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PubMed1997

Intra-amygdala infusion of 2-chloroadenosine suppresses amygdala-kindled seizures.

The seizure-modulating effects of 2-chloroadenosine (2-CLA) infused directly into the amygdala were investigated. Different groups of amygdala-kindled rats were infused (1 microliter) with 2-CLA (0.25, 1, 10 and 25 nM), caffeine (200 microM and 2 mM), a combination of the two or artificial cerebrospinal fluid (ACSF) applied directly through a cannula located in the amygdala. Infusion of 2-CLA dramatically suppressed seizure stage (SS), after discharge duration (ADD) and stage 5 seizure duration (S5D), while the latency to bilateral forelimb clonus (S4L) was significantly prolonged. These anticonvulsant effects were evident after 5 min, reached a maximum at the 60 min time point and were still detectable 360 min post-2-CLA infusion. Pretreatment with caffeine blocked the anticonvulsant effects of 2-CLA dose-dependently. These results may suggest that in amygdaloid-kindled rats, adenosine receptors located in the amygdala play a major role in the expression of the anticonvulsant activity of 2-CLA.

2-Chloroadenosine↗
PubMed1994

Response properties of single units in areas of rat auditory thalamus that project to the amygdala. II. Cells receiving convergent auditory and somatosensory inputs and cells antidromically activated by amygdala stimulation.

The purpose of this study was to further our understanding of the contribution of auditory thalamoamygdala projections to conditioned emotional memories formed when auditory and noxious somatosensory stimuli are associated. Single unit activity was recorded in the acoustic thalamus of chloral hydrate-anesthetized rats in response to auditory (white noise, clicks, tones) and somatosensory (foot-shock) stimulation. The thalamic areas focused on were the medial division of the medial geniculate body (MGm), the suprageniculate nucleus (SG), and the posterior intralaminar nucleus (PIN), thalamic areas that receive inputs from both the inferior colliculus and the spinal cord and that project to the lateral nucleus of the amygdala (AL). For comparison, recordings were also made from the specific thalamocortical relay nucleus, the ventral division of the medial geniculate body (MGv), which receives projections from the inferior colliculus but not from the spinal cord. Auditory but not somatosensory responses were recorded from MGv, while both auditory and somatosensory responses were frequently found in MGm, PIN, and SG. In these areas, convergent auditory and somatosensory responses were more frequently found rostrally than caudally. Within a thalamic subregion, the acoustic response properties of the convergence cells were not different from the response properties of unimodal auditory cells. Some cells that responded to somatosensory but not auditory stimuli showed a potentiated response when tested with simultaneous presentation of auditory and somatosensory stimuli. In some studies, thalamic cells that project to the amygdala were antidromically activated by stimulation of the AL. Consistent with anatomical tracing results, antidromically activated cells were found in MGm, PIN, and SG, but not in MGv. Antidromically activated cells were more likely to respond to auditory stimuli than to somatosensory stimuli, but unimodal somatosensory and convergence cells were also found. These findings, which provide the first characterization of acoustic response properties of multimodal cells in the auditory thalamus and of cells in the auditory thalamus that project to amygdala, suggest insights into the emotional functions of the thalamoamygdala pathway.

Acoustic Stimulation↗
PubMed1988

Bifunctional roles of catecholamines in the development of amygdala kindling demonstrated by continuous intra-amygdala infusion of 6-hydroxydopamine.

Details of seizure stage progression in amygdala kindling were studied in the cat under local denervation of catecholamine input to the amygdala. A chemitrode was used for both electrical stimulation and continuous infusion of 6-hydroxydopamine. The extent of denervation was confirmed by fluorescence histochemistry. The result has indicated that catecholamine afferents to the amygdala exert biphasic roles in normal kindling: inhibitory in the early local and late generalized seizure stages, whereas facilitatory in the intermediate stage.

Amygdala↗
PubMed1975

Improvement produced by lateral amygdala lesions on the instrumental alimentary performance imparied by dorsomedial amygdala lesions in dogs.

The dorsomedial and subsequent lateral amygdala lesions were performed on 6 dogs. Lesions of the dorsomedial part produced transient aphagia, decrease of body weight and either abolishment or impairment of instrumental performance. Subsequent lesions of the lateral amygdala produced restoration or improvement and stabilization of the instrumental performance. It is supposed that the prevailing inhibitory influences from the lateral amygdala are the main cause of the impairment of instrumental performance after dorso-medial amygdalar lesions. The removal of this source of inhibition enabled restoration of instrumental performance and other alimentary positive functions.

Amygdala↗
PubMed2005

Post-training intra-amygdala amphetamine injections given during acquisition of a stimulus-response (S-R) habit task enhance the expression of stimulus-reward learning: further evidence for incidental amygdala learning.

The effect of post-training intra-amygdala amphetamine injections was examined on the acquisition and expression of a visual discrimination task. Rats were trained to enter four lit arms for food (stimulus-response) and avoid unlit arms on an eight-arm radial maze visual discrimination task. Post-training intra-amygdala amphetamine injections (10 microg) were given for 4 consecutive days during the mid-point of training (days 20-23). The number of lit arm entries was used as a measure of stimulus-response habit learning 24 h after each injection. Twenty-four hours after the last injection, a transfer test was run to assess the effect of the same post-training manipulation. This transfer test assessed the amount of time spent in the lit arms and was used as a measure of stimulus-reward learning. Compared to saline-injected rats, rats that received post-training amphetamine spent more time in lit as opposed to dark arms during the transfer test. This occurred in the absence of an increase in the number of correct arm entries during visual discrimination training. This suggests that post-training amphetamine strengthened a stimulus-reward association that did not immediately affect behavioral output. This association may reflect a mnemonic representation stored in an ensemble of amygdala neurons.

Amphetamine↗
PubMed2004

Amygdala amino acid and monoamine levels in genetically Fast and Slow kindling rat strains during massed amygdala kindling: a microdialysis study.

We investigated the neurochemistry of epileptic seizures in rats selectively bred to be seizure-prone (Fast) vs. seizure-resistant (Slow) to amygdala kindling. Microdialysis was used to measure levels of amino acids [glutamate, aspartate and gamma-aminobutyric acid (GABA)] and monoamines (noradrenaline, dopamine and serotonin) during 'massed' stimulation (MS) (every 6 min) of the ipsilateral amygdala for a total of 40 stimulation trials. Behavioral seizure profiles together with their afterdischarge thresholds (ADTs) and associated durations were assessed during the procedure, and subsequently were redetermined 1, 7 and 14 days later. Then normal 'daily' kindling commenced and continued until the animal reached the fully kindled state. During MS, several generalized seizures were triggered in Fast rats that were associated with long afterdischarge (AD) durations and intermittent periods of elevated thresholds, but in Slow rats, most stimulations were associated with stable ADTs and short ADs. Progressively increasing extracellular glutamate and decreasing GABA was observed in Fast rats during the MS, whereas Slow rats showed levels similar to baseline values. Levels of noradrenaline and dopamine, but not of serotonin, were also increased in both strains throughout the MS treatment. In Fast rats, a dramatic lengthening of AD durations occurred 7 and 14 days following MS, as well as subsequent strong positive transfer to daily kindling, all of which were not seen in Slow rats. Together, these results show that repeated, closely spaced stimulations of the amygdala can differentially alter excitatory and/or inhibitory transmitter levels in a seizure network, and that sensitivity to this manipulation is genetically determined.

Amino Acids↗
PubMed1999

The extended amygdala: are the central nucleus of the amygdala and the bed nucleus of the stria terminalis differentially involved in fear versus anxiety?

Although there is a close correspondence between fear and anxiety, and the study of fear in animals has been extremely valuable for understanding the neural basis of anxiety, it is also clear that a richer animal model of human anxiety disorders would include measures of both stimulus-specific fear and something less stimulus specific, more akin to anxiety. Patients with posttraumatic stress syndrome seem to show normal fear reactions but abnormal anxiety measured with the acoustic startle reflex. Studies in rats, also using the startle reflex, indicate that highly processed explicit cue information (lights, tones) activates the central nucleus of the amygdala, which projects to and modulates the acoustic startle pathway in the brain stem. Less explicit information, such as that produced by exposure to a threatening environment or by intraventricular administration of corticotropin-releasing hormone, may activate another part of the extended amygdala, the bed nucleus of the stria terminalis, which also projects to the startle pathway. Because this information may be less specific and of long duration, activation of the bed nucleus of the stria terminalis may mediate anxiety, whereas activation of the central nucleus of the amygdala may mediate stimulus-specific fear.

Amygdala↗
PubMed1990

Transient elevation of amygdala alpha 2 adrenergic receptor binding sites during the early stages of amygdala kindling.

Enhanced noradrenergic neurotransmission retards but does not prevent the development of kindling. We previously reported that locus coeruleus (LC) alpha 2 adrenergic receptor binding sites are transiently elevated during the early stages of kindling development. Since the firing activity of LC noradrenergic neurons is partially regulated via an alpha 2 receptor-mediated recurrent inhibition, the transient elevation in LC alpha 2 receptors could decrease LC activity and consequently facilitate the development of kindling. Transient elevation of alpha 2 receptor binding sites during early stages of kindling may also occur on noradrenergic axon terminals projecting to forebrain sites. Using in vitro neurotransmitter autoradiography techniques, we investigated this hypothesis by measuring specific [3H]idazoxan binding in 5 different areas of rat forebrain at 2 different stages of kindling development. After 2 class 1 kindled seizures, specific [3H]idazoxan binding was elevated significantly in the amygdala, but not in other forebrain regions. No differences in specific [3H]idazoxan binding were observed in any of the 5 brain regions in rats kindled to a single class 5 kindled motor seizure. Saturation of binding experiments indicated that the increase in amygdala [3H]idazoxan binding, following 2 class 1 kindled motor seizures, was due to an increase in the total number of alpha 2 receptor binding sites without a change in the affinity of the binding sites for [3H]idazoxan. Thus, the transient increase in alpha 2 receptors that occurs in the LC in the early stages of kindling also occurs in the forebrain region in which the kindled seizure originates.

Amygdala↗
PubMed1997

The protective effect of 2-chloroadenosine against the development of amygdala kindling and on amygdala-kindled seizures.

The influence of 2-chloroadenosine, a non-metabolizable adenosine A1 receptor agonist, was tested on the development of electrically kindled amygdala and on the seizure responses of fully kindled rats. Focal intra-amygdaloid injection of 2-chloroadenosine (1-10 nmol/0.5 microl) 20 min before applying the daily kindling stimulus prevented the development of the kindling process. The behavioural seizure score and the afterdischarge duration were reduced below their initial values. The antiepileptogenic effects of 1 and 10 nmol of 2-chloroadenosine were reversible 8-10 days after withdrawal of the drug. When 2-chloroadenosine was tested on fully developed stage 5 amygdala-kindled seizures, it increased the generalised seizure threshold in a dose-dependent manner. A maximum efficiency of 125% (P < 0.001) was achieved with 5 nmol and the median effective dose was 0.55 nmol. Higher doses resulted in the reduced anticonvulsant effect (P < 0.05). With the same daily stimulation, 2-chloroadenosine 5 nmol in 0.5 microl vehicle, significantly reduced the maximum seizure score by 90%, the afterdischarge duration by 88% and completely blocked the generalised seizure duration. The antiseizure activity of the drug lasted for 3 days. In conclusion, 2-chloroadenosine not only acts as an anticonvulsant against electrically induced kindled seizures as described here, and against audiogenic seizures, electroshock and a variety of chemical convulsants as described by others, it prevents the development of the epileptic state by kindling-stimulation, i.e., it is antiepileptogenic. We theorise here that this is due to its blockade of presynaptic glutamate release.

2-Chloroadenosine↗
PubMed1998

Intra-amygdala infusion of an end-capped antisense oligodeoxynucleotide to c-fos accelerates amygdala kindling.

The changes produced by repeated stimulation of the brain that result in the kindling effect remain unknown. It is known, however, that activation of immediate early genes including c-fos is a very early event in the development of kindling. Here we show that c-fos expression in the amygdala can be knocked-down by an end-capped antisense oligodeoxynucleotide (but not by vehicle, or control antisense oligodeoxynucleotides) and that this results in an acceleration of kindling. These results suggest that, at least in the amygdala, the expression of c-fos is associated with an attempt by the brain to retard the development of kindling.

Amphetamine↗
PubMed1977

Neural mechanism for production of spasmodic expiratory response like cough induced by amygdala stimulation in the cat. I. Pathways from the amygdala to the lower brain stem.

The pathways descending from the amygdala to neural structures in the lower brain stem responsible for production of spasmodic expiratory response like cough (SER), which occurred upon electrical stimulation of the cortical nucleus of amygdala (Aco), were investigated using microinjection and ablation techniques in the cat. 1) Following transection of the bilateral stria terminalis (STT), the threshold for SER production was remarkably elevated. 2) SER was suppressed by administration of procaine (20 microgram) or diazepam (5 microgram) into either side of the hypothalamic ventromedial nucleus (Hvm); furthermore, SER completely disappeared after lesion of bilateral Hvm. After lesion of the ipsilateral Hvm to the side of stimulation, the threshold for SER was obviously elevated, but SER was not affected by lesion of the contralateral Hvm. 3) After section of the substantia grisea centralis at the midcollicular level, SER disappeared. 4) Both SER and peripherally-induced coughs were depressed by codeine (10 microgram), dextromethorphan (10 microgram) or procaine (20 microgram) administered into the solitary tract nucleus (STN) or the nucleus reticularis parvocellularis. 5) SER and coughs disappeared after lesion of the bilateral STN or nucleus ambiguus (AM). These results demonstrate that most of the efferent fibers from Aco get to Hvm via STT, and further to STN and AM in the medulla.

Amygdala↗
PubMed1996

The role of the basolateral nucleus of the amygdala in the pathway between the amygdala and the midbrain periaqueductal gray in the rat.

We electrophysiologically examined the connection between the basolateral nucleus of the amygdala (BLA) and the periaqueductal gray (PAG) and examined the role of the central nucleus of the amygdala (CNA) in this pathway. Train electrical stimulation of the BLA excited 21% (7/33) and inhibited 27% (9/33) of the cells recorded in the PAG. Chemical stimulation of the BLA excited 23% (13/56) and inhibited 16% (9/56) of the cells recorded in the PAG. Injection of lidocaine into the CNA by itself had no effect on PAG cells (n = 9) or on blood pressure but blocked the effect of BLA stimulation on PAG neurons in 78% of the cells recorded. It was concluded that: (1) PAG cells respond to BLA stimulation; (2) the majority of these cells are located in the dorsolateral and lateral columns of the PAG; and (3) the CNA modulates a majority of the activities of the BLA in the PAG.

Amygdala↗
PubMed1994

The effect of the non-NMDA receptor antagonist GYKI 52466 and NBQX and the competitive NMDA receptor antagonist D-CPPene on the development of amygdala kindling and on amygdala-kindled seizures.

A competitive (NBQX) and a non-competitive (GYKI 52466) AMPA antagonist, and a competitive NMDA antagonist (D-CPPene) were tested against the development of kindling and against fully kindled seizures in amygdala-kindled rats. GYKI 52466, 10 mg/kg given i.p. 5 min prior to electrical stimulation in fully kindled animals, reduces both the cortical after-discharge duration and the behavioural seizure score. GYKI 52466, 20 mg/kg, reduces seizure score and after-discharge duration significantly (after 5-30 min) but the animals show severe motor side effects and an irregular cortical and hippocampal EEG. Administration of GYKI 52466, 10 mg/kg, prior to kindling stimulation on days 3-8, does not slow the development of kindling. NBQX, 20 mg/kg or 40 mg/kg i.p., 30 min prior to stimulation, significantly reduces the seizure score in fully kindled animals. NBQX 20 mg/kg i.p. has no effect on the development of kindling. D-CPPene, 8 mg/kg or 12 mg/kg, 120 min prior to stimulation reduces the behavioural seizure score in fully kindled animals. D-CPPene, 8 mg/kg on days 3-8, delays the development of kindling. NMDA receptors play a key role in the kindling process. Expression of kindled seizures involves non-NMDA and NMDA receptors.

Amygdala↗
PubMed2005

Opposing influence of basolateral amygdala and footshock stimulation on neurons of the central amygdala.

BACKGROUND: The basolateral complex (BLA) and the central nucleus of the amygdala (CeA) are believed to mediate the expression of affective responses. After affective learning, conditioned stimulus-related information is thought to be conveyed from the BLA to the CeA; the medial CeA (Cem), in turn, projects to hypothalamic and brainstem structures involved with induction of affective responses. Although the conditioned stimulus and unconditioned stimulus both evoke affective responses, the precise response often differs. It is unknown whether this difference is represented by distinct activity patterns of single Cem neurons. Furthermore, the nature of the interaction between the BLA and Cem is unknown. METHODS: Using in vivo extracellular and intracellular recordings, we examined how the BLA affects the Cem and compared this with effects induced by footshock (unconditioned stimulus) in the same neurons. RESULTS: Our results demonstrate that, contrary to conventional views, BLA stimulation primarily inhibits Cem neurons by a polysynaptic circuit, and show that single Cem neurons respond to both BLA input and footshock in an opposite manner. CONCLUSIONS: These results demonstrate the predominantly inhibitory nature of the BLA-Cem interaction. These data further demonstrate the distinct cellular events that might lead to differential modulation of conditioned and unconditioned affective responses.

Action Potentials↗
PubMed2003

Antinociceptive effect of calcitonin gene-related peptide in the central nucleus of amygdala: activating opioid receptors through amygdala-periaqueductal gray pathway.

The central nucleus of amygdala (CeA) plays an important role in pain regulation. Calcitonin gene-related peptide (CGRP)-like immunoreactive fibers and CGRP receptors are distributed densely in CeA. The present study was performed to elucidate the role of CGRP in nociceptive regulation in the CeA of rats. Intra-CeA injection of CGRP induced dose-dependent increases in the hind-paw withdrawal latency tested by hotplate test and Randall Selitto Test, indicating an antinociceptive effect of CGRP in CeA. Furthermore, the antinociceptive effect of CGRP was blocked by intra-CeA administration of the CGRP receptor antagonist CGRP8-37, suggesting that CGRP receptor1 is involved in the CGRP-induced antinociception. The CGRP-induced antinociception was attenuated by s.c. injection of the opioid antagonist naloxone, suggesting an involvement of endogenous opioid systems in CGRP-induced antinociception. Moreover, it was demonstrated that opioid receptors in the periaqueductal gray, but not in CeA, contributed to the CGRP-induced antinociception, indicating the importance of the pathway between CeA and the periaqueductal gray in CGRP-induced antinociception. Combining retrograde fluorescent tracing with immunohistochemistry, we found that met-enkephalinergic neurons were innervated by CGRP-containing terminals in CeA. Furthermore, most neurons in the CeA retrogradely traced from the periaqueductal gray were contacted by CGRP-containing terminals and some of them were surrounded by characteristic basket-like structures formed by the terminals, suggesting that CGRP innervates the neurons which project from CeA to the periaqueductal gray. The results indicate that CGRP activates the met-enkephalinergic neurons, which project from CeA to the periaqueductal gray, producing antinociceptive effect in rats.

Amygdala↗
PubMed2005

Does the amygdala mediate anesthetic-induced amnesia? Basolateral amygdala lesions block sevoflurane-induced amnesia.

BACKGROUND: Amnesia for aversive events caused by benzodiazepines or propofol depends on the basolateral amygdala (BLA). Whether the amnesia of volatile anesthesia is also mediated through the BLA is unknown. If so, a general principle of anesthetic-induced amnesia may be emerging. Here, using an inhibitory avoidance paradigm, the authors determine whether BLA lesions prevent sevoflurane-induced amnesia. METHODS: Male Sprague-Dawley rats were separated into two groups: sham-operated controls (n = 22) and rats given bilateral N-methyl-D-aspartate lesions of the BLA (n = 32). After a 1-week recovery, the rats were randomly assigned to be trained during either air or sevoflurane (0.3% inspired, 0.14 minimum alveolar concentration) exposure. Animals learned to remain in the starting safe compartment of a step-through inhibitory avoidance apparatus for 100 consecutive seconds by administering foot shock (0.3 mA) whenever they entered an adjacent shock compartment. Memory was assessed at 24 h. Longer latencies to enter the shock compartment at 24 h imply better memory. RESULTS: Sham-air (n = 10) animals had a robust memory, with a median retention latency of 507 s (interquartile range, 270-600 s). Sham-sevoflurane (n = 6) animals were amnesic, with a latency of 52 s (27-120 s) (P < 0.01, vs. sham-air). Both the air-exposed (n = 5) and the sevoflurane-exposed (n = 8) animals with BLA lesions showed robust memory, with latencies of 350 s (300-590 s) and 378 s (363-488 s), respectively. The latencies for both did not differ from the performance of the sham-air group and were significantly greater than the latency of the sham-sevoflurane group (both P < 0.01). CONCLUSIONS: BLA lesions block sevoflurane-induced amnesia. A role for the BLA in mediating anesthetic-induced amnesia may be a general principle of anesthetic action.

Amnesia↗
PubMedDate not supplied

Memory enhancement induced by post-training intrabasolateral amygdala infusions of beta-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala.

Previous findings indicate that the noradrenergic, dopaminergic, and cholinergic innervations of the basolateral amygdala (BLA) modulate memory consolidation. The current study investigated whether memory enhancement induced by post-training intra-BLA infusions of a beta-adrenergic or muscarinic cholinergic agonist requires concurrent activation of dopamine (DA) receptors in the BLA. Rats with implanted BLA cannulae were trained on an inhibitory avoidance (IA) task and, 48 h later, tested for retention. Infusions of the beta-adrenergic agonist clenbuterol into the right BLA, but not the left, enhanced retention, and concurrent infusions of the nonspecific DA receptor antagonist cis-Flupenthixol (Flu) blocked the enhancement. Post-training infusions of the muscarinic agonist oxotremorine into the right BLA also enhanced retention, and concurrent infusions of Flu blocked this effect. Additional experiments investigated whether memory modulation was lateralized to the right BLA. Post-training DA infusions into the right BLA, but not the left, enhanced retention. Post-training infusions of lidocaine or muscimol, which impair retention when infused bilaterally, had no effect when infused unilaterally into either the right or left BLA. These findings, together with earlier work, suggest that the dopaminergic system in the BLA is critically involved in memory modulation induced by noradrenergic and cholinergic influences. Additionally, these findings indicate that the enhancement, but not impairment, of memory consolidation is lateralized to the right BLA.

Adrenergic beta-Agonists↗