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M E Corcoran

Publications and source records attributed to M E Corcoran.

At least 55 records · Page 3Linked to original sources
PubMed1988

Kindling in the deep prepyriform cortex of the rat.

Rats were electrically kindled in deep prepyriform cortex (DPC) and in immediately surrounding areas, pyriform cortex, and the basolateral amygdala in an effort to identify an area of the basal forebrain crucially involved in epileptogenesis and the kindling of seizures. Picomolar quantities of carbachol were also microinjected into DPC. All of these areas kindled at equivalent rates. Injection of picomolar quantities of carbachol failed to evoke epileptiform spiking, but injection of nanomolar quantities of carbachol usually evoked epileptiform spiking. Bilateral radiofrequency lesions of the DPC did not affect the rate of electrical kindling of the basolateral amygdala. We conclude that the DPC kindles readily at a rate that is similar to that of surrounding basal forebrain tissue and that the integrity of the DPC is not necessary for basolateral amygdaloid kindling.

Amygdala↗
PubMed1988

Characteristics of accelerated kindling after depletion of noradrenaline in adult rats.

The characteristics and pattern of the acceleration of kindling produced by 6-hydroxydopamine-induced depletion of noradrenaline (NA) were investigated in adult rats receiving electrical stimulation of the amygdala once daily. NA-depleted rats developed generalized seizures very rapidly by spending significantly less time than controls in the early stages of nonconvulsive or partial seizures, and they required significantly less cumulative total time in afterdischarge than controls to develop generalized seizures. The results suggest that attempts to identify noradrenergic correlates of kindling should be directed to the early stages of seizure development.

Animals↗
PubMed1987

Monoaminergic correlates of kindling.

High-performance liquid chromatography with electrochemical detection was used to measure the regional concentrations of monoamines and metabolites in the brains of rats killed 2 or 4 weeks after kindling of generalized seizures with amygdaloid stimulation. Each kindled rat was compared to a yoked control that received brief trains of non-convulsive low-frequency stimulation of the amygdala. Two weeks after kindling we found a significant depletion of noradrenaline (NA) in the ipsilateral frontal cortex, a significant depletion of serotonin (5-HT) in the stimulated amygdala and contralateral hypothalamus, and no significant changes in concentration of dopamine (DA). Four weeks after kindling we found significant depletions of NA in the stimulated amygdala and ipsilateral hypothalamus, a significant depletion of 5-HT in the ipsilateral hippocampus, and no significant changes in DA. These findings generally fail to replicate previous reports of monoaminergic correlates of kindling. Furthermore, the alterations in monoamines produced by kindling do not fall into a simple and readily interpretable pattern.

Animals↗
PubMed1987

Antagonism of central but not peripheral cholinergic receptors retards amygdala kindling in rats.

The effects of antagonism of muscarinic cholinergic receptors on the development of seizures produced by electrical stimulation of the amygdala (kindling) were assessed in three experiments. Rats pretreated with the muscarinic antagonist scopolamine developed seizures more slowly than did untreated rats. Whereas scopolamine retarded the development of seizures in a dose-dependent manner, it did not affect the intensity or duration of seizures when administered to kindled control rats. Pretreatment with methylscopolamine, a quaternary derivative of scopolamine that does not readily cross the blood-brain barrier, did not affect the rate of development of seizures, nor did it affect established seizures. Thus the prophylactic effects of scopolamine are produced in the central nervous system and not in the periphery. The results from these experiments are consistent with the idea that central cholinergic or cholinoceptive neurons are critically involved in amygdala kindling.

Amygdala↗
PubMed1986

Relations between amygdaloid and anterior neocortical kindling.

Primary kindling of generalized seizures with amygdaloid stimulation facilitated the subsequent kindling of generalized seizures with neocortical stimulation. Similarly, initial kindling of generalized seizures with anterior neocortical stimulation facilitated the kindling of generalized amygdaloid seizures. Unexpectedly, there were striking differences in the reliability with which seizures could be triggered by amygdaloid and neocortical stimulation. The results support the idea that there is a single mechanism that is responsible for seizure generalization.

Amygdala↗
PubMed1986

Failure to kindle seizures after repeated intracerebral administration of arginine vasopressin.

In an attempt to kindle seizures with arginine-vasopressin (AVP), we injected AVP into the amygdala or hippocampus of rats. Although behavioral and electrographic alterations were sometimes observed, seizures failed to develop, even in rats that had previously been kindled with electrical stimulation. This and previous failures to kindle seizures by intraventricular injections of AVP call into question the possibility of AVP kindling.

Amygdala↗
PubMed1985

Epileptiform effects of met-enkephalin, beta-endorphin and morphine: kindling of generalized seizures and potentiation of epileptiform effects by handling.

Repeated spaced injection of small amounts of beta-endorphin or Met-enkephalin into the hippocampus or posterior amygdala of the rat led to the development of kindled generalized convulsions. Similar injection of morphine into the hippocampus or anterior amygdala resulted in epileptiform spiking followed by tolerance. The epileptiform spiking and convulsive behavior varied in a dose-related manner. Naloxone blocked or greatly attenuated the electrographic seizure and convulsive behavior. Prior kindling with beta-endorphin or Met-enkephalin significantly facilitated electrical kindling of the amygdala. Handling or conspecific threat potentiated the epileptiform spiking and convulsive behavior in some cases. The results indicate that the epileptogenic response to intracerebrally applied opioid peptides is site-specific within the rat brain, and they support the idea that endogenous opioid mechanisms may play a role in convulsive seizures. They also suggest a possible opiate-based mechanism for the stress-induced exacerbation of seizures.

Amygdala↗
PubMed1984

Vasopressin and the kindling of seizures.

In an attempt to confirm a previous report that two intracerebroventricular injections of arginine-vasopressin (AVP) can kindle convulsive seizures, we injected AVP up to 14 times. Although behavioral and electrographic effects were observed, seizures failed to develop with any reliability. These results call into question the phenomenon of AVP kindling.

Animals↗
PubMed1984

Intracerebral beta-endorphin, met-enkephalin and morphine: kindling of seizures and handling-induced potentiation of epileptiform effects.

The effects of repeated infusion of small, initially subconvulsive amounts of beta-endorphin, met-enkephalin or morphine sulfate into the amygdala and hippocampus were investigated. beta-endorphin and met-enkephalin evoked epileptiform spiking when infused into the posterior amygdala or ventral hippocampus. Morphine evoked epileptiform spiking when infused into the anterior amygdala. Naloxone blocked or terminated the spiking. Repetition of the infusions led to the gradual development of bilateral generalized convulsions by beta-endorphin and met-enkephalin and to the development of tolerance to morphine. An unexpected observation was that handling, immobilization or conspecific threat potentiated the epileptiform effects of beta-endorphin and morphine in many cases. These results suggest that endogenous opiate mechanisms might play a role in convulsive seizures and that stressful stimuli can exacerbate opiate seizures.

Animals↗
PubMed1984

Depletion of noradrenaline fails to affect kindled seizures.

Convulsive seizures were kindled in rats by repeated stimulation of the amygdala, and the subjects then received intracerebral injections of 6-hydroxydopamine into the dorsal noradrenergic bundle. Although this treatment severely depleted noradrenaline, there was no effect on the intensity or duration of seizures, suggesting that noradrenaline does not regulate kindled seizures when they have developed.

Amygdala↗
PubMed1984

Amygdaloid kindling in Papio cynocephalus and subsequent recurrent spontaneous seizures.

Three baboons, Papio cynocephalus, (two photosensitive and one nonphotosensitive) were subjected to amygdaloid kindling. Electroclinical profile of seizure development-developed seizure compares very favourably to that described in photosensitive baboons, Papio papio, with rapid seizure progression and ultimate emergence of Stage 5 bisymmetrical and bisynchronous generalized convulsive state. In addition, one baboon developed spontaneous recurrent seizures which were identical to the kindled Stage 5 seizure. It is concluded that the state of exceptional seizure susceptibility observed in Papio papio is shared by Papio cynocephalus, although photosensitivity and kindled generalized convulsion appear to be independent variables.

Amygdala↗
PubMed1983

Facilitation of neocortical kindling by depletion of forebrain noradrenaline.

The role of forebrain noradrenaline in seizures induced by electrical stimulation of the anterior neocortex (kindling) was investigated in control rats and rats pretreated with bilateral injections of 6-hydroxydopamine (6-OHDA) into the mesencephalic trajectory of the dorsal tegmental noradrenergic bundle. Extensive depletion of forebrain noradrenaline significantly facilitated the rate of development of cortico-generalized seizures.

Animals↗
PubMed1983

Forebrain noradrenaline and oral self-administration of ethanol by rats.

The effects of 6-hydroxydopamine-induced depletion of forebrain noradrenaline (NA) on oral intake of ethanol were studied in male Wistar rats. Prior depletion of NA produced a smaller and significantly less variable intake of a concentrated solution of ethanol than that of control rats, and this effect was not accompanied by hyperreactivity to aversive solutions of quinine. NA-depleted rats also displayed rejection 'thresholds' for ethanol solutions that were significantly lower than those of controls. Depletion of forebrain NA did not, however, affect the punishing effects of ethanol injections measured in the conditioned taste aversion paradigm. In contrast to these effects of NA depletion on initiation of ethanol intake, depletion of forebrain NA after a preference for ethanol had been established failed to affect subsequent intake of ethanol. These results suggest that forebrain NA is involved in the initiation of ethanol intake by naive rats but not in the maintenance of established patterns of intake by experienced rats. Possible mechanisms for this differential involvement of NA are discussed.

Alcohol Drinking↗
PubMed1983

Optical depolarization changes on the diffraction pattern in the transition of skinned muscle fibers from relaxed to rigor state.

Light diffraction spectra from single or small bundles of skinned striated muscle fibers show large changes in polarization properties when muscles are placed into rigor. The technique of combining optical diffraction and ellipsometry measurements has previously been shown by Yeh and Pinsky to be a sensitive probe of periodic anisotropic regions of the fiber. In the present work, using this method, the observed spectrum shows marked decrease in the measured phase angle, delta, as the fiber approaches the rigor state. The degree of phase angle change is a function of sarcomere length: Maximum overlap of approximately 2.3 microns gives the most change in delta a delta delta R-R approximately 35 degrees decrease for a bundle of three fibers. At a sarcomere length of 2.9 microns this delta delta R-R value is only 10 degrees. At a nonoverlapping length of approximately 3.8 microns, delta does not vary at all upon the removal of ATP. The rigor state was confirmed by stiffness measurements made after small-amplitude (0.75%), quick length changes. Upon re-relaxation, the stiffness of the skinned fiber decreased to the value of the resting state (4 mM ATP) and the phase angle delta returned to its original value. A model based on either anisotropic subunit-2 (S-2) movements or other cross-bridge-related structural anisotropy (form birefringence) changes during the relaxed-rigor transition is suggested.

Adenosine Triphosphate↗
PubMed1980

Spontaneously recurrent seizures after intracerebral injections of kainic acid in rat: a possible model of human temporal lobe epilepsy.

Intrastriatal injection of kainic acid in rats acutely induced repeated episodes of clonic convulsions. Spontaneously recurrent generalized seizures and a potentiation of the convulsant effects of phentylenetetrazol were then observed in most of the injected rats several weeks after surgery. In addition to marked loss of striatial neurons, limbic pathological alterations similar to those found in human temporal lobe epilepsy were observed in the brains of the kainic-acid treated rats. It is proposed that this preparation might serve as an animal model of human temporal lobe epilepsy.

Animals↗