Disease relevance of Amygdala

• Generation of epileptic seizures by using kainic acid, a potent glutamate analog, elevated levels of NDF transcripts in limbic cortical areas, hippocampus, and amygdala [1].
• Thus, the present study suggests that a common mechanism may govern aggregation of alpha-synuclein and tau in the amygdala, and that aggregation of alpha-synuclein may play some role in the neurodegenerative process of a tauopathy (i.e. PDC) in which Abeta deposition is virtually absent [2].
• In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus [3].
• Lewy bodies in the amygdala: increase of alpha-synuclein aggregates in neurodegenerative diseases with tau-based inclusions [4].
• By using kindling by repetitive amygdala stimulation as a model of generalized seizure development in the rat, we have shown that dopamine receptor subsensitivity has been shown to occur in selected brain areas after the development of seizures [5].

Psychiatry related information on Amygdala

• Moreover, a single injection of morphine after SPARC infusion into the basolateral amygdala of previously uninjected mice substantially enhanced locomotor activity [6].
• Here we report that mice lacking Ras-GRF are impaired in the process of memory consolidation, as revealed by emotional conditioning tasks that require the function of the amygdala; learning and short-term memory are intact [7].
• We examined neural activity in rat orbitofrontal cortex and basolateral amygdala during instrumental learning in an olfactory discrimination task [8].
• MAIN OUTCOME MEASURES: Self-reports of depressive symptoms and anxiety were measured, as were global and relative glucose metabolism in the orbitofrontal, cingulate, lateral prefrontal, and insular cortices and the amygdala, striatum, and cerebellum [9].
• Therefore, decreased function of CREB in the central nucleus of the amygdala might regulate anxiety and alcohol intake via decreased expression of NPY, and might provide a common link between anxiety and alcohol abuse disorders [10].

High impact information on Amygdala

• stathmin, a gene enriched in the amygdala, controls both learned and innate fear [11].
• We identified the Grp gene, encoding gastrin-releasing peptide, as being highly expressed both in the lateral nucleus of the amygdala, the nucleus where associations for Pavlovian learned fear are formed, and in the regions that convey fearful auditory information to the lateral nucleus [12].
• Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala, in a pattern similar to that observed experimentally in animals after the administration of kainic acid, which is also structurally similar to glutamate and domoic acid [13].
• In the basolateral amygdala, endocannabinoids and CB1 were crucially involved in long-term depression of GABA (gamma-aminobutyric acid)-mediated inhibitory currents [14].
• Dopamine-mediated modulation of odour-evoked amygdala potentials during pavlovian conditioning [15].

Chemical compound and disease context of Amygdala

• Long-term satiation of mink increased the level of 5-hydroxyindole acetic acid in the lateral hypothalamus and amygdala and enhanced the latency of predatory aggression [16].
• Instrumental learning, but not performance, requires dopamine D1-receptor activation in the amygdala [17].
• These results suggest that exposure to a stressful event transiently activates NMDA receptors in basolateral/lateral nuclei of the amygdala and thereby induces a persistent enhancement of associative learning [18].
• Rats with bilateral, excitotoxic lesions of the basolateral amygdala readily acquired the i.v. self-administration of cocaine under a continuous reinforcement schedule, initially administering more infusions and maintaining a slightly elevated level of self-administration than controls [19].
• GABA-producing transplants had no significant effect on the rate of amygdala kindling, but the latency to the first generalized seizure during kindling was significantly increased in animals receiving GABA-producing cells [20].

Biological context of Amygdala

• Here we show that glutamatergic synaptic transmission to inhibitory interneurons in the basolateral amygdala is mediated solely by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors [21].
• Exposure to these cues increased ERK phosphorylation in the central, but not the basolateral, amygdala after 30 d, but not 1 d, of withdrawal [22].
• Visual stimuli induce expression of the immediate early gene Fos (also known as c-fos) in the auditory thalamus and the lateral amygdala in rewired mice, similar to the way auditory stimuli do in control mice [23].
• Specifically, seizure induction by KA injection into the amygdala induces tPA activity and cell death in both hippocampi, and unilateral treatment of rats with neuroserpin, a natural inhibitor of tPA in the brain, enhances neuronal survival in both hippocampi [24].
• When brain slices were incubated with tritium-labeled vasopressin, an intense concentration of binding sites was identified which included the medial aspects of the amygdala [25].

Anatomical context of Amygdala

• beta-Endorphin alters luteinizing hormone secretion via the amygdala but not the hypothalamus [26].
• Here we report for the first time that NMDA receptors of the dentate gyrus, where they do not normally contribute to the generation of synaptic potentials, become actively involved in synaptic transmission following long-lasting neuronal changes induced by daily electrical stimulation (kindling) of the amygdala or hippocampal commissures [27].
• POMC peptides have been detected immunohistochemically and biochemically in the medial basal hypothalamus, the amygdala and throughout the brain stem [28].
• In the nucleus accumbens somatostatin levels were increased threefold, while in the amygdala thyrotropin-releasing hormone levels were elevated [29].
• Severe deficits in the acquisition of an olfactory learning-set task resulted from lesions of the central (olfactory) component of the mediodorsal thalamic nucleus but not from large lesions that destroyed olfactory projections to the amygdala [30].

Associations of Amygdala with chemical compounds

• Second-order fear conditioning prevented by blocking NMDA receptors in amygdala [31].
• Prompted by this finding, we injected known acetylcholine (ACh) agonists and cholinesterase (ChE) inhibitors into the rat amygdala and found that either class of agent reproduces this type of S-BD syndrome [32].
• We have observed that DPE induces the S-BD syndrome by systemic but not intra-mygdaloid injection, whereas an oxidized DPE derivative which structurally resembles the cholinergic agonist oxotremorine is effective when injected into the amygdala [32].
• Increased sensitivity to the stimulant effects of morphine conferred by anti-adhesive glycoprotein SPARC in amygdala [6].
• Mechanism of the rapid effect of 17 beta-estradiol on medial amygdala neurons [33].

Gene context of Amygdala

• These results provide novel evidence of a requirement of PI-3 kinase activation in the amygdala for synaptic plasticity and memory consolidation, and this activation may occur at a point upstream of MAPK activation [34].
• The NPSR mRNA is widely distributed in the brain, including the amygdala and the midline thalamic nuclei [35].
• Lhx6 delineates a pathway mediating innate reproductive behaviors from the amygdala to the hypothalamus [36].
• Other regions such as hypothalamic nuclei and the central nucleus of the amygdala, also related to central CRH system but involved in the processing of the ascending visceral information and neuroendocrine-autonomic response to stress, did not show CRH-mediated ERK1/2 activation [37].
• Behavior consistent with increased anxiety was observed principally in ERbeta mutant females and was associated with a reduced threshold for the induction of synaptic plasticity in the basolateral amygdala [38].

Analytical, diagnostic and therapeutic context of Amygdala

• Microinjection of the cholecystokinin B antagonist L-365,260 into the amygdala blocked associative tolerance [39].
• We used intracerebral microdialysis to directly sample extracellular dopamine in the human amygdala during the performance of cognitive tasks [40].
• Western blot analysis of neuronal tissues taken from fear-conditioned rats showed a selective activation of phosphatidylinositol 3-kinase (PI-3 kinase) in the amygdala [34].
• As shown by immunohistochemistry and confocal microscopy analysis, CRH administration increased p-ERK1/2 levels specifically in the CA3 and CA1 hippocampal subfields and basolateral complex of the amygdala, both structures related to external environmental information processing and behavioral aspects of stress [37].
• The amygdala showed prominent expression, and overexpressing ASIC1a enhanced fear conditioning, an animal model of acquired anxiety [41].

References