Septal networks: relevance to theta rhythm, epilepsy and Alzheimer's disease

Colom, Luis V.

doi:10.1111/j.1471-4159.2005.03630.x

Cited by 131 publications

(125 citation statements)

References 115 publications

(258 reference statements)

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“…An alternative explanation has to consider the CV damage localization, that could be essential for the changes in EEG rhythmicity. CV lesions in the thalamocortical pathway could affect preferentially the oscillatory activity of the a frequency peak (Steriade and Llinas, 1988;Llinas et al, 1999;Jellinger, 2002Jellinger, , 2005, whereas lesions in cortico-basal or cortico-septal pathways could affect preferentially the oscillatory activity of the transition frequency between a and h frequency bands (Colom, 2006). Obviously, given the correlative nature of this study, these conclusions have to be considered with caution.…”

Section: Eeg Frequency Indices Of a Rhythms And CV Damagementioning

confidence: 79%

“…Therefore, a h band power increase significantly based on the CV damage could occur when the axonal destructuration reaches a well-defined stage during the course of the disease. Alternatively, a pathological increase of the h band power could be due to a specific vascular impairment of the anatomical network ascending from the brainstem towards the medial septum-hippocampal formation involved in the generation of the h rhythm (Colom, 2006).…”

Section: Relative Power Spectral Density and CV Damagementioning

confidence: 99%

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Vascular damage and EEG markers in subjects with mild cognitive impairment

Moretti

Miniussi

Frisoni

et al. 2007

Clinical Neurophysiology

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Objective: We evaluated the changes induced by cerebrovascular (CV) damage on brain rhythmicity recorded by electroencephalography (EEG) in a cohort of subjects with mild cognitive impairment (MCI). Methods: We enrolled 99 MCI subjects (Mini-Mental State Examination [MMSE] mean score 26.6). All subjects underwent EEG recording and magnetic resonance imaging (MRI). EEGs were recorded at rest. Individual EEG frequencies were indexed by the h/a transition frequency (TF) and by the individual a frequency (IAF) with power peak in the extended a range (5-14 Hz). Relative power was separately computed for d, h, a1, a2, and a3 frequency bands on the basis of the TF and IAF values. Subsequently, we divided the cohort in four sub-groups based on subcortical CV damage as scored by the age-related white matter changes scale (ARWMC). Results: CV damage was associated with 'slowing' of TF proportional to its severity. In the spectral bandpower the severity of vascular damage was associated with increased d power and decreased a2 power. No association of vascular damage was observed with IAF and a3 power. Moreover, the h/a1 ratio could be a reliable index for the estimation of the individual extent of CV damage. Conclusions: EEG analysis may show physiological markers sensitive to CV damage. The appropriate use of this EEG index may help the differential diagnosis of different forms of cognitive decline, namely primary degenerative and secondary to CV damage. Significance: The EEG neurophysiological approach, together with anatomical features from imaging, could be helpful in the understanding of the functional substrate of dementing disorders.

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Section: Eeg Frequency Indices Of a Rhythms And CV Damagementioning

confidence: 79%

Section: Relative Power Spectral Density and CV Damagementioning

confidence: 99%

Vascular damage and EEG markers in subjects with mild cognitive impairment

Moretti

Miniussi

Frisoni

et al. 2007

Clinical Neurophysiology

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“…A smaller monosynaptic excitatory input to the ipsilateral hippocampal formation projects from the septal region through fornix/fimbria (Crutcher et al, 1981;Swanson and Cowan, 1979). The cell bodies of this largely cholinergic septohippocampal pathway reside in the medial septum with contributions from both the vertical and horizontal limbs of the diagonal band of Broca (Amaral and Kurz, 1985); the bulk of lateral septal efferents projects to medial septal nuclei with little or no input to the hippocampal formation (Colom, 2006). These cells project to the supra-and infragranular layers of the dentate gyrus (Chandler and Crutcher, 1983) and the hippocampus (Amaral and Kurz, 1985).…”

Section: Discussionmentioning

confidence: 99%

Asymmetric accumulation of hippocampal 7S SNARE complexes occurs regardless of kindling paradigm

et al. 2007

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Modifications of neurotransmission may contribute to the synchronization of neuronal networks that are a hallmark of epileptic seizures. In this study we examine the synaptosomal proteins involved in neurotransmitter release to determine if alterations in their interactions correlate with the chronic epileptic state. Using quantitative western blotting, we measured the levels of 7S SNARE complexes and SNARE effectors in the effected hippocampi from animals that were electrically kindled through stimulation from one of three different foci. All three kindling paradigms, amygdalar, entorhinal, and septal, were associated with an accumulation of 7S SNARE complexes in the ipsilateral hippocampus, measured one month after completion of kindling. Of the eight SNARE effectors examined (α-SNAP, NSF, SV2A/B, Munc18a/nSec1, Munc13-1, Complexin 1, 2, and synaptotagmin I), there was a statistically significant bihemispheric increase of hippocampal SV2 and decrease of NSF upon kindling; neither by itself would be expected to account for the asymmetry of SNARE complex distribution. These data suggest that an ipsilateral hippocampal accumulation of SNARE complexes is a permanent alteration of kindling-induced epilepsy, regardless of stimulation pathway. The significance of these findings toward a molecular understanding of epilepsy will be discussed.

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“…This diversity in firing properties among basal forebrain cholinergic neurons may be related to connectivity. In this case, neurochemically identified medial septal cholinergic neurons may be more electrophysiologically diverse than formerly proposed due to specific connectivity patterns present in each medial septal subregion (Colom, 2006).Our initial analysis of current-clamp recordings from MS/DB neurons revealed that the firing properties of medial septal neurons exhibited great variability. Heterogeneity of firing characteristics was evident in all of the classically-described electrophysiological phenotypes including regular firing, fast spiking and burst-firing neurons.…”

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confidence: 99%

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Garrido-Sanabria¹,

Perez²,

Bañuelos³

et al. 2007

Neuroscience

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Slow firing septal neurons modulate hippocampal and neocortical functions. Electrophysiologically, it is unclear whether slow firing neurons belong to a homogeneous neuronal population. To address this issue, whole-cell patch recordings and neuronal reconstructions were performed on rat brain slices containing the medial septum/diagonal band complex (MS/DB). Slow firing neurons were identified by their low firing rate at threshold (< 5Hz) and lack of time-dependent inward rectification (I h ). Unsupervised cluster analysis was used to investigate whether slow firing neurons could be further classified into different subtypes. The parameters used for the cluster analysis included latency for first spike, slow afterhyperpolarizing potential, maximal frequency and action potential (AP) decay slope. Neurons were grouped into three major subtypes. The majority of neurons (55%) were grouped as cluster I. Cluster II (17% of neurons) exhibited longer latency for generation of the first action potential (246.5±20.1 ms). Cluster III (28% of neurons) exhibited higher maximal firing frequency (25.3±1.7 Hz) when compared to cluster I (12.3±0.9 Hz) and cluster II (11.8±1.1 Hz) neurons. Additionally, cluster III neurons exhibited faster action potentials at suprathreshold. Interestingly, cluster II neurons were frequently located in the medial septum whereas neurons in cluster I and III appeared scattered throughout all MS/DB regions. Sholl's analysis revealed a more complex dendritic arborization in cluster III neurons. Cluster I and II neurons exhibited characteristics of "true" slow firing neurons whereas cluster III neurons exhibited higher frequency firing patterns. Several neurons were labeled with a cholinergic marker, , and cholinergic neurons were found to be distributed among the three clusters. Our findings indicate that slow firing medial septal neurons are heterogeneous and that soma location is an important determinant of their electrophysiological properties. Thus, slow firing neurons from different septal regions have distinct functional properties, most likely related to their diverse connectivity. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 January 22. Published in final edited form as:Neuroscience. (Griffith et al., 1991, Matthews and Lee, 1991, Jones et al., 1999, Morris et al., 1999, Knapp et al., 2000, Henderson et al., 2001, Sotty et al., 2003. Slow firing neurons are characterized by slow firing rates and pronounced slow post-spike afterhyperpolarization potenti...

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Septal networks: relevance to theta rhythm, epilepsy and Alzheimer's disease

Cited by 131 publications

References 115 publications

Vascular damage and EEG markers in subjects with mild cognitive impairment

Vascular damage and EEG markers in subjects with mild cognitive impairment

Asymmetric accumulation of hippocampal 7S SNARE complexes occurs regardless of kindling paradigm

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

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