Hippocampal amnesia

Abstract

A 35-year-old right-handed woman (CK) showed deficits in sorting and rating emotional facial expressions and experienced temporary emotional hyperarousal with panic attacks during a T2-signal enhancement of the reglon of the right amygdala. In a sorting task CK was able to match positive, but not negative, basic emotions. Furthermore CK rated most facial emotions as unpleasant and unaroused. In the further course, the neuroradiologically demonstrated lesion dlsappeared, as well as the Impaired Identification and judgement of emotional faclal expressions. The results suggest that a lesion of the right amygdala is sufficient to disturb the processing of emotional facial expressions.     

Hippocampal Amnesia

This article reviews 147 cases of amnesia following damage including the hippocampus or fornix as reported in 179 publications. The aetiology, mnestic abilities and reference(s) are tabulated for each case. Consistent findings across cases include the association of bilateral hippocampal damage with a deficit in anterograde episodic memory combined with spared procedural and working memory. The limited nature of retrograde amnesia following lesions to the fornix is also noted. Less consistent and thus more controversial findings, include effects of lesion size or laterality, deficits in semantic memory or familiarity-based recognition and the extent of retrograde amnesia. The evidence concerning these issues is reviewed across cases.     

移植齿状回颗粒细胞重建海马神经网络的方法研究

目的:探讨新生大鼠齿状回颗粒细胞在培养的海马组织切片上迁移特征。方法:从生后3d的绿色荧光蛋白(GFP)基因导入的SD大鼠海马组织中分离颗粒细胞层组织,分别移植到生后7d的宿主(野生型)SD大鼠海马组织切片的不同区域,施行共同培养6d,观察表达GFP的齿状回颗粒细胞的迁移方向和纤维投射。结果:当移植物移植到齿状回门区附近时,表达GFP的齿状回颗粒细胞迁移到宿主海马组织的齿状回门区和颗粒细胞层,并发出树突和轴突分别投射到齿状回的内分子层和CA3区。结论:移植的齿状回颗粒细胞在海马组织切片上迁移并发出神经纤维投射到CA3区,提示移植的齿状回颗粒细胞可能参与海马的局部神经网络。     

Hippocampal theta sequences

The activity of individual hippocampal principal neurons is spatially localized such that each neuron is active only when the animal occupies an area of the environment known as the cell's place field. Additionally, the activity of hippocampal neurons exhibits a particular temporal relationship to the hippocampal EEG, such that spikes fired by the neuron occur at progressively earlier phases of the co-occurring theta rhythm in the EEG as the animal traverses the place field. This relationship is known as theta precession. A long-standing prediction following the observation of theta precession has been that among a collection of hippocampal neurons recorded simultaneously, the neurons will fire in sequences reflecting the behavioral order of the place fields. Here we examine this prediction. We show that clear, ordered sequences occur during theta, which we name theta sequences, in which a portion of the animal's spatial experience is played out in forwards order. We further investigate the relationship of theta sequences to phase precession by shuffling spike phases in such a way as to preserve the relationship between spike phase and position. This jitter significantly reduces the prevalence of theta sequences while leaving theta phase precession intact, suggesting that the presence of theta phase precession is not trivially predictive of theta sequences. Finally, we discuss the relationship between theta sequences and individual place fields, and the possible functional role of theta sequences in navigational learning.     

Hippocampal sclerosis revisited

Studies dating back more than 150 years reported a relationship between hippocampal sclerosis and epilepsy. Retrospective studies of patients who underwent temporal lobectomy for intractable partial epilepsy found a relationship between a history of early childhood convulsions, hippocampal sclerosis, and the development of temporal lobe epilepsy. Many believe that febrile seizures lead to hippocampal damage and this in turn predisposes the patient to the development of temporal lobe epilepsy. Studies in adult rats have shown that seizures can lead to hippocampal damage and unprovoked recurrent seizures. However, many questions remain as to the relevance of early childhood seizures to hippocampal sclerosis and temporal lobe epilepsy. Human prospective epidemiologic studies have not shown a relationship between early childhood seizures and temporal lobe epilepsy. Recent MRI studies in humans suggest that a preexisting hippocampal lesion may predispose infants to experience febrile seizures, later on hippocampal sclerosis, and possibly temporal lobe epilepsy may occur. Unlike the studies in adult rats, normal immature rats with seizures have not been shown to develop hippocampal damage or unprovoked seizures in adulthood. Furthermore, animal studies reveal that preexisting brain abnormalities can predispose to hippocampal damage following seizures early in life. This paper reviews evidence for and against the view that early childhood convulsions, hippocampal sclerosis, and temporal lobe epilepsy are related, while also exploring clinical and animal studies on how seizures can lead to hippocampal damage, and how this can result in temporal lobe epilepsy. By better understanding the cause and effect relationship between early childhood seizures and hippocampal injury in normal and abnormal brains specific treatments can be developed that target the pathogenesis of epilepsy.     

Hippocampal polysynaptic computation

Neural circuitry is a self-organizing arithmetic device that converts input to output and thereby remodels its computational algorithm to produce more desired output; however, experimental evidence regarding the mechanism by which information is modified and stored while propagating across polysynaptic networks is sparse. We used functional multineuron calcium imaging to monitor the spike outputs from thousands of CA1 neurons in response to the stimulation of two independent sites of the dentate gyrus in rat hippocampal networks ex vivo. Only pyramidal cells were analyzed based on post hoc immunostaining. Some CA1 pyramidal cells were observed to fire action potentials only when both sites were simultaneously stimulated (AND-like neurons), whereas other neurons fired in response to either site of stimulation but not to concurrent stimulation (XOR-like neurons). Both types of neurons were interlaced in the same network and altered their logical operation depending on the timing of paired stimulation. Repetitive paired stimulation for brief periods induced a persistent reorganization of AND and XOR operators, suggesting a flexibility in parallel distributed processing. We simulated these network functions in silico and found that synaptic modification of the CA3 recurrent excitation is pivotal to the shaping of logic plasticity. This work provides new insights into how microscopic synaptic properties are associated with the mesoscopic dynamics of complex microcircuits.     

Hippocampal neurons in schizophrenia

Summary. The hippocampus is crucial for normal brain function, especially for the encoding and retrieval of multimodal sensory information. Neuropsychiatric disorders such as temporal lobe epilepsy, amnesia, and the dementias are associated with structural and functional abnormalities of specific hippocampal neurons. More recently we have also found evidence for a role of the hippocampus in the pathophysiology of schizophrenia. The most consistent finding is a subtle, yet significant volume difference in schizophrenia. Here we review the cellular and molecular basis of smaller hippocampal volume in schizophrenia. In contrast to neurodegenerative disorders, total hippocampal cell number is not markedly decreased in schizophrenia. However, the intriguing finding of a selective loss of hippocampal interneurons deserves further study. Two neurotransmitter receptors, the GABAA and AMPA/kainate glutamate receptors, appear to be abnormal, whereas changes of the NMDA glutamate receptor are less robust. The expression of several genes, including those related to the GABAergic system, neurodevelopment, and synaptic function, is decreased in schizophrenia. Taken together, recent studies of hippocampal cell number, protein expression, and gene regulation point towards an abnormality of hippocampal architecture in schizophrenia. Received February 21, 2002; accepted March 1, 2002     

Hippocampal sclerosis-Origins and imaging

The association between hippocampal sclerosis (HS) and epilepsy has been known for almost two centuries. For many years, HS was studied in postmortem series; however, since the mid-20th century, surgical specimens from temporal lobe resections have provided important new knowledge. HS is the most common pathology underlying drug-resistant mesial temporal lobe epilepsy (MTLE), a syndrome with a characteristic history and seizure semiology. In the early 1990s, it was recognized that magnetic resonance imaging (MRI) could detect HS. The standard MRI protocol for temporal lobe abnormalities uses coronal slices perpendicular to the long axis of the hippocampus. The MRI features of HS include reduced hippocampal volume, increased signal intensity on T(2) -weighted imaging, and disturbed internal architecture. The histopathologic diagnosis of HS is usually straightforward, with neuronal loss and chronic fibrillary gliosis centered on the pyramidal cell layer. There are several patterns or subtypes of HS recognized from surgical series based on qualitative or quantified assessments of regional neuronal loss. The pathologic changes of HS include granule cell dispersion, mossy fiber sprouting, and alterations to interneurons. There may also be more extensive sclerosis of adjacent structures in the medial temporal lobe, including the amygdala and parahippocampal gyrus. Subtle cortical neuropathologies may accompany HS. The revised classification of dysplasias in epilepsy denotes these as focal cortical dysplasias type IIIa. Sometimes, HS occurs with a second lesion, either in the temporal lobe or extratemporal, most often ipsilateral to the HS. HS on preoperative MRI strongly predicts good seizure outcome following temporal lobe resection (TLR). If adequate MRI shows no structural correlate in patients with MTLE, functional imaging studies are valuable, especially if they are in agreement with ictal electroencephalography (EEG) findings. Focal hypometabolism on 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) ipsilateral to the symptomatic temporal lobe predicts a good surgical outcome; the added value of (11) C-Flumazenil-PET (FMZ-PET) and proton magnetic resonance spectroscopy (MRS) is less clear. Surgical methods have evolved, particularly resecting less tissue, aiming to preserve function without compromising seizure outcome. Around two thirds of patients operated for MTLE with HS obtain seizure freedom. However, the best surgical approach to optimize seizure outcome remains controversial.     

Human Hippocampal Seizure Spread Studied by Depth and Subdural Recording: The Hippocampal Commissure

Eleven patients had seizures with unilateral temporal lobe onset recorded with simultaneous bilateral medial temporal depth electrodes and neocortical (subdural) electrodes at least on the side of seizure onset. Of a total of 55 seizures, four had simultaneous onset in neocortex and hippocampus, and 51 had onset in unilateral hippocampus. None originated solely in temporal neocortex. Three reproducible patterns of seizure spread from hippocampus were defined in which seizures spread initially to ipsilateral neocortex (32 seizures), spread first to contralateral hippocampus (13 seizures), or spread simultaneously to ipsilateral neocortex and contralateral hippocampus. Although the region of hippocampus in which seizures arose was constant, patterns of spread sometimes varied in the same patient. When contralateral neocortical involvement occurred, it was after or with contralateral hippocampus but never before. These results suggest the existence of an operational hippocampal commissure in humans.     

Hippocampal neurons inhibit meal onset

There is extensive research regarding the neural mechanisms involved in satiety and meal termination; in contrast, there is very limited understanding of how meal onset is regulated. On the basis of several converging lines of evidence, we hypothesized that hippocampal neurons form a memory of a meal and inhibit meal onset during the postprandial period. As a first step, we tested whether reversible inactivation of the hippocampus with muscimol infusions after the end of one meal would accelerate the onset of the next meal. To test this, adult male Sprague–Dawley rats (N = 23) were implanted with a cannula aimed at the right or left dorsal hippocampus and then trained to consume a 32% sucrose solution at a scheduled time daily. On the experimental day, hippocampal neuronal activity was temporarily disrupted during the postprandial period by infusing muscimol (0.5 μg/μl; 1 μl) 5 min after the rats stopped consuming the sucrose solution. Compared to vehicle infusions, muscimol infusions significantly decreased the latency to start the postinfusion meal and increased the size of the postinfusion meal. In addition, muscimol disrupted the relationship between the size of a meal and length of the following postprandial period. These effects of muscimol on meal onset were not due to an effect on the speed of consumption. Collectively, these findings are consistent with the hypothesis that hippocampal neurons suppress meal initiation during the postprandial period. Given that overeating can impair hippocampal function, these findings suggest that impaired hippocampal functioning is a cause and consequence of overeating and obesity. © 2012 Wiley Periodicals, Inc.