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PubMed1996

Posterodorsal amygdaloid lesions in rats: long-term effects on body weight.

Bilateral lesions in the most posterodorsal aspects of the amygdala in female rats resulted in immediate and dramatic weight gains on a standard lab chow diet. The rate of weight gain returned to normal by Day 20, but the difference in body weight between animals with amygdaloid lesions and those with sham lesions was maintained for the duration of the study (60 days). Because rats with posterodorsal amygdaloid lesions have also been found to be hyperinsulinemic, it is hypothesized that the lesions result in a similar, though smaller, version of the syndrome that follows lesions of the ventromedial hypothalamus.

Amygdala↗
PubMed2006

Immunohistochemical localisation of the NK1 receptor in the human amygdala: preliminary investigation in schizophrenia.

The amygdala has a role in the modulation of moods and emotion, processes that are known to be affected in people with psychiatric disorders such as schizophrenia and depression. The tachykinin NK(1) receptor is known to be expressed in the amygdala. However to date, there is limited knowledge of the distribution of the NK(1) receptor in this region. This study used immunohistochemistry to analyse the distribution of the NK(1) receptor in fixed human amygdala tissue in control subjects with no history of psychiatric illness and matched subjects with a diagnosis of schizophrenia (n=4 pairs). The NK(1) receptor was observed sparsely distributed in cell bodies in all amygdaloid nuclei with the basolateral and lateral having a greater relative density of NK(1) receptor-immunoreactive cell bodies than the other nuclei. Double labelling with antibodies to microtubule associated protein and the NK(1) receptor revealed that the NK(1) receptor is expressed by large pyramidal, small stellate and large bipolar neurons. Interestingly, the basal nucleus of Meynert, which is just dorsal to the amygdala, was observed to have a significantly higher relative density of NK(1) receptor-immunoreactive cell bodies compared to any of the amygdaloid nuclei. Preliminary analysis of the density of NK(1) receptor-immunoreactive cell bodies in the major amygdaloid nuclei and the basal nucleus of Meynert revealed no significant differences between schizophrenia and control subjects. Real-time PCR showed that the mRNA for both the short and long isoforms of the NK(1) receptor was expressed at low levels in fresh frozen human amygdala tissue from control subjects and that this was not different in matched subjects with schizophrenia (n=11 pairs). In conclusion, this study has demonstrated that the NK(1) receptor is widely distributed in the amygdala, and has shown for the first time a high relative density of NK(1) receptor-immunoreactive cell bodies in the basal nucleus of Meynert.

Adult↗
PubMed2001

A neuropathological study of the disturbance of the nigro-amygdaloid connections in brains from patients with dementia with Lewy bodies.

We neuropathologically and immunohistochemically investigated characteristics of the central amygdaloid nucleus lesion and its relationship with the substantia nigra lesion in dementia with Lewy bodies (DLB) brains. Nine DLB, four Parkinson's disease (PD) and four Alzheimer-type dementia (ATD) cases were examined. The degree of neuronal loss in the substantia nigra was (+)-(+++) in DLB cases, (+++) in PD cases and (+) in ATD cases. All DLB cases showed spongy change and ubiquitin-positive spheroids in the central nucleus. The degree of spongy change was (+)-(+++) in DLB cases, (+) in PD cases and (-)-(+) in ATD cases, which was correlated with the degree of neuronal loss in the substantia nigra in DLB cases. The number of ubiquitin-positive spheroids was parallel to the degree of spongy change. The central nucleus receives dense dopaminergic fibers from the substantia nigra. Many ubiquitin-positive spheroids were also positive to alpha-synuclein and tyrosine-hydroxylase, suggesting that they derive from the degeneration of terminal or distal axons of Lewy body-bearing dopaminergic neurons in the substantia nigra. The disturbance of the dopaminergic connections from the substantia nigra to the central nucleus may be responsible for psychotic symptoms in DLB patients.

Aged↗
PubMed2001

[A 64-year-old man with parkinsonism as an initial symptom followed by dementia associated with marked abnormal behaviours].

We report a 64-year-old man with parkinsonism as an initial symptom, which was followed by dementia and abnormal behaviours. He was well until 1985, when he was 49 years old, when he noted rest tremor in his right hand. Soon tremor appeared in his left hand as well. He was seen in our clinic and levodopa was prescribed. He was doing well with this medication, however, in 1993, he started to suffer from on-off phenomenon. He also noted visual hallucination. In 1994, he stole a watermelon and ate it in the shop. He repeated such abnormal behaviours. In 1995, he was admitted to the neurology service of Hatsuishi Hospital. On admission, he was alert and oriented. He did not seem to be demented; however, he admitted stealing and hypersexual behaviours. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, downward gaze was markedly restricted. He showed masked and seborrhoic face, and small voice. No motor palsy was noted, but he walked in small steps with freezing and start hesitation. Marked neck and axial rigidity was noted. Tremor was absent except for in the tongue. No cerebellar ataxia was noted. Deep tendon reflexes were diminished. Plantar response was extensor bilaterally. Forced grasp was noted also bilaterally. He was treated with levodopa and pergolide, but he continued to show on-off phenomenon. His balance problem and akinesia became progressively worse; still he showed hypersexual behaviour problems. He also showed progressive decline in cognitive functions. In 1997, he started to show dysphagia. He developed aspiration pneumonia in July of 1998. In 1999, he developed emotional incontinence and became unable to walk. He also developed repeated aspiration pneumonia. He died on March 1, 2000. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had corticobasal degeneration. Other diagnoses entertained included dementia with Lewy bodies, diffuse Lewy body disease, and frontotemporal dementia. Majority of the participants thought that diffuse Lewy body disease was most likely. Post-mortem examination revealed marked nigral neuronal loss, gliosis and Lewy bodies in the remaining neurons. Abundant Lewy bodies of cortical type were seen wide spread in the cortical areas, but particularly many in the amygdaloid nucleus. Lewy bodies were also seen in the subcortical structures such as the dorsal motor nucleus, oculomotor nucleus, Meynert nucleus, putamen, and thalamus. What was interesting was marked neuronal loss of the pontine nuclei, demyelination of the pontocerebellar fiber, and moderate neuronal loss of the cerebellar Purkinje neurons, a reminiscent of pontocerebellar atrophy. However, the inferior olivary nucleus was intact.

Brain↗
PubMed1988

Pattern of in vivo release of endogenous histamine in the mamillary body and the amygdala.

The mamillary body and the medial amygdaloid nucleus of cats anaesthetized with sodium pentobarbital were bilaterally and simultaneously superfused through push-pull cannulae with CSF and the release of endogenous histamine was determined in the superfusates. Collection of the superfusates in 10 min time periods revealed that histamine was rhythmically released in the two areas with frequencies of one cycle/90 min (mamillary body) or one cycle/135 min (medial amygdaloid nucleus). Collection of the superfusates in time periods of 2 min revealed the existence of an additional ultradian rhythm with a frequency of approximately one cycle/19 min in both areas. Bilateral lesions of the suprachiasmatic nucleus did not seem to influence the pattern of histamine release in the mamillary body and the medial amygdaloid nucleus, but the rate of histamine release was decreased in the mamillary body. It is concluded that the ultradian rhythms of histamine release in the mamillary body and the medial amygdaloid nucleus are not dependent on the integrity of the suprachiasmatic nucleus. The rate of histamine release in the mamillary body seems to be under the influence of excitatory neurons which originate from the suprachiasmatic nucleus.

Activity Cycles↗
PubMedDate not supplied

Peptidergic transmission in the brain. VI. Behavioral consequences of central activation.

Having described a peptidergic transmitter system in the rat brain, we now begin to evaluate its behavioral function. We stimulated cell bodies in the medial amygdaloid nucleus (AME) with indwelling bilateral electrodes. These cell bodies contain a vasopressin-like peptide and send fibers to the hippocampus where the peptide is released upon stimulation. There the peptide inhibits hippocampal output in the awake rat just as it does in the anesthetized rat and in the rat brain slice. The stimulation reorganizes behavior with the same latency and duration as the hippocampal effect. For about 15-20 minutes after the brief stimulus, rats remain motionless with eyes wide open. This "freezing" state is punctuated by episodes of exploratory behavior. The stimulus appears to have a positive affective quality. Review of the literature in light of the present results indicates a probable role for this peptidergic system in the generation of sexual behavior in male rats.

Amygdala↗
PubMed2006

The distribution pattern of pathology and cholinergic deficits in amygdaloid complex in Alzheimer's disease and dementia with Lewy bodies.

We studied the distribution pattern of pathology and cholinergic deficits in the subnuclei of the amygdaloid complex (AC) in five patients with Alzheimer's disease (AD), eight with dementia with Lewy bodies (DLB) and five normal controls. In controls, the basal nucleus contained the highest choline acetyltransferase activity; the activity in the lateral and central nuclei and those in the cortical, medial and accessory basal nuclei were comparable. In AD, there was a significant decrease in choline acetyltransferase activity in the accessory basal and lateral nuclei, in DLB a significant decrease was observed in the accessory basal, lateral and cortical nuclei. Compared to controls the hyperphosphorylated tau-pathology burden was significantly higher in the basal, central and medial nuclei in AD and in the central, cortical, lateral and medial nuclei in DLB. The amyloid plaque burden was significantly higher in the accessory basal, basal, lateral and cortical nuclei in AD and in all nuclei in DLB. The alpha-synuclein burden was significantly higher in all nuclei in both AD and DLB. Compared to AD alpha-synuclein burden was higher in all nuclei in DLB. There were no correlations between the distribution pattern of hyperphosphorylated tau-pathology, amyloid plaques and alpha-synuclein-positive structures, and choline acetyltransferase activity, except the lateral nucleus in DLB. In conclusion we found no relationship between the pattern of cholinergic deficits and the distribution pattern of lesions in the AC of patients with AD or DLB. Cholinergic deficits were more prominent in the nuclei of basolateral (BL) group in AD, whereas the nuclei of both BL and corticomedial groups were involved in DLB, which may be due to the involvement of both basal forebrain and brainstem cholinergic nuclei in the latter.

Aged↗
PubMed1997

Thalamic and amygdaloid connections of the auditory association cortex of the superior temporal gyrus in rhesus monkey (Macaca mulatta).

Thalamic and amygdaloid connections of three association auditory areas (AA1, AA2, AA3) of the superior temporal gyrus (STG) were investigated. In order to define the projections of the particular areas, injections of fluorescent tracers were made in three monkeys. Distribution of labeling indicates that area AA1 differs from areas AA2 and AA3 in patterns of both thalamo-cortical and amygdalo-cortical connections. Area AA1 receives its predominant inputs from the ventral and dorsal nuclei of the medical geniculate body (MGB). The amygdaloid projection to the area AA1 originates from the basal nuclei, whereas input from the lateral nucleus was not found. The characteristic thalamic projections to areas AA2 and AA3 originate from the dorsal MGB nucleus and the polymodal nuclei of the posterior thalamus. The density of projections from the dorsal nucleus gradually decreases from area AA1 to area AA3 while projections from the Plm, Sg and Lim nuclei increase in the same direction. Areas AA2 and AA3 are the source of strong connections with the lateral nucleus of amygdala, which density increases progressively when injections shift from area AA2 to AA3. The basal and accessory basal nuclei are the source of a less significant amygdalofugal projections to both cortical areas. Thus, our experimental data indicate that influence of the polymodal thalamic nuclei increases substantially in the direction of the higher order association areas. The strong relation of the same cortical areas with the lateral amygdaloid nucleus might suggest that areas AA2 and AA3, in addition to auditory input are the site of transfer of complex sensory information to the amygdala.

Amygdala↗
PubMed1991

Patterns of histamine release in the brain.

The pattern of histamine release has been investigated in various brain areas of anaesthetized cats and conscious, freely moving rats by the push-pull technique. In the hypothalamus, medial amygdaloid nucleus and mamillary body of the anaesthetized cat, histamine was found to be released according to an ultradian rhythm with a frequency of 1 cycle per 1-2 h. Additionally, oscillations have been observed in the medial amygdaloid nucleus and mamillary body with a frequency of 1 oscillation per 10 min. In the posterior hypothalamus of the conscious rat, histamine is also released rhythmically with a frequency of 1 cycle per 1.5 h. Moreover, the release rate of histamine is increased in the night.

Amygdala↗
PubMed1983

Study of inhibitory effect of amygdaloid stimulation on auditory response of medial geniculate body (MGB) and analysis of transmissive pathway of the said effect.

Experiments performed on 103 rabbits immobilized with Flaxedil, and the recording of the electrical discharges of single MGB neuron caused by clicks, burst or sustained tone showed marked inhibition of the reaction of 47 out of 75 (62.7%) MGB units responding to sound stimuli, when the amygdaloid complex was stimulated. The latent period of such an inhibitory effect was 5-12 msec and its duration about 2-13 msec. Evoked responses with the latency of 1-2 msec for the stimulation of medial, central and lateral nuclei of amygdala could be recorded from the temporal and parietal cortex. The largest response was recorded from Woolsey's AI area of the temporal cortex. Stimulation of the Woolsey's AI auditory area could also result in a distinct inhibition of the spontaneous as well as the evoked discharges of MGB neurons in response to sound stimulation. Moreover, application of 1% procaine to the surface of auditory cortex could block the inhibitory effect of the amygdala on the MGB neurons. Based on the facts mentioned above, the authors have reason to believe that the inhibitory effect of the amygdaloid complex on the activity of MGB units might be transmitted via the amygdala-auditory cortex-MGB circuit. The biological significance of such an suppressive effect has been discussed.

Acoustic Stimulation↗