Electrophysiological analysis of the hippocampal-septal projections: I. Response and topographical characteristics

DeFrance, Jon F.; Kitai, S.T.; Shimono, T.

doi:10.1007/bf00234861

Cited by 29 publications

(11 citation statements)

References 26 publications

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“…Reciprocal connections via the dorsal fimbria fornix connect the medial septal nucleus with the dentate gyrus, CA1, CA2, subiculum, and entorhinal cortex. 23-25…”

Section: Introductionmentioning

confidence: 99%

“…Reciprocal connections via the dorsal fimbria fornix connect the medial septal nucleus with the dentate gyrus, CA1, CA2, subiculum, and entorhinal cortex. [23][24][25] We hypothesize that, after neonatal hypoxicischemic brain injury, axonal injury emerges in interconnecting white matter tracts related to the hippocampus over a delayed period, resulting in injury in a systems-preferential manner to interconnected remote target regions whose susceptibility to injury is directed by their connection to the primary/initial site of injury.…”

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confidence: 99%

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Delayed neural network degeneration after neonatal hypoxia‐ischemia

Stone¹,

Zhang²,

Mack³

et al. 2008

Annals of Neurology

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Objective-Clinical MR studies show delayed and ongoing neurodegeneration following neonatal hypoxia-ischemia (HI), but the mechanisms and timing of this neurodegeneration remain unclear. We use ex vivo Diffusion Tensor Imaging (DTI) and brain neuropathology to determine if selective injury to white matter tracts occurs following neonatal HI in mice resulting in neural system associated attrition in remote regions and at delayed time points. Methods-TheRice Vannucci model (unilateral carotid ligation + 45 minutes of hypoxia FIO2=0.08) was used to cause brain injury in postnatal (p)7 C57BL6 mice and ex vivo DTI and correlative neuropathology were performed at p8,p11,p15,p21,p28, and p42.Results-DTI provides excellent contrast visualization of unmyelinated white matter in the immature mouse brain. Acute severe ipsilateral injury to the hippocampus is seen with both histopathology and diffusion-weighted MRI 24 hours post injury. Injury to axons is evident 24 hours after HI in the hippocampal alveus. By p11 and continuing until p28, the ipsilateral fimbria fornix degenerates. Beginning at p15, there is injury and loss of axons entering the ipsilateral septal nucleus followed by ipsilateral septal atrophy. Volume loss in the hippocampus is rapid and severe but is subacute and significantly slower in the ipsilateral septum. Neonatal HIE, also interrupts the normal developmental increase in fractional anisotropy in the ipsilateral fimbria but not in the contralateral fimbria from p8 to p42.Interpretation-In the neonatal brain there is a progressive systems-preferential injury following HI. DTI allows unparalleled visualization of this neural-network associated attrition so that it can be followed longitudinally in the developing brain.

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“…Reciprocal connections via the dorsal fimbria fornix connect the medial septal nucleus with the dentate gyrus, CA1, CA2, subiculum, and entorhinal cortex. 23-25…”

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Delayed neural network degeneration after neonatal hypoxia‐ischemia

Stone¹,

Zhang²,

Mack³

et al. 2008

Annals of Neurology

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“…investigations have revealed that much of the innervation which the lateral septal complex (LX) receives from the hippocampal formation by way of the fimbria-fomix (fi-fx) fibers, is excitatory (9,10,20,23). Data indicating that the innervation is mediated by an excitatory amino acid were obtained from biochemical studies.…”

Section: Electrophysiologicalmentioning

confidence: 99%

Amino acid neurotransmission between fimbria-fornix fibers and neurons in the lateral septum of the rat: A microiontophoretic study

Joëls¹,

Urban²

1984

Experimental Neurology

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We investigated the nature of the excitatory amino acid and the type of amino acid receptor involved in the projection of fimbria-fomix (fi-fx) fibers on neurons in the lateral septal complex (LSC) of the rat. It appeared that neurons which were strongly orthodromically activated (SOA) by stimulation of fi-fx fibers were excited by glutamate (GLU) and aspartate (ASP) at much lower ejecting currents than neurons which were only weakly orthodromically excited. In addition, GLU was a stronger agent than ASP, particularly in SOA septal cells. Two amino acid antagonists tested, glutamic acid diethylester (GDEE) and 2-amino-S-phosphonovaleric acid (2-APV), selectively antagonized responses to the amino acid agonists quisqualate (QUIS) and N-methyl-D-aspartate (NMDA), respectively. They also depressed GLU-and ASP-induced responses, although in that case the antagonists frequently had to be expelled with currents higher than those needed to block QUIS-and NMDA-evoked excitations. Furthermore, GDEE frequently antagonized GLU-induced responses better than ASPevoked excitations, whereas 2-APV often blocked responses to ASP more effectively than those to GLU. It was observed that GDEE, ejected with currents that blocked responses to QUIS reversibly, decreased the number of synaptic responses induced in SOA cells by fi-fx stimuli. Synaptically induced excitation in these neurons was consistently una&cted by 2-APV, even when the antagonist was expelled with high currents. According to these results, LSC neurons, in particular the SOA neurons, are more Abbreviations: li-fx-fimbria-fomix; LSC-lateral septal complex; SOA, WOA-strongly, weakly orthodromically activated; GLU-glutamate; ASP-aspartate; GDEE-glutamic acid diethylester, 2-APV-2-amino%phosphonovaleric acid; QUIS-quisqualate; NMDA-N-methylDaspartate; KA-kainic acid.

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“…The calvaria was removed and the cortex gently aspirated away to expose the septal nuclei and the hippocampal fimbrial-fornix system. This preparation has been described elsewhere in detail (DeFrance, Kitai, and Shimono, 1973).…”

Section: Physiologicalmentioning

confidence: 99%

“…The I econd criterion was examined with histamine agonistlantagonist challenge of the adenylate cyclase activation of CAMP. The third criterion was examined with iontophoretic application of histaminergic agonists and appropriate antagonists to responses in nucleus accumbens elicited by fimbria stimulation because the responses have been characterized previously (DeFrance, Kitai, and Shimono, 1973) in the lateral septa1 gray (Fox, 1940) and because the hippocampus to nucleus accumbens axis has been implicated as being significant in affective disorders (Mesalum and Geschwind, 1978). Therefore, the present investigations were designed to explore anatomic, pharmacologic, and physiologic parameters of histamine action in rabbit nucleus accumbens.…”

Section: Introductionmentioning

confidence: 99%

Histamine: Correlative studies in nucleus accumbens

et al. 1982

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The role of histamine as a neurotransmitter has been the subject of considerable controversy. Recent evidence suggests it to be involved in such complex activities as arousal and affect. The purpose of the present study is to examine the possible source, function, and pharmacology of histamine in the nucleus accumbens, an area of the brain also implicated in complex activities such as affect. The anatomical studies suggest that the most probable source of the histamine in nucleus accumbens is the complex region lateral to the mammillary nuclei. These areas are the intercalated nucleus and the tuberomammillary nucleus (nuclei gemini hypothalami). To a lesser degree, the supramammillary complex may also contribute histamine-containing axons to the accumbens area. Adenylate cyclase in the rabbit nucleus accumbens displayed activation in response to histamine agonists (histamine, 2-Me-histamine, and 4-Me-histamine). The action of the H1 antagonist promethazine was greater than the H2 antagonist metiamide in reducing enzyme activation by histamine and 2-Me-histamine. In contrast, metiamide was more potent than promethazine toward antagonism of the action of 4-Me-histamine. However, no additive effects were noted when agonists were added in combination. Based upon these data, it is suggested that activation of adenylate cyclase in the rabbit nucleus accumbens is mediated in part by mixed H1 and H2 receptors or cellular disruption reflects the loss of receptor specificity. Physiological studies demonstrated that the H2 agonist 4-Me-histamine had an inhibitory effect on the activity of neurons driven by stimulation of the fimbria. The magnitude of the effect was frequency dependent. The H1 agonist 2-Me-histamine had no significant effect. Iontophoretic application of 4-Me-histamine had minimal effect upon low frequency volleys (0.5 Hz) but had a pronounced effect upon higher frequency volleys (6.0 Hz). These effects were antagonized by metiamide. Iontophoretic application of metiamide alone produced an effect only upon the P component of the field response, which is also bicuculline sensitive. Bicuculline coadministration was also effective in antagonizing the 4-Me-histamine effect. The physiological data suggest that histamine works through H2 receptors in nucleus accumbens, perhaps by potentiating the effects of gamma-aminobutyric acid (GABA). Thus, histamine in nucleus accumbens appears to function as a modulatory substance whose effect is dependent upon the activity of other transmitter and afferent systems.

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Electrophysiological analysis of the hippocampal-septal projections: I. Response and topographical characteristics

Cited by 29 publications

References 26 publications

Delayed neural network degeneration after neonatal hypoxia‐ischemia

Delayed neural network degeneration after neonatal hypoxia‐ischemia

Amino acid neurotransmission between fimbria-fornix fibers and neurons in the lateral septum of the rat: A microiontophoretic study

Histamine: Correlative studies in nucleus accumbens

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