Electrical Stimulation Of Amygdala Research Articles

Influence of hippocampal low-frequency stimulation on GABAA R α1, ICER and BNDF expression level in brain tissues of amygdala-kindled drug-resistant temporal lobe epileptic rats

This study investigated the therapeutic effect of hippocampal low-frequency stimulation (Hip-LFS) and its influence on the type A γ-aminobutyric acid receptor α1 subunit (GABAA R α1 subunit), inducible cAMP early repressor (ICER) and brain-derived neurotrophic factors (BNDF). The model of epilepsy was induced by chronic electrical stimulation in amygdala. Drug-resistant and drug-sensitive epileptic rats were selected by testing their seizure response to phenytoin and phenobarbital. The changes of GABAA R α1 subunit, ICER and BDNF expression were detected via immunohistochemistry and western blot. The expression levels of ICER and BDNF were increased remarkably but the GABAA R α1 subunit decreased significantly in the drug-resistant epileptic rats. However, the expression levels of ICER, BDNF were decreased and the expression of the GABAA R α1 subunit increased significantly in the drug-resistant epileptic rats after two weeks of Hip-LFS. Meanwhile, the seizure degree was reduced and the electroencephalograms were improved. The present study demonstrated thatincreased ICER and BDNF might be associated with the development of drug-resistance. The effect of Hip-LFS in the treatment of drug-resistant epileptic rats might be associated with increasing the levels of the ICER and the BDNF.

Electrical Low Frequency Stimulation of the Kindling Site Preserves the Electrophysiological Properties of the Rat Hippocampal CA1 Pyramidal Neurons From the Destructive Effects of Amygdala Kindling: The Basis for a Possible Promising Epilepsy Therapy

BackgroundDeep brain stimulation (DBS) has emerged as a potential therapeutic strategy in the treatment of neurological disorders including epilepsy. However, the cellular mechanism responsible for the effects of DBS remains largely undefined. Therefore, using electrophysiological approach, we aimed to determine the antiepileptic effects and restorative potential of low frequency stimulation (LFS) on amygdala kindling-induced changes in electrophysiological properties of rat hippocampal CA1 pyramidal neurons. MethodsAnimals were kindled by electrical stimulation of amygdala in a rapid kindling manner (12 times per day). In one group of animals, immediately after termination of daily 12 rapid kindling stimulations, the kindling site was subjected to 4 packages of LFS at intervals of 5 min (each package contained 200 monophasic square-wave pulses, 0.1 ms pulse duration at 1 Hz). Whole cell patch clamp recording under current clamp conditions was performed on visually identified pyramidal neurons in hippocampal slice preparations obtained from amygdala-kindled rats and the rats receiving LFS. ResultsKindling of the right basolateral amygdala profoundly affected spontaneous firing behavior and repetitive discharge characteristics of pyramidal neuronal electrophysiological properties. Application of LFS at the kindling site almost completely prevented the development of epilepsy and the disruptive effects of kindling on neuronal electrical activity through restoration of the normal electrophysiological characteristics. ConclusionsThe results of this study implied that application of LFS during kindling acquisition prevents the kindling induced changes in functional electrical properties of CA1 pyramidal neurons, suggesting that this action may be involved in the antiepileptogenic mechanism of LFS.

Raphe region mediates changes in cutaneous vascular tone elicited by stimulation of amygdala and hypothalamus in rabbits

Raphe pallidus/parapyramidal neurons control cutaneous vasoconstriction induced by noxious stimuli. To determine whether they mediate forebrain-induced cutaneous vasoconstriction, we assessed changes in ear pinna blood flow elicited by electrical stimulation of amygdala and hypothalamus before and after injection of muscimol into the raphe/parapyramidal region. We compared ear flow with simultaneously recorded mesenteric flow. Experiments were performed in rabbits anesthetized with urethane (1.25–1.5 g/kg), paralysed and mechanically ventilated. Amygdala stimulation reduced skin conductance from 0.32±0.06 to 0.10±0.02 cm/s per mm Hg ( P<0.05, n=9), without effect on mesenteric conductance. Hypothalamic stimulation caused vasoconstriction in both cutaneous and mesenteric beds (conductances fell from 0.27±0.05 to 0.05±0.02 cm/s per mm Hg and from 0.27±0.06 to 0.14±0.04 cm/s per mm Hg ( P<0.05, n=9), respectively). Muscimol microinjection (5 nmol in 100 nl) to raphe/parapyramidal region eliminated amygdala- and hypothalamus-induced skin vasoconstriction (pre-stimulus conductance 0.42±0.13 and 0.41±0.11 cm/s per mm Hg, post-stimulus 0.41±0.12 and 0.39±0.10 cm/s per mm Hg, respectively), but not hypothalamically-induced mesenteric vasoconstriction (pre-stimulus 0.29±0.06, post-stimulus 0.16±0.03 cm/s per mm Hg, P<0.05, n=8). The latter was strongly attenuated by bilateral injection of muscimol to the rostral ventrolateral medulla. Data suggest that descending hypothalamo–spinal and amygdala–spinal pathways constricting the cutaneous vascular bed relay in the raphe/parapyramidal area. A relay in the rostral ventrolateral medulla contributes substantially to mesenteric vasoconstriction elicited from the hypothalamus.

Limbic ictus as a condition for anxiety attacks

Episodes of anxiety have been reported to be the most common psychological symptoms in patients with partial seizures. They may occur before, during and after seizures and can also appear in isolation without any convulsive symptoms. The epileptic anxiety syndrome is strikingly similar to panic attacks, and panic disorder is an important differential diagnosis. The close relationship between epileptic seizures and panic attacks is of special interest for a better pathophysiological understanding of panic attacks. In the literature an epileptiform neuronal activity is discussed as a possible underlying mechanism for panic disorder. The finding that anxiety was the most common experiential phenomenon produced by electrical stimulation of amygdala and hippocampus with depth electrodes points in this direction. PET has demonstrated abnormalities of hippocampal structures during the nonpanic state of patients with panic disorder. In addition, some EEG studies have demonstrated a high incidence of epileptiform EEG patterns in patients with panic disorder with or without agoraphobia. This was the reason why several investigators proposed that a subset of panic attacks may be related to abnormal epileptiform neuronal activity in the limbic system. The size of this subset is difficult to determine because discharges in the depth of the limbic system often cannot be seen in the scalp EEG. Concerning the hypothetical pathophysiological mechanism of panic disorder therapeutic measures were taken with antiepileptic agents. The best results were obtained for valproic acid. It seems to be reasonable to make a therapeutic trial with antiepileptic medication after nonresponse to standard pharmacotherapy.

Distinct motor patterns of cricothyroid muscle in larynx evoked by electrical stimulation in amygdala and lateral hypothalamus

Distinct motor patterns of cricothyroid muscle in larynx evoked by electrical stimulation in amygdala and lateral hypothalamus

Cardiovascular responses to chemical and electrical stimulation of amygdala in rats

Electrical stimulation of the amygdala has been shown to produce changes in cardiovascular variables. To locate neuronal cell bodies responsible for these changes, responses of arterial pressure (AP) and heart rate (HR) to DL-homocysteate (DLH, 0.15 M, 50-100 nl) microinjected into sites in three amygdaloid nuclei were compared with responses to electrical (90-150 microA) stimulation of the same sites in 35 artificially ventilated, paralyzed, urethan-anesthetized rats. Electrical stimulation resulted in depressor responses in most sites (89%). Changes in AP were accompanied by variable changes in HR. Chemical stimulation produced significantly fewer (25%) depressor responses. Similar results were obtained with injections of 1.0 M DLH. To eliminate the influence of the anesthetic on these responses, AP was recorded in nine conscious rats while stimulating the amygdala. Changes in behavior and AP in these animals could be obtained only by electrical stimulation. These results may be interpreted to indicate either that cell bodies responsible for changes in cardiovascular variables during electrical stimulation are not located in the amygdala or that chemical and electrical stimulation affect different neuronal elements in circuits located in the same anatomic site.

Slowing of scalp EEG after electrical stimulation of amygdala in man.

Electrical Stimulation (60 Hz) of the amygdala in anaesthetized patients caused a predominantly ipsilateral slowing of the scalp EEG. The slowing appeared a few seconds after cessation of Stimulation and lasted for 2–3 min. The frequency of the slow waves was 1–1.5 Hz and the amplitude 200–400 µV.

Effects of tetrahydrocannabinols on kindled amygdaloid seizures and photogenic seizures in Senegalese baboons, Papio papio.

Intraperitoneal injections of delta 8-tetrahydrocannabinol (THC) and delta 9-THC failed to affect myoclonic response to photic stimulation in Senegalese baboons (Papio papio). However, both isomers of THC exerted dose-related antiepileptic effects upon established kindled convulsions provoked by electrical stimulation of amygdala in the same species. Delta 9-THC was more potent than delta 8-THC, in terms of both antiepileptic effects and general toxicity. The antiepileptic effects of the THC isomers appear to be due mainly to the suppression of propagation of the induced afterdischarge to distant cerebral structures, although high doses also seem to suppress afterdischarge at the site of stimulation.

ADH release from cut pituitary stalk and intact pituitary gland during hippocampal stimulation of various frequencies in rats.

Changes in antidiuretic substance (i.e., vasopressin) release from the cut pituitary stalk and the intact pituitary gland were observed during electrical stimulation of amygdala medial nucleus. Electr

Amnesia produced by brief electrical stimulation of amygdala or dorsal hippocampus in cats.

Amnesia produced by brief electrical stimulation of amygdala or dorsal hippocampus in cats.

Influences of amygdala and medial forebrain bundle on self-stimulation in the septum

Effects of lesions and electrical stimulation in the amygdala or medial forebrain bundle on rewarding stimulation of the septum were investigated. Rats were trained to press a bar for septal stimulation. Some rats learned to self-stimulate (pressers) and others did not (nonpressers). Following production of bilateral lesions in the amygdala (AMY), both pressers and nonpressers showed increased rates of self-stimulation. Bilateral lesions in the anterior medial forebrain bundle (MFB) resulted in no significant change. Rats with no lesions were used as controls. Other rats received 3 sets of chronic electrodes, one set each in the septum, AMY, and anterior MFB. After training for septal self-stimulation, the rats received noncontingent electrical stimulation in AMY during septal self-stimulation sessions. The AMY stimulation decreased bar pressing rates. Subsequently the rats received stimulation in MFB during septal self-stimulation sessions. Half of the group showed increased bar-pressing rates during MFB stimulation while the other half showed a long-lasting decrease in response rates. The results suggest that in terms of septal self-stimulation AMY has an inhibitory influence on the septum, and that MFB may carry 2 modulatory systems that influence the septum, one being inhibitory and the other facilitatory.

Behavioral reactions to electrical stimulation of amygdala in cats

The following main behavioral, motor, and autonomic reactions were observed in chronic experiments on 18 cats using monopolar electrical stimulation of the amygdala: The last two reactions could be evoked from all the nuclei of the amygdala and the piriform cortex, and also from the corpus striatum.

Effect of noradrenaline on phosphatase activity in synaptic membrane of the rat brain.

THE classical experiments of Loewi1 demonstrated the transmitter substance of the sympathetic nervous system to be adrenaline or noradrenaline2,3. Several further investigations have shown a transmitter substance to be present in the central nervous system (CNS), that is, the hypothalamus, the central grey matter of mesencephalon and the area postrema4,7. Differential centrifugation of a CNS homogenate has demonstrated the presence of noradrenaline in the synaptic vesicles of the synaptic junction8–10. Electrophysiological investigation has revealed that electrical stimulation of amygdala or of terminals of bulbo-spinal neurones leads, in both instances, to a reduction of the noradrenaline content of certain areas of the brain11–13. The molecular basis for the action of noradrenaline in the CNS is, however, unknown. Previous investigations of the pharmacological action of noradrenaline, particularly on different enzyme systems14–16, have not provided the experimental evidence basic to a theoretical understanding of physiological events of depolarization and repolarization. The relationship of changes in the ion-flux across the synaptic membrane to the action of a transmitter substance has not been denned. Investigation (our report in preparation) of the distribution of phospholipids and glycolipids free from sialic acid in the sub-cellular fractions of hypothalamus revealed a preponderance of phosphatidyl-serine in the sub-mitochondrial fraction B–C19 using the method of De Robertis et al.8,9. This discovery stimulated us to search for a possible function of phosphatidyl-serine in the synaptic endings. In vitro investigations revealed phosphatidyl-serine to be the only major lipid among phospholipids or glycolipids free from sialic acid of the CNS which binds the noradrenaline17.

Delayed puberty following electrical stimulation of amygdala in female rats.

ARTICLESDelayed puberty following electrical stimulation of amygdala in female ratsM Bar-Sela, and V CritchlowM Bar-Sela, and V CritchlowPublished Online:01 Nov 1966https://doi.org/10.1152/ajplegacy.1966.211.5.1103MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByGnRH pulse generator frequency is modulated by kisspeptin and GABA ‐glutamate interactions in the posterodorsal medial amygdala in female mice28 October 2022 | Journal of Neuroendocrinology, Vol. 34, No. 11Role of Posterodorsal Medial Amygdala Urocortin-3 in Pubertal Timing in Female Mice17 May 2022 | Frontiers in Endocrinology, Vol. 13Optogenetic stimulation of kisspeptin neurones within the posterodorsal medial amygdala increases luteinising hormone pulse frequency in female mice11 February 2020 | Journal of Neuroendocrinology, Vol. 32, No. 2Role of the posterodorsal medial amygdala in predator odour stress‐induced puberty delay in female rats29 April 2019 | Journal of Neuroendocrinology, Vol. 31, No. 6Kisspeptin signaling in the amygdala modulates reproductive hormone secretion11 March 2015 | Brain Structure and Function, Vol. 221, No. 4The Posterodorsal Medial Amygdala Regulates the Timing of Puberty Onset in Female RatsEndocrinology, Vol. 156, No. 10Overexpression of Corticotropin Releasing Factor in the Central Nucleus of the Amygdala Advances Puberty and Disrupts Reproductive Cycles in Female RatsEndocrinology, Vol. 155, No. 10Stress Regulation of Kisspeptin in the Modulation of Reproductive Function16 February 2013The Role of the Medial and Central Amygdala in Stress-Induced Suppression of Pulsatile LH Secretion in Female RatsEndocrinology, Vol. 152, No. 2Effects of Gonadal Steroids on Neuronal Morphology in the Adult Mammalian Brain: A Life History PerspectiveEffect of stimulation and destruction of the amygdaloid nuclei on the ovaries of sexually mature and infantile female ratsNeuroscience and Behavioral Physiology, Vol. 9, No. 3The efferent connections of the ventromedial nucleus of the hypothalamus of the rat,The Journal of Comparative Neurology, Vol. 169, No. 4Electrophysiological evidence for sexual dimorphism and synaptic convergence in the preoptic and anterior hypothalamic areas of the rat1 January 1997 | Proceedings of the Royal Society of London. Series B. Biological Sciences, Vol. 193, No. 1113An electrophysiological study of amygdalohypothalamic projections to the ventromedial nucleus of the ratBrain Research, Vol. 105, No. 1Evaluation of extrahypothalamic control of reproductive physiology21 June 2005Atlas of estrogen-concentrating cells in the central nervous system of the squirrel monkeyThe Journal of Comparative Neurology, Vol. 160, No. 43 Dynamics of hypothalamic-pituitary function during pubertyClinics in Endocrinology and Metabolism, Vol. 4, No. 1The Search for the Determinants of Puberty in the RatThe Localization of Sex in the BrainTwenty-four-Hour Patterns of Luteinizing Hormone Secretion in Humans: Ontogenetic and Sexual ConsiderationsChanges in volume and incorporation of [35S]- or [3H]-methionine in the amygdala before and after puberty in male and female miceBrain Research, Vol. 50, No. 1Correlated Changes in Gonadotropin Release and Electrical Activity of the Hypothalamus Induced by Electrical Stimulation of the Hippocampus in Immature and Mature RatsNeural control of pubertyJournal of Psychosomatic Research, Vol. 16, No. 4Amygdaloid-Hypothalamic Neurophysiological InterrelationshipsDas Hypothalamus-Hypophysenvorderlappen-Keimdrüsen-SystemSites of Steroid Binding and Action in the BrainFactors influencing sex hormone uptake by rat brain regions. I. Effects of neonatal treatment, hypophysectomy, and competing steroid on estradiol uptakeBrain Research, Vol. 21, No. 1Sexual Differentiation of the Brain: Effects of Testosterone on Brain RNA Metabolism in Newborn Female RatsNature, Vol. 226, No. 5248Control of Synthesis and Release of Anterior Pituitary Hormones in vivoFACTORS AFFECTING HYPOTHALAMIC FUNCTIONS: THE PHARMACOLOGY OF PUBERTYSome endocrine aspects of forebrain inhibitionBrain Research, Vol. 6, No. 1Control of the Onset of Puberty More from this issue > Volume 211Issue 5November 1966Pages 1103-1107 Copyright & PermissionsCopyright © 1966 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1966.211.5.1103PubMed5924030History Published online 1 November 1966 Published in print 1 November 1966 Metrics

Central representation of affective reactions in forebrain and brain stem: electrical stimulation of amygdala, stria terminalis, and adjacent structures.

Central representation of affective reactions in forebrain and brain stem: electrical stimulation of amygdala, stria terminalis, and adjacent structures.