Biomedical subjects

E Gilat

Publications and source records attributed to E Gilat.

At least 19 recordsLinked to original sources

PubMed2006

Seizure duration following sarin exposure affects neuro-inflammatory markers in the rat brain.

The current study was aimed to characterize for the first time the alterations in the characteristic neuro-inflammatory markers triggered by sarin exposure in the rat's brain, and to investigate its dependency on seizure duration. Centrally mediated seizures are a common consequence of exposure to organophosphates (OP) despite conventional treatment with atropine and an oxime. In the present study midazolam, was used to control duration and intensity of seizures. The levels of the pro-inflammatory cytokine peptides IL-1beta, IL-6, TNF-alpha and prostaglandin E2 (PGE2) were monitored at various times after sarin exposure in the hippocampus and cortex of rats treated with midazolam following 5 or 30 min of seizure activity. Biochemical evaluation of brain tissues revealed a significant increase in the level of the pro-inflammatory peptides starting at 2 h and peaking at 2-24 h following sarin. Hippocampal values of IL1-beta increased from 1.2+/-0.1 pg/mg tissue (control), to 2.4+/-0.3 at 2 h (5 min seizure) and to 9.3+/-2.5 at 8h (30 min seizure). PGE2 level in the hippocampus increased up to 24 h following exposure (from 56+/-3 to 175+/-26 and 277+/-28 pg/mg tissue) following 5 and 30 min of seizure activity respectively. Thus, unlike limitation of seizures to 5 min by midazolam, delayed treatment (30 min) resulted in prolonged seizures and pronounced increase in cytokines and PGE2. In addition, a second increase in inflammatory markers was observed 30 days following sarin exposure only in rats treated following 30 min of seizure activity. Histological evaluation of the rat brain, conducted in this study, revealed lack of damage in the hippocampus and piriform cortex with minor lateral ventricles enlargement in few animals following 5 min of sarin-induced seizure activity. In contrast, marked histological damage to the brain was demonstrated following 30 min of seizure activity, consisting severe damage to the hippocampus, piriform cortex and some thalamic nuclei. In summary, a novel characterization of the prolonged central neuro-inflammatory process that accompanies sarin exposure is presented. The timing of the anticonvulsive treatment was shown to be crucial in modulation of the neuro-inflammatory response, and may implicate the consequent long-term brain damage.

Animals↗

PubMed2005

Anticonvulsant treatment of sarin-induced seizures with nasal midazolam: an electrographic, behavioral, and histological study in freely moving rats.

Centrally mediated seizures and convulsions are common consequences of exposure to organophosphates (OPs). These seizures rapidly progress to status epilepticus (SE) and contribute to profound brain injury. Effective management of these seizures is critical for minimization of brain damage. Nasal application of midazolam (1.5 mg/kg) after 5 min of sarin-induced electrographic seizure activity (EGSA) ameliorated EGSA and convulsive behavior (238 +/- 90 s). Identical treatment after 30 min was not sufficient to ameliorate ECoG paradoxical activity and convulsive behavior. Nasal midazolam (1.5 mg/kg), together with scopolamine (1 mg/kg, im) after 5 min of EGSA, exerted a powerful and rapid anticonvulsant effect (53 +/- 10 s). Delaying the same treatment to 30 min of EGSA leads to attenuation of paroxysmal ECoG activity in all cases but total cessation of paroxysmal activity was not observed in most animals tested. Cognitive tests utilizing the Morris Water Maze demonstrated that nasal midazolam alone or together with scopolamine (im), administered after 5 min of convulsions, abolished the effect of sarin on learning. Both these treatments, when given after 30 min of convulsions, only decreased the sarin-induced learning impairments. Whereas rats which were not subject to the anticonvulsant agents did not show any memory for the platform location, both treatments (at 5 min as well as at 30 min) completely abolished the memory deficits. Both treatments equally blocked the impairment of reversal learning when given at 5 min. However, when administered after 30 min, midazolam alone reversed the impairments in reversal learning, while midazolam with scopolamine did not. Rats exposed to sarin and treated with the therapeutic regimen with the exclusion of midazolam exhibited severe brain lesions that encountered the hippocampus, pyriform cortex, and thalamus. Nasal midazolam at 5 min prevented brain damage, while delaying the midazolam treatment to 30 min of EGSA resulted in brain damage. The addition of scopolamine to midazolam did not alter the above observation. In summary, nasal midazolam treatment briefly after initiation of OP-induced seizure leads to cessation of EGSA and prevented brain lesions and behavioral deficiencies in the rat model.

Administration, Intranasal↗

PubMed2002

Nasal midazolam as a novel anticonvulsive treatment against organophosphate-induced seizure activity in the guinea pig.

Seizures and status epilepticus, which may contribute to brain injury, are common consequences of exposure to organophosphorus (OP) cholinesterase inhibitors. Effective management of these seizures is critical. To investigate the efficacy of nasal midazolam as an anticonvulsive treatment for OP exposure, as compared to intramuscular midazolam, guinea pigs were connected to a recording swivel for electrocorticograph (ECoG) monitoring and clinical observation. The experimental paradigm consisted of pyridostigmine pretreatment (0.1 mg/kg i.m.) 20 min prior to sarin exposure (1.2x LD(50,) 56 micro g/kg i.m.). One minute post-exposure, atropine (3 mg/kg i.m.) and TMB-4 (1 mg/kg im) were administered. Within 3-8 min after sarin exposure all animals developed electrographic seizure activity (EGSA), with convulsive behavior. Treatment with midazolam (1 mg/kg i.m.) 10 min after the onset of EGSA abolished EGSA within 389+/-181 s. The same dose was not effective, in most cases, when given 30 min after onset. However, a higher dose (2 mg/kg) was found efficacious after 30 min (949+/-466 s). In contrast, nasal application of midazolam (1 mg/kg) was found most effective, with significant advantages, in amelioration of EGSA and convulsive behavior, when given 10 min (216+/-185 s) or 30 min (308+/-122 s) following the onset of EGSA ( P<0.001). Thus, nasal midazolam could be used as a novel, rapid and convenient route of application against seizure activity induced by nerve agent poisoning.

Administration, Intranasal↗

PubMed2000

Beneficial effects of topical anti-inflammatory drugs against sulfur mustard-induced ocular lesions in rabbits.

Ocular injuries following sulfur mustard (HD) exposure are characterized by an inflammatory response, observed as eyelid swelling, conjunctivitis, corneal oedema and cellular infiltration starting 1-4 h after exposure, depending on dose. These effects heal partially during the first 1-2 weeks after exposure, with the later appearance of neovascularization, recurrent erosions and recurrent oedema of the cornea (delayed response). We have shown previously that topically applied steroid treatment, administered after HD exposure, attenuated the extent of neovascularization, one of the characteristics of delayed ocular pathology in rabbits. The present study was designed to characterize further the initial inflammatory response and to elucidate the role of anti-inflammatory (AI) drugs as a potential therapy. Rabbit eyes were exposed to HD vapour (390 microg l(-1) for 2 min) and were treated with a topical commercial ophthalmic solution of dexamethasone or diclofenac, starting 1 h post-exposure (four times a day). Inflammation was evaluated by clinical observations, biochemical analysis of aqueous humour and by histology. Sulfur mustard exposure initiated typical clinical ocular symptoms within 4-6 h after exposure. Biochemical analysis of aqueous humour showed that protein content and prostaglandin E (PGE) increased significantly at 6 h and were still high 48 h after HD exposure. Light microscopy evaluation revealed severe damage to the cornea, characterized by epithelial denudation, oedema and cellular infiltration (mostly eosinophiles) in the stroma. Both treatments were effective in alleviating the clinical symptoms and in preventing the HD-induced increase in protein and PGE in the anterior chamber, as well as the cellular infiltration, in the corneal stroma. However, the AI treatments had no therapeutic effect on corneal erosions, and a short delay in epithelial regeneration was noted. It is concluded that AI drugs are potential candidates for the treatment of ocular lesions following HD exposure.

Animals↗

PubMed1999

The involvement of the NMDA receptor complex in the protective effect of anticholinergic drugs against soman poisoning.

Organophosphate poisoning is associated with adverse effects on the central nervous system such as seizure/convulsive activity and long term changes in neuronal networks. This study reports on investigations designed to assess the consequences of soman exposure on excitatory amino acids receptors in the rat brain. In addition, the protective effects of caramiphen which acts at these receptors, and scopolamine, which does not, was determined on soman-induced alteration in rat brain functions. Administration of soman (1xLD50) to pyridostigmine pretreated rats produced seizure activity (measured by EEG monitoring) in all animals tested. Estimation of [3H]MK-801 binding to brain membranes from intoxicated rats revealed a marked decrease in Bmax value 24 but not 2 hrs following soman administration. The specific nature of these effects of soman was demonstrated by the findings that [3H]flunitrazepam binding to central benzodiazepine receptors remained unchanged in soman-poisoned rat brain membranes. Both scopolamine and caramiphen, when used prophylactically prevented the lethal effect of soman and completely blocked the development of electrographic seizure activity (EGSA). In contrast, only caramiphen abolished soman-induced modifications in NMDA/ion channel characteristics. Caramiphen displaced [3H]MK-801 bound to the NMDA/ion channel complex, possibly by interacting with the Zn2+ site whereas scopolamine did not. Moreover, caramiphen, but not scopolamine, partially protected mice from NMDA-induced lethality. Thus, it is suggested that an important component of the protective efficacy of caramiphen against organophosphate poisoning might be attributed to its ability to modulate NMDA receptors in addition to its anticholinergic properties.

Animals↗

PubMed1998

Prophylaxis against soman inhalation toxicity in guinea pigs by pretreatment alone with human serum butyrylcholinesterase.

Human butyrylcholinesterase (HuBChE) has previously been shown to protect mice, rats, and monkeys against multiple lethal toxic doses of organophosphorus (OP) anticholinesterases that were challenged by i.v. bolus injections. This study examines the concept of using a cholinesterase scavenger as a prophylactic measure against inhalation toxicity, which is the more realistic simulation of exposure to volatile OPs. HuBChE-treated awake guinea pigs were exposed to controlled concentration of soman vapors ranging from 417 to 430 micrograms/liter, for 45 to 70 s. The correlation between the inhibition of circulating HuBChE and the dose of soman administered by sequential i.v. injections and by respiratory exposure indicated that the fraction of the inhaled dose of soman that reached the blood was 0.29. HuBChE to soman molar ratio of 0.11 was sufficient to prevent the manifestation of toxic signs in guinea pigs following exposure to 2.17x the inhaled LD50 dose of soman (ILD50, 101 micrograms/kg). A slight increase in HuBChE:soman ratio (0.15) produced sign-free animals after two sequential respiratory exposures with a cumulative dose of 4.5x ILD50. Protection was exceptionally high and far superior to the currently used traditional approach that consisted of pretreatment with pyridostigmine and postexposure combined administration of atropine, benactyzine, and an oxime reactivator. Quantitative analysis of the results suggests that in vivo sequestration of soman, and presumably other OPs, by exogenously administered HuBChE, is independent of the species used or the route of challenge entry. This assuring conclusion significantly expands the database of the bioscavenger strategy that now offers a dependable extrapolation from animals to human.

Animals↗

PubMed1998

Angiotensin-converting enzyme inhibition produces electrophysiologic but not antiarrhythmic effects in the intact heart.

Although angiotensin-converting enzyme (ACE) inhibitors are known to influence favorably the structural remodeling of the heart after myocardial infarction, the mechanisms by which ACE inhibitors improve survival are not well understood. The hypothesis that ACE inhibitors may possess antiarrhythmic activity has been studied in various isolated tissue preparations. However, the electrophysiologic effects of ACE inhibitors in the intact heart are not well understood. The effect of the ACE inhibitor enalaprilat on intact heart electrophysiology was studied by using multisite optical action-potential recordings with voltage-sensitive dyes. Action potentials were recorded simultaneously from 128 left ventricular epicardial sites in 15 Langendorff perfused hearts subjected to an endocardial cryoablation procedure, which was used to restrict propagation to a thin viable rim of epicardium. Action-potential duration (APD) was significantly prolonged in 67% of preparations perfused with 5 mg/L enalaprilat. Higher concentration of enalaprilat (50 mg/L) prolonged APD in all preparations tested. This APD-prolonging effect persisted over a broad range of stimulus rates, indicating the absence of reverse use-dependent properties. Enalaprilat did not modify conduction velocity, nor did it affect spatial dispersion of repolarization times. In addition, enalaprilat had no effect on ventricular fibrillation threshold and failed to suppress the initiation of ventricular tachycardia using an anatomically defined reentrant circuit. These findings indicate that in the intact heart, enalaprilat does indeed have electrophysiologic effects that cause APD prolongation, particularly at high drug concentrations. However, this effect was not of sufficient magnitude in the guinea pig to suppress the initiation of ventricular fibrillation or reentrant ventricular tachycardia.

Action Potentials↗

PubMed1990

Phorbol ester enhances synaptic transmission at crustacean neuromuscular junctions.

Effects of phorbol ester (PE) (4 beta-phorbol-12,13-dibutyrate) on transmitter release were studied in the deep extensor neuromuscular system of the prawn, Macrobrachium rosenbergii. Our findings show that PE enhances transmitter release as indicated by an increase in the quantal content. PE had no post-synaptic effects. The increase in release is accompanied by a slight decline in twin pulse facilitation, suggesting a minor increase in Ca2+ entry. The fact that the increase in Ca2+ entry has a minor contribution to the PE effect is supported by the following observations: the duration of facilitation was not affected by PE, and 3,4-diaminopyridine (3,4-DAP), which by itself increased release, did not reduce the effect of PE. The time course of release was measured from synaptic delay histograms, upon which PE had no effect. This finding indicates that protein kinase C (PKC) is probably not involved in the rate limiting step of the process of secretion. The log/log plot of the initial part of the delay histogram is not affected by PE, suggesting a lack of effect on cooperativity of the release process. Increased release by loading the presynaptic terminal with Ca2+ either by pretreatment with Ca2+ ionophore or by frequent stimulation prevented further increase in release by PE. We conclude that the main effect of PE is confined to stages of release that are secondary to the first elevation in presynaptic Ca2+. PKC in this system probably plays a role in long term modulation of release, and it can be activated in processes leading to presynaptic Ca2+ accumulation.

Animals↗

PubMed1990

The role of reduced potassium conductance in generating triggered activity in guinea-pig ventricular muscle.

This study investigates the role of reducing potassium conductance (gK) in generating delayed afterdepolarizations and triggered activity in small preparations of ventricular muscle from guinea-pig hearts. We used agents believed to reduce gK (low or absent K0, tetraethylammonium (TEA), CsCl) and we used ouabain (10(-6) M) to induce delayed afterdepolarizations. Treatment with ouabain only caused subthreshold delayed afterdepolarizations or occasionally non-sustained triggered activity. Exposure to Tyrode's solution with K reduced from 4 to 2 mM or K-free Tyrode's solution, with or without ouabain, caused subthreshold delayed afterdepolarizations and sometimes non-sustained triggered activity. Exposure to Tyrode's solution containing TEA and ouabain caused sustained triggered activity, supporting the hypothesis that accumulation of extracellular K inhibits the development of triggered activity. Presumably, the reduction in gK caused by TEA is not reversed by accumulation of extracellular K so that the delayed afterdepolarizations in the presence of persistently reduced gK are large enough to induce sustained triggered activity. Under extreme conditions, when Cs replaced K and half the NaCl was replaced by TEA, delayed afterdepolarizations occurred in the presence of markedly reduced gK, the result being the rapid development of sustained triggered activity, even at the basic drive rate of 1 Hz. Our results suggest that reduced gK plays an important role in the development of triggered activity.

Animals↗

PubMed1990

The inhibitory chloride channel of the lobster Panulirus penicillatus neuromuscular junction.

1. Single channel activity was recorded from muscle membranes of the lobster Panulirus penicillatus using the patch-clamp technique. 2. Cell-attached, outside-out and inside-out patches were prepared from the deep abdominal extensor muscle. 3. Low amplitude single channel currents were observed in most patches, and were identified as being chloride-currents. 4. The chloride channel was active spontaneously, and tended to desensitize when outside-out patches were exposed to a small jet of glutamate. 5. Amplitude histograms of single channel currents presented a well defined peak of 8 pA at a membrane potential of -160 mV, while open and closed time histograms were fit to single exponential functions with tau open of 3.27 msec and tau closed of 31.58 msec.

Animals↗

PubMed1990

Triggered activity induced by K(+)-free, Na(+)-deficient solution in guinea pig ventricular muscle: the effects of ouabain, lidocaine, and Ca2+ channel blockers.

Triggered activity induced by delayed afterdepolarizations has been suggested as a cellular mechanism for some arrhythmias. The development of triggered activity should be favored by conditions that increase myoplasmic Ca2+ and increase membrane resistance. A solution which could create these conditions was devised. After perfusion with normal Tyrode's solution, 24 trabeculae were exposed to the experimental solution. All preparations developed triggered activity after exposure to the experimental solution, 83% developed delayed afterdepolarizations before the onset of triggered activity, and triggered activity stopped in all trabeculae after reperfusion with normal Tyrode's solution. The interaction of ouabain, lidocaine, and three Ca2+ channel blockers with triggered activity induced by the experimental solution is described. Verapamil inhibited triggered activity but not underlying voltage oscillations, whereas nisoldipine and Mn2+ inhibited both triggered activity and voltage oscillations. Lidocaine did not inhibit afterdepolarizations or triggered activity. Exposure to ouabain for 10 min caused delayed afterdepolarizations but not triggered activity. Our results show that the experimental solution induced triggered activity, which was highly reliable and readily reversible. The high reproducibility of this activity enables the study of interactions of pharmacological agents with this triggered activity. This may contribute to the further understanding of the mechanism underlying some arrhythmias.

Action Potentials↗

PubMed1987

Effects of thyroid hormone on the action potential and membrane currents of guinea pig ventricular myocytes.

We studied the effects of thyroid hormone on the action potential and membrane currents recorded from enzymatically dissociated guinea pig ventricular myocytes, by means of the whole-cell recording technique. Hypothyroidism was associated with an increase in action potential duration, whereas hyperthyroidism was associated with a decrease in duration. These effects are similar to those reported in multicellular preparations. Hypo- and hyperthyroidism were also associated with a decrease and an increase, respectively, in the slope of the action potential plateau. Resting potential and action potential amplitude were unaffected by the alterations in the thyroid state. The voltage-clamp experiments revealed that as compared with euthyroid myocytes, the peak calcium current was bigger in hyperthyroid myocytes and smaller in hypothyroid myocytes. The potassium outward current (at a membrane potential = 50 mV) was of similar amplitude in hypo- and euthyroid myocytes and bigger in hyperthyroid myocytes. Our major conclusion is that thyroid hormones regulate the amplitude of the calcium current and that this effect may be responsible in part for the modulation of myocardial contractility by thyroid hormones.

Action Potentials↗

PubMed1987

Electrophysiological effects of a novel antiarrhythmic drug, EO-122, on guinea pig ventricular muscle and isolated myocytes.

EO-122, a newly developed structural analog of lidocaine, has recently been shown to suppress ventricular arrhythmias in a few clinical studies in patients and in experimental animals. In the present study, we investigated the effects of EO-122 on the electrophysiological properties of guinea pig papillary muscle and ventricular myocytes by means of standard microelectrode and whole-cell recording techniques, respectively, At the concentration range of 10(-7)-10(-4) M (cycle length, 2000 ms), resting potential and action potential duration (APD90) were not altered by the drug. Action potential amplitude and APD50 were reduced (p less than 0.01) by 10(-4) M, and Vmax was reduced (p less than 0.01) by EO-122 greater than or equal to 10(-5) M. The effect of EO-122 on Vmax was use-dependent. At 10(-6) and 10(-5) M (cycle length, 2000 ms), the time constant for onset of block (tau on) was 37.0 +/- 13.2 and 26.0 +/- 3.4 s, respectively. The recovery kinetics from use-dependent block was not monoexponential, and the estimated "time constant" for recovery was 76.5 s. We examined the effects of EO-122, 10(-5) M, on the membrane currents in ventricular myocytes and found that the drug attenuated the slow inward current (Isi). EO-122 reduced peak Isi by 68.6 +/- 5.2% (p less than 0.005), whereas the outward current was unchanged. The present study demonstrates that EO-122 blocks both the fast inward (Na+) and the slow inward (Ca2+) channels, and these effects are probably responsible for the antiarrhythmic effects of the drug.

Action Potentials↗

PubMed1987

Effect of sodium pentobarbital on the transmembrane action potential and the slow inward current of guinea pig ventricular myocytes.

Barbiturates, which are widely used in clinical anesthesia, exert a negative inotropic effect on the myocardium. To investigate the mechanism for the negative inotropism, we studied the effect of sodium pentobarbital (SP) on the action potential and the slow inward current recorded from guinea pig ventricular myocytes. We found that SP at 0.6, 1.0, and 1.6 microM decreased action potential duration at 50% repolarization by 17 +/- 6, 25 +/- 11, and 29 +/- 8%, respectively (p less than 0.05, n = 4). At the concentration range of 0.6-1.6 microM, resting potential and action potential amplitude were unaffected. Voltage-clamp studies in ventricular myocytes demonstrated that SP at 0.6, 1.0, and 1.6 microM reduced the peak slow inward current by 30 +/- 4, 36 +/- 14, and 67 +/- 5%, respectively (p less than 0.005, n = 4). In conclusion, SP, a frequently used anesthetic, decreases the slow inward current in guinea pig ventricular myocytes at clinically relevant concentrations.

Action Potentials↗

PubMed1986

The giant fiber and pectoral fin adductor motoneuron system in the hatchetfish.

In the medulla of the hatchetfish each Mauthner fiber forms chemical synapses on a number of large myelinated axons termed giant fibers. The giant fibers form rectifying electrotonic synapses on pectoral fin adductor motoneurons, and in this fish bilateral pectoral fin adduction is an important component of the Mauthner fiber-mediated escape reflex. The branching patterns of giant fibers were determined by intracellular injection of Lucifer yellow. Dye coupling to the motoneuron somata was not observed, although a low level of transfer might have been obscured by autofluorescence. Individual giant fibers terminate primarily on pectoral fin motoneurons contralateral to their cell bodies, but may also send a branch back across the midline to ipsilateral motoneurons. The rostral process of each giant fiber ends on neurons presumably associated with cranial musculature. The number and geometry of the pectoral fin motoneurons were determined using Golgi and Nissl staining and serial reconstruction methods.

Animals↗

PubMed1985

Ultrastructure of the rectifying electrotonic synapses between giant fibres and pectoral fin adductor motor neurons in the hatchetfish.

Synapses formed by giant fibres on pectoral fin adductor motor neurons were identified by horseradish peroxidase (HRP) injection. The synapses were distributed in clusters on the somata and proximal dendrites of the motor neurons. All of the labelled synapses contained synaptic vesicles and often had clearly defined active zones characteristic of chemical synapses. Some synapses also showed gap junctions with the motor neuron soma, often directly adjacent to an active zone. The gap junctions were asymmetrical, with a thick layer of electron dense material on the postsynaptic side. Previous electrophysiological data indicate that giant fibre inputs to motor neurons are purely electrotonic and that these electrical synapses rectify.

Action Potentials↗

PubMed1985

Delayed afterdepolarizations and triggered activity in ventricular muscle from rats with streptozotocin-induced diabetes.

Previous studies have shown that myocardium of the diabetic rat has impaired myoplasmic calcium metabolism. Delayed afterdepolarizations and triggered activity are potentiated by conditions believed to increase intracellular calcium concentration therefore, we performed this study to investigate the possibility that myocardium of the diabetic rat is more susceptible than normal tissue to develop afterdepolarizations and triggered activity. We used standard microelectrode techniques to record the electrical activity of papillary muscles from hearts of control rats and rats made diabetic with streptozotocin. We compared the response of control and diabetic preparations to conditions presumed to create progressively more severe degrees of myoplasmic calcium loading, viz. perfusion with solutions containing ouabain (5 X 10(-5) M) and increasing concentrations of calcium (2.4, 4.8, 7.2, and 9.6 mM). Our results showed the following. Ventricular muscle from diabetic rats was more prone than normal myocardium to develop delayed afterdepolarizations and triggered activity under conditions believed to cause myoplasmic calcium overload. The external calcium concentration correlated with the incidence but not the magnitude or coupling interval of the delayed afterdepolarizations in fibers of diabetic rats. The action potentials in fibers of diabetic rats decreased markedly in duration after exposure to ouabain, whereas normal action potentials were not affected significantly; as external calcium was increased with ouabain still present, the action potential duration in diabetic fibers decreased slightly more, whereas the action potential duration in normal fibers did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Single unit activity in the auditory cortex and the medial geniculate body of the rhesus monkey: behavioral modulation.

Three Rhesus monkeys were trained to respond to a given auditory signal, the nature of which could be predicted from a preceding visual stimulus. The activity of 28 units in the auditory cortex and 53 units in the Medial Geniculate Body (MGB) of the monkey was recorded during task-performance conditions, as well as in the non-performance conditions. The activity of about one third of the cortical and MGB units was independent of the behaving status of the animal. In other units, the response to an auditory signal delivered during task-performance conditions as compared to the response recorded during non-performance periods was either augmented or attenuated. Furthermore, it was found that the spontaneous activity of most of the MGB and cortical units was continuously affected by either an excitatory or an inhibitory input, activated by the behavioral state. The temporal characteristics of behavioral modulation were studied by computing an amplification curve for all MGB units characterized by a 'through stimulus excitation' type of response. Analysis of these curves together with the behavioral effect on the spontaneous activity allows the suggestion of possible mechanisms by which the behavioral state of the monkey modulates the activity in the thalamocortical segment of the auditory system.

Animals↗