Relationship of some open-field behaviors to amygdaloid kindled convulsions in Wistar rats

Repeated low-intensity electrical stimulation (kindling) of the amygdala eventually produces convulsive behavior in animals. The present study examined the relationship between behaviors displayed in a novel open-field situation with behavioral characteristics of the kindled clonic convulsion (CC). Wistar rats were given two open-field tests and were subsequently kindled to clonic convulsions. A multiple regression analysis indicated that rats which urinated more often in the open-field tests tended to show longer latencies to CC onset. Thus, open-field urination was a significant predictor of latency to CC onset. It is suggested that an emotionality construct may be related to rate of kindling.     

Divergent axon collaterals to cerebellum and amygdala from neurons in the parabrachial nucleus, the nucleus locus coeruleus and some adjacent nuclei

Summary After injections in the cat of Rhodamine labelled latex microspheres in the amygdala and of Fast Blue in the cerebellum neurons labelled with one of these tracers as well as some double labelled neurons were found in the parabrachial nucleus, the nucleus locus coeruleus and some adjacent nuclei (the nucleus subcoeruleus and the pontine tegmental reticular formation). All double labelled cells were located on the ipsilateral side. A few double labelled neurons were also found bilaterally in the dorsal raphe nucleus. It therefore appears that a certain number of cerebellar projecting neurons in these brain stem nuclei by means of divergent axon collaterals also project to the amygdala. The location of the double labelled cells found in this study suggests that at least some of the neurons are catecholaminergic. The findings are related to previous reports on the distribution of catecholaminergic neurons and on the amygdaloid and cerebellar projections from this part of the brain stem, and the possible involvement of these connections in cerebellar non-somatic responses are discussed. Some comments are made concerning the use of fluorescent latex microspheres for double labelling studies in combination with another fluorescent tracer.     

不同剂量托吡酯对癫癎大鼠临床发作与脑电活动的影响

目的:观察不同剂量托吡酯对癫癎大鼠临床发作及脑电活动的影响。方法:选取雄性健康Wistar大鼠60只制作杏仁核点燃模型,然后用托吡酯(分20、40、80 mg／kg三组)进行灌胃,记录用药后杏仁核后放电阈值、皮层及杏仁核后放电持续时间及大鼠双前肢抽动时间。结果:托吡酯灌胃后相同强度电刺激点燃大鼠所需刺激次数明显增加;托吡酯(40、80 mg／kg)灌胃后4 h,杏仁核后放电阈值升高、杏仁核及皮层后放电时程缩短、双前肢抽动时间缩短。结论:托吡酯可明显缩短杏仁核点燃大鼠癫 癎发作时间,缩短杏仁核及皮层后放电持续时间,升高杏仁核后放电阈值。     

Neuroanatomical Correlates of Skin Conductance Orienting in Normal Humans: A Magnetic Resonance Imaging Study

Although little is known about the neuroanatomical basis of skin conductance orienting in intact normal humans, the limited literature on animals and humans with neurological and clinical disorders implicate prefrontal, temporal/amygdala, and pons brain areas in mediating skin conductance orienting. This study relates area of these structures using magnetic resonance imaging techniques to skin conductance orienting responses in 17 normal humans in order to test hypotheses that larger area of these excitatory structures will be associated with more orienting responses. Left and right hand skin conductance orienting was significantly associated with left and right prefrontal area (r = .44-.60), area of the pons (r = .43-.54), and left but not right temporal/amygdala area (r = .47-.53). No relationships were observed with areas thought to be unrelated to skin conductance activity (cerebellum, nonfrontal cortical area), medial prefrontal cortex, or the third ventricle. This appears to be the first study relating brain structure to skin conductance orienting in intact normal humans. Although preliminary at the present time, these results implicate prefrontal, pons, and temporal/amygdala areas in the mediation of skin conductance orienting in normal humans.     

Physostigmine and norepinephrine: Effects of injection into the amygdala on taste associations

The present investigation was conducted to determine whether norepinephrine or acetylcholine systems of the amygdala could be involved in two adaptive feeding behaviors in the rat: development of taste aversion and recovery from neophobia. In a taste aversion paradigm, a single bilateral injection of physostigmine directly into the amygdala at the onset of an apomorphine-induced illness experience produced a time-dependent attenuation in the development of taste aversion; in contrast, norepinephrine had no disruptive effects. In a neophobia paradigm, norepinephrine injected directly into the amygdala after a novel taste experience resulted in a time-dependent attenuation in recovery from neophobia; however, physostigmine produced no disruptive effects. Hence, acetylcholine appears to mediate taste-illness associations, while norepinephrine plays an important role in recovery from neophobia, i.e., taste-“learned safety” associations.     

Amygdala kindling and muricide in rats

It was demonstrated that home cage muricide in the Wistar rat was uneffected by bilateral amygdala after-discharge threshold (ADT) reduction. The subsequent kindling of the amygdala, however, resulted in an apparent facilitation in the onset of the predatory response. In a larger predatory arena, the above manipulations had no effect upon the muricide response of Royal Victoria Hooded rats. There were no obvious amygdala EEG correlates of muricidal versus non-muricidal rats, e.g., differences in ADT, AD duration, kindling rate, etc. In addition, the ADT of the two amygdalae were seemingly independent. Similarly, ADT reduction and/or kindling had no effect upon the contralateral amygdala ADT. As has been previously shown, kindling of one amygdala significantly facilitated the rate of motor seizure development from the second, as well as provoking changes in the onset latency to motor seizure. The muricide data were discussed in the context of kindled induced synaptic facilitation and functional lesion effects.     

Clinical patterns of patients with temporal lobe epilepsy and pure amygdalar atrophy

PURPOSE: MRI volumetric measurements (MRIvol) have been proven reliable in determining mesial temporal atrophy in patients with TLE. We attempted to correlate the clinical features with different patterns of hippocampal formation (HF) and amygdala (AM) atrophy in patients with TLE without foreign tissue lesion. METHODS: We studied 65 patients with refractory TLE. They were divided into five groups according to MRIvol results: pure AM atrophy (n = 11, 10 unilateral and one bilateral), unilateral HF atrophy (n = 16), bilateral HF atrophy (n = 12), unilateral AM + HF atrophy (n = 13), and patients with normal volumes of AM and HF (n = 13). MRIvol of AM and HF were performed by using a protocol previously described by Watson et al. (Neurology 1992;42:1743-50). RESULTS: Patients with AM atrophy had later onset of seizures compared with those with unilateral HF atrophy (p < 0.01). History of febrile convulsions (p < 0.0001) and frequent secondarily generalized tonic-clonic seizures (GTCSs) were more often found in patients with HF atrophy compared with those with pure AM atrophy and those with normal volumes (p = 0.04). Prolonged postictal confusion was more often found with AM atrophy (p = 0.05). Memory impairment was more severe in patients with HF atrophy than in those with AM atrophy only or in those with normal volumes (p = 0.03). There were no significant differences among the five groups in the following parameters: age, duration of epilepsy, seizure frequency, and presence and type of aura. CONCLUSIONS: Prolonged postictal confusion appeared to be related to AM atrophy, in keeping with previous clinical observations. These patients also had a lower incidence of early febrile convulsions, older age at epilepsy onset, lower frequency of secondary GTCS, and lesser memory dysfunction compared with patients with hippocampal atrophy.     

Environmental Influences on Neural Plasticity, the Limbic System, Emotional Development and Attachment: A Review

The effects of early environmental influences on neural plasticity, the limbic system, and social and emotional development are reviewed and an illustrative case study is briefly discussed. Deprived or abnormal rearing conditions induce severe disturbance in all aspects of social and emotional functioning, and effect the growth and survival of dendrites, axons, synapses, interneurons, neurons, and glia. The amygdala, cingulate, and septal nuclei develop at different rates which correlate with the emergence of wariness, fear, selective attachments, play behavior, and the oral and phallic stages of development. These immature limbic nuclei are experience-expectant, and may be differentially injured depending on the age at which they suffer deprivation. The medial amygdala and later the cingulate and septal nuclei are the most vulnerable during the first three years of life. If denied sufficient stimulation these nuclei may atrophy, develop seizure-like activity or maintain or form abnormal synaptic interconnections, resulting in social withdrawal, pathological shyness, explosive and inappropriate emotionality, and an inability to form normal emotional attachments.     

Enhanced conditioned inhibition following repeated pretreatment with d-amphetamine

We have shown that prior repeated exposure to d-amphetamine facilitates appetitive Pavlovian conditioning. However, animals sensitised in this manner also show elevated levels of stimulated activity. To investigate whether enhanced conditioning was dependent upon increased activity, a conditioned inhibition task was employed in the present study. Rats received d-amphetamine (2 mg/kg, IP) or vehicle once per day for 7 days. After a 7-day drug-free period, an activity assay confirmed that repeated d-amphetamine treatment markedly elevated the locomotor response to a subsequent challenge with 0.5 mg/kg d-amphetamine. Conditioning began 6 days later. In phase 1, stimulus A+ (light or tone) immediately preceded sucrose availability (excitatory conditioning). In phase 2, sucrose again was presented after A+ alone, but not after presentation of a compound of A+ with a second stimulus (AB−). Sensitisation enhanced the acquisition of conditioned approach behaviour to the excitatory stimulus A+ in phase 1. Furthermore, acquisition of conditioned inhibition to the stimulus compound, AB−, was also facilitated. Thus, sensitised rats showed reduced levels of responding to the stimulus compound far sooner than controls. Finally, a retardation test was carried out in stage 3, in which the inhibitory stimulus B- was paired alone with sucrose reward. Sensitised rats initially showed retarded acquisition of excitatory conditioned responding relative to controls, suggesting that B possessed stronger inhibitory associations in these animals. However, sensitised animals again exhibited higher levels of responding in later sessions, consistent with the enhanced excitatory conditioning shown in phase 1. These findings suggest that prior repeated d-amphetamine enhanced the acquisition of inhibitory and excitatory Pavlovian associations; a propensity not readily attributable to stimulated locomotor hyperactivity. Received: 29 December 1997/Final version: 21 July 1998