Intrahippocampal kainic acid, seizures and local neuronal degeneration: Relationships assessed in unanesthetized rats

French, Edward D.; Aldinio, C.; Schwarcz, Robert

doi:10.1016/0306-4522(82)90212-3

Cited by 88 publications

(37 citation statements)

References 35 publications

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“…On the other hand, glutamate regulation of VTA neurons is target-specific, and stimulation of NMDA and AMPA receptors in the VTA produce different effects (Takahata and Moghaddam, 2000). Nevertheless, the present findings support previous findings that inhibition of the HIP with lidocaine infusions suppressed activity (Flicker and Geyer, 1982) in a dose-dependent manner (Bast et al, 2001), whereas stimulation of the vHIP with low dose NMDA produced hyperactivity (French et al, 1982;Bardgett and Henry, 1999;Bast et al, 2001). Our data are consistent with previous report that dopamine antagonists suppressed enhanced Fos expression following vHIP stimulation, and that enhanced locomotion produced by stimulation of the vHIP required both D1 and D2 receptors (Bardgett and Henry, 1999).…”

Section: Inhibition and Stimulation Of Vhip On Amphetamine-induced Hysupporting

confidence: 81%

“…Although we have not measured these behaviors systematically, these behavioral characteristics appear to be similar to the wet-dog shakes and oral stereotypy reported by French et al (1982). However, a low dose of NMDA (0.5 lg/ll/site) used in the present study produced no obvious signs of seizures that are typically produced with high doses (0.74 lg/ll or greater) of NMDA (Legault and Wise, 1999; also our unpublished observation).…”

Section: Effects Of Inhibition or Stimulation Of Vhip On Hyperlocomotsupporting

confidence: 67%

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Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

2006

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Using lesions and infusions, the present study investigated the way in which and the extent to which the ventral hippocampus (vHIP) modulates amphetamine-induced hyperactivity in rats. Rats were lesioned (excitotoxic or sham) in the vHIP or were implanted with cannulae for subsequent infusions. A high dose (12.5 microg/microl) of N-methyl-D-aspartate (NMDA) was used to make excitotoxic lesions and a low dose (0.5 microg/microl) of NMDA to cause activation of the hippocampus. Lidocaine was used to inactivate the hippocampus. Lidocaine or a low dose of NMDA was infused into the vHIP in combination with either systemic injection or intra-accumbens infusions of amphetamine. The effects of these treatments on locomotor activity were measured by distance traveled in 10-min intervals for 40-60 min. Lesions and deactivation of the hippocampus attenuated amphetamine-induced hyperlocomotion, compared to the controls. Stimulation of the hippocampus augmented amphetamine-induced hyperlocomotion. The present findings provide evidence that the hippocampus exerts excitatory modulation on the expression of behavioral excitation produced by amphetamine, likely via the nucleus accumbens.

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Section: Inhibition and Stimulation Of Vhip On Amphetamine-induced Hysupporting

confidence: 81%

Section: Effects Of Inhibition or Stimulation Of Vhip On Hyperlocomotsupporting

confidence: 67%

Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

2006

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“…The most striking procedural difference between the studies is the choice of neurotoxins (kainic acid vs ibotenic acid). Kainic acid is known to cause recurrent epileptic seizures even after nanogram infusions in the hippocampus (French et al, 1982;Bouilleret et al, 1999), and such seizures may lead to structural or functional damage in hippocampal target areas. It remains to be determined whether extrahippocampal damage or other factors account for the different effects on adrenocortical activity.…”

Section: Discussionmentioning

confidence: 99%

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

et al. 2003

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It has been proposed that the hippocampus exerts a tonic inhibitory influence on the hypothalamic-pituitary-adrenal (HPA) stress axis. This claim rests, in particular, on the upregulation of corticosterone secretion and other measures of HPA activity after nonselective lesions of the hippocampal formation. We measured plasma corticosterone concentrations after selective neurotoxic damage to the hippocampus and the subiculum in rats. Concentrations were estimated during rest in the rat's home cage and at several time points after varying degrees of stress. Lesions of the hippocampus did not increase the concentration of corticosterone relative to control rats in any condition. Temporary inactivation of the hippocampus or the ventral subiculum by infusion of the GABA A receptor agonist muscimol also failed to induce hypersecretion, although hippocampal infusions did impair spatial memory. These results suggest that the hippocampus is not necessary for tonic inhibition of adrenocortical activity and imply that the HPA axis receives efficient negative feedback inhibition from other brain systems too.

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“…The duration of the transient improvement after PEX is consistent with removal and subsequent spontaneous reaccumulation of pathogenic autoantibodies (9). The effect of the circulating factors removed by PEX is comparable to the dose-related effects of experimental epileptogenic agents, such as local application of penicillin (14) or glutamate agonists (15)(16)(17). Twyman et al reported that GluR3 antibodies raised in rabbits immunized with a putative extracellular portion of GluR3 protein, and sera from RE patients with increased GluR3 antibodies, rapidly and reversibly activated glutamate receptors on a subpopulation of cultured fetal mouse cortical neurons (18).…”

Section: Discussionmentioning

confidence: 55%

Clinical and Electroencephalographic Correlates in Rasmussen's Encephalitis

1997

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Summary:Purpose: Rasmussen's encephalitis (RE) is a progressive childhood disease characterized by unilateral brain dysfunction, seizures, and inflammatory histopathology. Converging lines of evidence suggest that an autoimmune process is important in the pathogenesis of RE.Methods: Two patients with pathologically confirmed RE and increased levels of circulating glutamate receptor subunit (GluR3) antibodies were studied prospectively before, during, and after trials of plasmapheresis (PEX) and other immunomodulation. Frequency, duration, and intensity of clinical seizures were directly correlated with the abundance of interictal epileptiform activity on serial EEGs.Rasmussen's encephalitis (RE) is a rare childhood syndrome of unilateral brain dysfunction and focal seizures (1-3). Unihemispheric dysfunction progresses relentlessly in severity and degree over months to decades, culminating in hemiparesis and dementia. Seizures are refractory to antiepileptic drugs (AEDs). Partial corticectomy may temporarily control seizures, but spread of the process to the rest of the hemisphere eventually follows. Functional hemispherectomy is the recommended alternative (3,4). Neuroimaging shows progressive atrophy of the affected hemisphere (33). Neuropathology characteristically shows perivascular lymphocytic cuffing and proliferation of microglial nodules in the cortex of the affected hemisphere, with sparing of the contralateral hemisphere, basal ganglia, and posterior fossa structures (1,6). Converging lines of evidence suggest an autoimmune process is important in the pathogenesis of RE, and that the glutamate receptor subunit, GluR3, may be an important autoantigen (7-9).This report correlates clinical and EEG features of 2 patients with RE who underwent therapeutic plasmaphaAccepted September 27, 1996. Address correspondence and reprint requests to Dr. P. I. Andrews at Division of Neurology, Sydney Children's Hospital, High St., Randwick, Australia, 2031.Results: Serial EEGs in these patients suggest that early in the course of RE interictal epileptiform activity is localized to the affected hemisphere and that disease progression is associated with increasingly frequent bilaterally synchronous and contralateral epileptiform activity.Conclusions: The clinical and EEG parameters of epileptogenesis were transiently diminished by PEX, which suggests that circulating factors induce dose-dependent, reversible epileptogenic effects in some patients with RE. Key Words: Rasmussen's encephalitis-Electroencephalography-Autoimmune4lutamate receptor-False lateralization. resis (PEX), highlighting the progression of EEG abnormalities over time. METHODSTwo previously reported patients (7,9) with pathologically confirmed RE were enrolled sequentially in a series of therapeutic trials of PEX and other immunemodulating therapies, with the approval of the Duke University Medical Center Institutional Review Board and informed consent of the families. Data were collected prospectively. Daily seizure diaries were recorded by the parents. ...

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Intrahippocampal kainic acid, seizures and local neuronal degeneration: Relationships assessed in unanesthetized rats

Cited by 88 publications

References 35 publications

Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

Selective Hippocampal Lesions Do Not Increase Adrenocortical Activity

Clinical and Electroencephalographic Correlates in Rasmussen's Encephalitis

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