Facilitatory and inhibitory effects of electrochemical stimulation of the amygdala on the release of luteinizing hormone

Beltramino, C.; Taleisnik, S.

doi:10.1016/0006-8993(78)90437-7

Cited by 107 publications

(43 citation statements)

References 26 publications

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“…The cortical amygdala lesions which we have demon strated to significantly attenuate the morphine-induced de pression of LH correspond with sites diagrammed as inhibi tory to gonadotropin release by Bellramino and Taleisnik [4]. Thus, our demonstration of the attenuation of mor phine's depression of serum levels of LH following such ex trahypothalamic lesions is consistent with the observed in hibitory influence of the amygdala revealed by electrical stimulation in this area.…”

Section: Discussionsupporting

confidence: 77%

“…Likewise, bilateral microinjections of luteiniz ing releasing hormone (LHRH) into the PAG induces lor dosis in female rats [40,44], The PAG region has projections to the amygdaloid nuclei [ 1,18, 34], including ascending se rotonergic projections from the raphe [3,6,14,15,31] which provide an inhibitory influence on amygdaloid neuronal activity [49]. The amygdala has been demonstrated to exert both facilitatory and inhibitory influences on the neuro endocrine regulation of LH release [4] as well as an electrophysiological influence on various hypothalamic nuclei [39]. Like the PAG, high concentrations of opiate receptors in the rhesus monkey and rat brain are present in the amyg dala [2,27].…”

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confidence: 99%

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Attenuation of Morphine’s Depression of Serum Luteinizing Hormone by Lesions in the Amygdala

Lakoski¹,

Gebhart²

1981

Neuroendocrinology

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The administration of morphine or opioid peptides produces alterations in the neuroendocrine regulation of anterior pituitary hormone secretion, including the depression of serum levels of luteinizing hormone (LH). Central nervous system sites mediating the opioid-induced depression of serum levels of LH are not well understood. Discrete bilateral electrolytic lesions of amygdaloid nuclei or the periaqueductal central gray (PAG) were employed to investigate the role of these extrahypothalamic regions in the morphine-induced depression of serum levels of LH in the male rat. Lesions of the cortical amygdaloid nucleus, but not the medial, central or basolateral nuclei, significantly attenuated the depression of serum levels of LH 60 min following the acute administration of morphine (7.5 mg/kg). These results were independently replicated in different 10- and 22-day postlesion studies. Bilateral lesions of the medial region of the PAG, which did not encroach upon the dorsal raphe nucleus, elevated basal levels of serum LH. While morphine-treated subjects with bilateral lesions of the PAG exhibited significantly elevated serum levels of LH compared to sham lesion control subjects, no attenuation of the morphine-induced depression of serum levels of LH was observed 21 days following lesions of the PAG. These results indicate that the cortical nucleus of the amygdala, but not other amygdaloid nuclei or the PAG, is an extrahypothalamic site involved in the mediation of narcotic-induced changes in gonadotropin secretion in the male rat.

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Section: Discussionsupporting

confidence: 77%

mentioning

confidence: 99%

Attenuation of Morphine’s Depression of Serum Luteinizing Hormone by Lesions in the Amygdala

Lakoski¹,

Gebhart²

1981

Neuroendocrinology

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“…When male rats are exposed to urine from an estrous female, LH levels are increased within several minutes (Kamel et al, 1977). Electrical stimulation of the MeA is known to increase LH secretion (Beltramino and Taleisnik, 1978), and the MeA is well positioned anatomically to mediate signals from the AOB to the neurons that regulate LH release (De Vries and Simerly, 2002). Evidence in support of left-sided control of LH comes from a study of women with temporal lobe epilepsy.…”

Section: Laterality Of Meapd Sexual Dimorphismmentioning

confidence: 99%

Sexually Dimorphic Synaptic Organization of the Medial Amygdala

2005

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The medial amygdala is important in social behaviors, many of which differ between males and females. The posterodorsal subnucleus of the medial amygdala (MeApd) is particularly sensitive to gonadal steroid hormones and is a likely site for gonadal hormone regulation of sexually dimorphic social behavior. Here we show that the synaptic organization of the MeApd in the rat is sexually dimorphic and lateralized before puberty. With the use of whole-cell voltage-clamp recording and quantitative electron microscopy, we found that, specifically in the left hemisphere, prepubertal males have ϳ80% more excitatory synapses per MeApd neuron than females. In the left but not the right MeApd, miniature EPSC (mEPSC) frequency was significantly greater in males than in females; mEPSC amplitude was not sexually dimorphic. Paired-pulse facilitation of EPSCs, an index of release probability, also was not sexually dimorphic, suggesting that greater mEPSC frequency is caused by a difference in excitatory synapse number. Electron microscopy confirmed that the asymmetric synapse-to-neuron ratio and the total asymmetric synapse number were significantly greater in the left MeApd of males than of females. In contrast to results for excitatory synapses, we found no evidence of sexual dimorphism or laterality in inhibitory synapses. Neither the frequency nor the amplitude of mIPSCs was sexually dimorphic or lateralized. Likewise, the number of symmetric synapses measured with electron microscopy was not sexually dimorphic. These findings show that the excitatory synaptic organization of the left MeApd is sexually differentiated before puberty, which could provide a sexually dimorphic neural substrate for the effects of hormones on adult social behavior.

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“…Additionally, LHRH immunoreactive fibers project to the interpeduncu lar nucleus and dorsal midbrain, regions which contain neurons strongly responsive to lordosis trigger stimuli, and where lesions impair lordosis in hamsters [29,30]. We can not say whether vomeronasal signals normally lead to the release of LHRH, or whether LHRH influences lordosis in dependently: however, there is evidence which implicates the accessory olfactory system in LHRH release [2][3][4]10] and in raised serum luteinising hormone, an effect that can be prevented by vomeronasal organ removal [5].…”

Section: Discussionmentioning

confidence: 89%

Removal of the Vomeronasal Organ Impairs Lordosis in Female Hamsters: Effect Is Reversed by Luteinising Hormone-Releasing Hormone

Mackay‐Sim¹,

Rose

1986

Neuroendocrinology

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In female golden hamsters, vomeronasal organ removal disrupts the elicitation of lordosis by lumbosacral tactile stimulation. A similar disruption occurs if the nasopalatine ducts are closed, without removing the vomeronasal organ. Injection of luteinising hormone-releasing hormone reverses the effect of vomeronasal organ removal. These findings suggest that chemosensory signals from the male hamster act via the accessory olfactory system, to facilitate the triggering of lordosis by somatic stimulation.

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Facilitatory and inhibitory effects of electrochemical stimulation of the amygdala on the release of luteinizing hormone

Cited by 107 publications

References 26 publications

Attenuation of Morphine’s Depression of Serum Luteinizing Hormone by Lesions in the Amygdala

Attenuation of Morphine’s Depression of Serum Luteinizing Hormone by Lesions in the Amygdala

Sexually Dimorphic Synaptic Organization of the Medial Amygdala

Removal of the Vomeronasal Organ Impairs Lordosis in Female Hamsters: Effect Is Reversed by Luteinising Hormone-Releasing Hormone

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