute intraperitoneal injection. Animals sacrificed 21 h after 0.75 LD50 of each chemical had significantly increased frequencies of micronucleated PCE in adult and foetal tissues (p < 0.05). Heliotrine resulted in the largest increases in mean value of micronucleated PCE, of 5.4% in adult bone marrow and 6.9% in foetal liver compared to control values of 0.7% and 0.9% for adult and foetal tissue respectively (p < 0.005). The induction of MN was significantly higher in foetal than adult cells for 0.75 LD50 monocrotaline and benzidine after 21 h (p < 0.0005), and for one LD50 heliotrine at 12, 24 and 30 h after injection in a time-response study (p < 0.02). Induction of MN following LD50 heliotrine showed peak MN expression in PCE at 18 h after injection for adult bone marrow (2.6%) and at 24 h for foetal liver (7.9%). The majority of micronucleated PCE in adult and foetal tissue contained only one MN (mean 74% in mice treated with chemicals and 91% in untreated mice). This study demonstrated the sensitivity of the transplacental MN assay for detecting clastogenic damage in mice induced by chemicals and their metabolites. The importance of monitoring indicators of toxicity was highlighted by changes in erythrocyte population composition and the presence of basophilic stippling following exposure to LD50 heliotrine.

Animals↗
PubMed1986

The effects of arginine-8 vasopressin on the cerebral cortex of rats anaesthetised with urethane.

The effects of arginine-8 vasopressin (AVP) on the spontaneous electrical activity of the cerebral cortex were investigated in rats anaesthetised with urethane. Direct application of a relatively large concentration of AVP (0.5-2.0 mU AVP/microliter; 1.25-5.00 ng AVP/microliter) to the pial surface of a small area of the parietal cortex produced a complete cessation of spontaneous neural activity, which was often preceded by a short-lasting increase in frequency of discharge. There was also a decline in the number of large waves in the local electrocorticogram. These changes occurred after 1-4 min. A slow recovery began 10-30 min later, but was sometimes still incomplete after more than an hour. Only the first application of AVP produced the local effects described above. A second application, 2 hr later, was without effect. Direct application to a small area of one hemisphere did not alter the electrical activity of the contralateral cortex. Smaller concentrations of AVP (0.005-0.200 mU AVP/microliter; 12.5 pg-0.5 ng AVP/microliter) were variable in their actions. Occasionally, no effect at all was seen, while sometimes the cells stopped firing completely. However, the most usual consequence was a reduction in discharge frequency, the magnitude of which appeared to be related to the concentration of AVP applied. A second application of a small concentration of AVP usually failed to reduce the rate of spontaneous discharge.

Animals↗