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At least 19 recordsLinked to original sources
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↗
PubMed1977

Amygdala afferents from the mediobasal hypothalamus: an electrophysiological and neuroanatomical study in the rat.

Electrophysiological techniques and the retrograde transport of horseradish peroxidase (HRP) were used to determine the efferent projections from the caudal mediobasal hypothalamus to the amygdala. In pentobarbital anesthetized rats, the activity of 1780 mediobasal hypothalamic neurons was examined for response to stimulation sites in the amygdala and stria terminalis. Evidence of orthodromic activation from both stimulation sties was commonly observed. Sixty-five cells mostly located in the ventromedial nucleus displayed antidromic invasion from the basolateral, basomedial or cortical amygdala over a latency range of 5-34 msec (mean 15.3 +/- 6.7 msec S.D.). Three of 440 tested cells displayed antidromic activation from stimulation on the stria terminalis. Amygdala evoked antidromic responses were still present after lesions of the stria terminalis. May ipsilateral ventromedial hypothalamic neurons and a few cells in the ipsilateral arcuate nucelus and periventricular region and contralateral ventromedial nucleus displayed retrograde transport of HRP after an infection into the amygdala. Lesions of the stria terminalis had little effect on the numbers of HRP labeled neurons. Relatively more neurons were labeled retrogradely after medial injections than after lateral injections in the amygdala. Data from both electrophysiological and anatomical techniques therefore indicate that certain mediobasal hypothalamic neurons, particularly those located in the ipsilateral ventromedial nucleus, project to the amygdala probably via a route other than the stria terminalis. Thus there is substantial evidence in the rat for reciprocal connections between the amygdala and the hypothalamic ventromedial nucleus.

Afferent Pathways↗
PubMed1977

Modulation of the proestrous surge of luteinizing hormone by electrochemical stimulation of the amygdala and hippocampus in the unanesthetized rat.

The roles played by the amygdala and hippocampus in controlling the release of pituitary luteinizing hormone (LH) were studied in the freely moving rat. Monopolar stainless steel electrodes were implanted into the corticomedial (CM) amygdala, basolateral (BL) amygdala and dorsal hippocampus of female rats. When the animal had recovered from surgery and shown two consecutive 4-day estrous cycles, a chronic atrial cannula was introduced during the afternoon of diestrus II. On the following day (proestrus) electrochemical stimulation (ECS) was applied (20--50 micronA anodal DC 120 sec) bilaterally to the amygdala or hippocampus and blood samples were taken every 90 min from 12.00 to 21.00 h for radioimmunoassay (RIA) of LH. Next day, uterine tubes were examined for ova as evidence of ovulation. ECS of the amygdala exerted two divergent influences on LH release. Stimulation of the BL amygdala at 13.45 h, just before the critical period (14.00--16.00 h), was effective in delaying and reducing the LH surge, whereas ECS of the CM amygdala at 12.00 h resulted in an early synchronization in the timing of the LH curves. All of the rats in both groups ovulated, in contrast to the results of applying ECS to the dorsal hippocampus; there the LH surge and ovulation were completely blocked in 7 out of 9 rats. Thus, in the freely moving rat, the hippocampus can exert a potent inhibitory influence on LH release whereas the amygdala plays a modulatory role in the process.

Amygdala↗
PubMed1976

Influence of amygdala stimulation on the activity of identified tuberoinfundibular neurones in the rat hypothalamus.

1. Extracellular action potentials were recorded from 1246 neurones in the mediobasal hypothalamus of pentobarbitone or urethane anaesthetized male rats. Antidromic invasion from the surface of the median eminence identified 165 cells, located in the arcuate and ventromedial nuclei and the periventricular area, as tuberoinfundibular neurones. The majority (65%) of these cells displayed no spontaneous activity. 2. Latencies for antidromic invasion from median eminence ranged from 0-5 to 14-0 msec (mean 4-3 +/- 2-9 msec, S.D.). Conduction velocities for axons of tuberoinfundibular neurones were under 1-0 m/sec, and were slowest (under 0-2 m/sec) for those tuberoinfundibular neurones located in the arcuate nucleus. 3. Single 1 HZ stimulation of amygdala evoked short latency (mean 18-8 +/- 7-0 msec; n = 30) excitation of tuberoinfundibular neurones in the ventromedial nucleus. Stria terminalis stimulation evoked similar responses at a shorter latency (mean 10-2 +/- 3-5 msec; n = 12) from other ventromedial tuberoinfundibular neurones. Three of these neurones were also excited by amygdala stimulation at comparably longer latencies. In spontaneously active tuberoinfundibular cells, the initial excitation was followed by a decrease in excitability lasting 70-150 msec. Tuberoinfundibular neurones soldom followed orthodromic activation at frequencies beyond 30 HZ. 4. An initial decrease in activity at latencies of 18-40 msec (mean 29-2 +/- 10-2 msec) characterized the amygdala evoked responses from nine tuberoinfundibular neurones. A similar response from one other tuberoinfundibular neurone followed stria terminalis stimulation at a latency of 11 msec. Most of these tuberoinfundibular neurones were located in the dorsal part of the ventromedial nucleus. 5. Two ventromedial tuberoinfundibular neurones also displayed antidromic invasion from the amygdala; interaction studies suggested an axon collateral pathway that originated close to the origin of the axon. 6. Tuberoinfundibular neurones unresponsive to amygdala stimulation were usually located in the arcuate nucleus or periventricular area. 7. These results provide electrophysiological evidence for a direct influence of the amygdala on the activity of tuberoinfundibular neurones in the ventromedial hypothalamic nucleus. There are also data to indicate that some ventromedial tuberoinfundibular neurones have axon collaterals that return to the amygdala. These reciprocal connexions between the amygdala and ventromedial tuberoinfundibular neurones may indicate neural circuits important for extrahypothalamic modulation of adenohypophyseal secretion.

Amygdala↗
PubMed1978

Catecholamine innervation of the basal forebrain. II. Amygdala, suprarhinal cortex and entorhinal cortex.

The catecholamine (CA) innervation of the posterior basal forebrain, the amygdala, suprarhinal cortex and entorhinal cortex, was studied in the rat using biochemical assay and fluorescence histochemistry. The assay studies demonstrate a moderate norepinephrine (NE) content in the amygdala and entorhinal cortex with a lower value for the suprarhinal cortex. Following destruction of the locus coeruleus, the decrease in NE content of these basal forebrain structures indicates that their principal NE innervation is from locus coeruleus. An additional small NE input arises from the medullary NE neuron groups. Ablation of dopamine (DA) cell groups (substantia nigra-ventral tegmental area, SN-VTA) indicates that the DA input to the amygdala arises from the lateral VTA and medial half of the SN. Fluorescence histochemical studies using the glyoxylic acid-Vibratome technique demonstrate the presence of four distinct types of CA neuron terminal plexus in the posterior basal forebrain. These include two different DA fiber types arising in SN-VTA, small NE fibers with small varicosities arising in locus coeruleus and NE fibers with larger varicosities arising in other brainstem NE cell groups. The large NE fibers appear to enter the amygdala via the ansa peduncularis-ventral amygdaloid bundle to innervate the central and basolateral nucleus and the anterior amygdaloid area. The locus coeruleus NE fibers appear to enter the posterior basal forebrain via both the stria terminalis and ansa peduncularis-ventral amygdaloid bundle system to form a moderately dense innervation of the central and basolateral nuclei of the amygdala and a less dense innervation of the other areas. The DA neuron axons are concentrated in the central and basal nuclei and intercalated cell groups. Other areas receive a more diffuse DA input, with the exception of the moderately dense innervation of the suprarhinal cortex and DA "islands" in the ventral-anterrior entorhinal cortex, The DA input to the posterior basal forebrain is complex and heterogeneous and the axonal morphology differs greatly among the terminal fields within the amygdala and adjacent cortical areas.

Amygdala↗
PubMedDate not supplied

[Effect of ablation of the basolateral and corticomedial portions of the amygdala on the performance of food-getting conditioned reflexes in rats].

In experiments on 66 albino rats an electrolytic coagulation of the basolateral amygdala caused facilitation while that of the corticomedial amygdala caused inhibition of alimentary conditioned reflexes. The corticomedial amygdala forms a part of the excitatory and the basolateral amygdala--of the inhibitory system of the rat's brain. In intact rats the basolateral amygdala function dominates over the corticomedial amygdala activity in feeding behaviour.

Amygdala↗
PubMed1976

Temporal neocortical afferent connections to the amygdala in the rhesus monkey.

The temporal neocortical afferent connections to the amygdala were investigated in the rhesus monkey using the silver impregnation and autoradiographic tracing methods. A large topographically organized projection to the amygdala was found to originate from the anterior superior temporal gyrus (area TA), the anterior middle and inferior temporal gyri (area TE), and the medial and lateral aspects of the temporal pole (area TG). These projections terminate in discrete adjacent regions of the lateral and basal amygdaloid nuclei. The temporal pole projection terminates in the ventral two thirds of the medial one half of the lateral nucleus and in the accessory basal nucleus, the anterior superior temporal gyrus projection terminates in the ventral two thirds of the lateral one half of the lateral nucleus, and the anterior middle and inferior temporal gyri projection terminates in the dorsal parts of the lateral and lateral basal nuclei. A projection from the perirhinal cortex to the medial basal nucleus of the amygdala is also discussed. Our findings reveal that a far greater proportion of the temporal neocortex than previously described contributes afferents to the amygdala, further strengthening the view that the amygdala occupies a key anatomical position linking the neocortex with diencephalic structures.

Afferent Pathways↗
PubMed1977

Inhibiton of neurons in the amygdala by dorsal raphe stimulation: mediation through a direct serotonergic pathway.

This study presents data showing that the dorsal raphe nucleus (DRN) has a marked inhibitory influence upon neurons in the amygdala and that this inhibitory effect is mediated by a direct DRN-amygdala serotonergic pathway. The evidence may be briefly summarized as follows:(1) on the same amygdaloid cells, both iontophoresis of serotonin (5-HT) and electrical stimulation of the DRN markedly inhibited spontaneous single unit activities; (2) the latency of DRN-induced inhibition was relatively short and is compatible with the conduction velocities (which were determined by antidromic activation of the 5-HT pathway) of unmyelinated 5-HT fibers; (3) destruction of 5-HT projections by 5,7-dihydroxytryptamine (5,7-DHT) or pharmacological depletion of 5-HT by parachlorophenylalanine (PCPA) prevented the inhibitory responsed to DRN stimulation in the great majority of cells studied; (4) in PCPA-pretreated animals, injection of 5-hydroxytryptophan (5-HTP) reversed the PCPA effect, restoring the responses of amygdaloid cells to DRN stimulation. In the amygdala, the presumptive 5-HT antagonists which we tested did not block the inhibitory effects of 5-HT except that intravenously administered LSD blocked the inhibitory responses produced by submaximal DRN stimulation. The implications of these results for the possible functions of 5-HT in the amygdala is discussed.

5-Hydroxytryptophan↗
PubMed1977

Unit activity of amygdala and hippocampal neurons: effects of morphine and benzodiazepines.

The effects of morphine sulfate and two benzodiazepine derivatives, chlordiazepoxide HCl and diazepam, were evaluated upon single unit activity of the amygdaloid nuclear complex and hippocampal formation in immobilized cats. All surgical procedures were performed under halothane anesthesia and all wound margins were infiltrated with Lidocaine after halothane withdrawal. Single unit activity was recorded extracellularly with platinum-iridium microelectrodes. Chlordiazepoxide HCl, 10.0-20.0 mg/kg i.v., or diazepam, 0.05-0.20 mg/kg i.v., suppressed spontaneous firing rates of the amygdala and the hippocampal neurons. In contrast, the spontaneous firing rates of neurons in these limbic structures were augmented by morphine sulfate, 0.50-2.00 mg/kg i.v. The morphine-induced augmentation of hippocampal neuronal activity was effectively antagonized by naloxone, 0.10-0.20 mg/kg i.v. However, naloxone, 0.20-0.40 mg/kg i.v., only partially suppressed the morphine induced augmentation of amygdala neuronal activity. In a dose-dependent fashion, chlordiazepoxide and diazepam administration prevented or antagonized morphine-induced augmentation of amygdala and hippocampal neuronal activity. Our results suggest that, in the cat, the amygdala and hippocampus may play an important role for morphine-induced behavioral responses. Moreover, our data imply that these two limbic structures may be the sites of tranquillizing actions of diazepam and chlordiazepoxide.

Action Potentials↗
PubMed1977

Brightness discrimination learning under conditions of cue enhancement by rats with lesions in the amygdala or hippocampus.

Three groups of rats, one with amygdala lesions, one with hippocampal lesions and a control group were trained on a brightness discrimination task under one of three different conditions, enhancement of the negative cue, enhancement of the positive cue or a non-enhanced condition. Animals with amygdala lesions showed retarded learning compared with normal animals and those with hippocampal lesions under the positive cue enhancement condition. Under the negative cue enhancement condition animals with hipocampal lesions were significantly handicapped compared with the other two groups. Results are discussed in relation to the Douglas and Pribram concept of a reciprocal linking of the amygdala and hippocampal systems in discrimination learning with the amygdala functioning as a reinforce register system and the hippocampus as an error evaluation system.

Amygdala↗
PubMed1979

Effects of focal vs generalized kindled convulsions from anterior neocortex or amygdala on CER acquisition in rats.

Kindling of the anterior neocortex (AC) was shown to produce a brief focal motor seizure, characterized by a clonic-tonic-clonic response of the forelimbs with the animal in a prone posture. These same brief seizures, as previously reported, did not produce retrograde amnesia in a CER paradigm. With repeated evocations, over several days, the AC convulsions exhibited a dramatic increase of the second clonic phase (generalized) and came to appear similar to amygdala kindled convulsions. These generalized AC convulsions, like briefly kindled amygdala convulsions, produced good retrograde amnesia for a CER. With extensive amygdala kindling prior to CER training, a severe CER acquisition deficit was observed. These latter as well as other data suggest that protracted amygdala kindling produces a subsequent reduced ability to acquire fear motivated responses.

Amygdala↗
PubMed1978

Effects of posttraining injection of cholinergic agonists and antagonists into the amygdala on retention of passive avoidance training in rats.

Rats were given a single footshock while licking a water tube and tested 24 hr later for retention of the footshock experience. A single bilateral injection of a subseizure dose of physostigmine into the amygdala applied immediately, but not 18 hr, after the footshock imparied retention. This effect appeared to be somewhat localized, as physostigmine injected into the hippocampus or lateral ventricles did not disrupt retention. Conversely, a subseizure dose of atropine sulfate into the amygdala, given immediately or 18 hr after the footshock did not impair retention. Atropine injected concurrently with physostigmine into the same amygdaloid loci counteracted a potential physostigmine-induced retention deficit. Injection of carbachol into the amygdala also impaired retention; however, carbachol precipitated seizures and possibly exerted proactive consequences on performance. The time-dependent nature of the deficit following physostigmine is consistent with the view that injection of cholinergic agonists into the amygdala disrupts memory for the footshock experience.

Amygdala↗
PubMed1976

Suppression and disinhibition of instrumental alimentary reactions after successive lesions of the dorsomedial and lateral amygdala in dogs.

Damage of the dorsomedial amygdala produced impairment of instrumental performance to CS(+) with no changes to CS(-). Subsequent lesion of the lateral amygdala resulted in restoration of instrumental performance to CS(+) and transient disinhibition to CS(-). These results support the hypothesis that the dorsomedial amygdala is involved in facilitation, while the lateral amygdala in inhibition of alimmentary reactions.

Amygdala↗
PubMed2025

Histone Arginine Methylation Regulates Neuropeptide Y Expression in the Basolateral Amygdala to Promote Reward-Seeking Behaviour.

The basolateral amygdala (BLA) serves in the evaluation of reward. However, the causal molecular substrates in the BLA necessary for reward seeking behaviour are largely unknown. Reward conditioning induces long-lasting changes in epienzymes in limbic areas, including the amygdala. The current study probed the role of histone arginine methylation as a novel epigenetic mechanism in neuropeptide Y (NPY) gene regulation in the BLA during reward and reinforcement. For reward conditioning, adult Wistar rats were trained to self-administer sucrose pellets in a nose-poke operant chamber. Reward conditioning increased protein arginine methyltransferase 4 (PRMT4) and NPY in the BLA. Moreover, after operant conditioning, histone arginine methylation (H3R17me2a) and PRMT4 occupancy at the NPY promoter were heightened. PRMT4 was predominantly colocalised in the nucleus of the NPY-expressing cells in the BLA. Intra-BLA administration of specific siRNA or inhibitor of PRMT4 after conditioning waned the nose-poke activity, which was further reinstated during the subsequent 5 days. These effects of PRMT4 repression were correlated with the NPY expression and H3R17me2a levels at the NPY promoter. Furthermore, NPY peptide administration after PRMT4 siRNA or inhibitor infusion in BLA restored the nose-poke activity. PRMT4 is known to interact with CREB-binding protein (CBP). Therefore, co-occupancy of PRMT4 and CBP resulted in heightened histone acetylation (H3K14ac) in the conditioned rats. The current study suggests a pivotal role of PRMT4-mediated histone arginine methylation in NPY gene expression in the amygdala necessary for the reward-seeking behaviour.

Animals↗
PubMed1979

Differential effects of basolateral amygdala lesions on behavior, corticosterone, and prolactin responses.

The present experiment examines hormone-behavior relationships following manipulation of the amygdala. Affective behavior and levels of corticosterone and prolactin were compared in rats with lesions of the basolateral amygdala and in nonlesioned and sham-operated controls. Animals with lesions of the basolateral amygdala were found to be hyperreactive and to have normal resting levels of corticosterone and prolactin but potentiated corticosterone responses to stress. Normal prolactin stress responses were unaltered by the lesion. The results are discussed in relation to behavioral and endocrine changes seen following other limbic system lesions.

Amygdala↗
PubMedDate not supplied

[Role of the amygdala in the occurence of oro-alimentary signs of during epileptic seizures in man (author's transl)].

The authors study the role of amygdala dysfunction in cases of oro-alimentary signs occuring in seizures recorded during a series of stereo-electroencephalographic investigations (S.E.E.G.) carried out for neurosurgical purposes. The patients under study have an epilepsy that is resistant to drug therapy. This work concerns 89 seizures with "oro-alimentary motor activity" recorded in 59 patients with whom it was possible to establish sufficiently rigourous anatomical - electrical - clinical correlations. This study enabled us to show that : --a seizure characterized by "oro-alimentary motor" signs (with the exclusion of swallowing movements) is related to a discharge that directly involves the amygdala. --a critical discharge affecting the anterior temporal region is expressed as : oro-alimentary activity either accompanied or not by other signs (breaking contact is exceptional). --late "oro-alimentary motor activity" also indicates disorganization of the amygdala, but offers no conclusion on the origin of the discharge.

Amygdala↗
PubMed1976

Interactions of amygdala lesions with effects of pilocarpine and d-amphetamine on mouse killing, feeding, and drinking in rats.

Repeated injections of 7.5 mg/kg pilocarpine induced mouse killing in both amygdala-lesioned and sham-operated rats, but more injections were required in the lesioned animals. Killing was evoked least readily in rats that showed substantial weight loss after surgery and that had damage to more medial regions of the amygdala. d-Amphetamine (.75, 1.50, or 3.00 mg/kg), administered either before or after a killing test, inhibited pilocarpine-induced killing in both surgical groups. Amygdala lesions attenuated pilocarpine-facilitated drinking in sated animals but did not alter the inhibitory effects of either pilocarpine or d-amphetamine on feeding or drinking.

Aggression↗