Focal injection of 2-amino-7-phosphonoheptanoic acid into prepiriform cortex protects against pilocarpine-induced limbic seizures in rats

Millan, M.H.; Patel, Smita S.; Mello, Luiz E.; Meldrum, Brian S.

doi:10.1016/0304-3940(86)90439-8

Cited by 61 publications

(20 citation statements)

References 6 publications

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“…Even histological techniques used by some groups, such as paraffin wax embedding (Liu et al, 1991) may alter the accuracy of the observed result, as wax embedding shrinks the brain to about 25% of its original size. In the study by Millan et al (1986b), a radioactive AHP compound was injected in order to localise and validate the site of injection in the prepiriform cortex. In a small group of animals they measured the rostro-caudal diffusion of the drug only.…”

Section: Discussionmentioning

confidence: 99%

“…While there have been few studies that have reported performing microinjections into these and other regions (Aker and Onat, 2002;Hosford et al, 1997a,b;Liu et al, 1991;Millan et al, 1986a,b;Snead, 1991), there has been very little systematic studies validating the accuracy of these injections and how far the drug diffuses away from the injection site into surrounding structures. One epilepsy study measured the spread of a tritium labelled 2-amino-7-phosphoheptanoic acid ([ 3 H] APH) in the prepiriform cortex (Millan et al, 1986b). However, the study used small animal numbers and large, 0.5 l injection volumes, which generally result in a significant back flow of the injected compound up the cannula tract.…”

Section: Introductionmentioning

confidence: 99%

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Validation of a method for localised microinjection of drugs into thalamic subregions in rats for epilepsy pharmacological studies

Lohman

Liu

Morris

et al. 2005

Journal of Neuroscience Methods

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Validation of a method for localised microinjection of drugs into thalamic subregions in rats for epilepsy pharmacological studies

Lohman

Liu

Morris

et al. 2005

Journal of Neuroscience Methods

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“…The PC receives a dense cholinergic and noradrenergic innervation (Foote et al, 1983;Woolf et al, 1986;Senut et al, 1989). Excitatory amino acids have an established role in the PC neural transmission and seizures (Collins, 1982;Millan et al, 1986;Collins and Howlett, 1988). The NMDA antagonist, MK-801, inhibits the maintenance of soman-induced seizures (Sparenborg et al, 1990).…”

Section: Astrocytesmentioning

confidence: 98%

Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

1997

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Neurons in the piriform cortex and the pontine nucleus locus coeruleus express elevated levels of the immediate early gene protein product, Fos, within 30-45 minutes of a seizurogenic dose of the anticholinesterase, soman (Zimmer et al., [1997] J. Comp. Neurol. 378:468-481). By 24 hours following soman injection, there is marked neuropathology in the piriform cortex. These findings suggest selective, regional vulnerability in response to the seizurogenic actions of soman. In the present study, we determined that soman-induced seizures also cause selective, rapid activation of astrocytes and microglia in the piriform cortex and other brain regions. Animals were killed at different intervals between 1 hour and 24 hours after a convulsive dose of soman. Brain sections were processed for immunocytochemical detection of astrocytes with antibodies against glial fibrillary acidic protein, and microglia and macrophages with antibodies against the complement receptor 3 protein, OX-42. The results demonstrate that following soman administration: (1) there is a rapid increase in glial fibrillary acidic protein staining in astrocytes of the piriform cortex (1 hour); (ii) reactive astrocytes are specifically restricted to layer II and the superficial boundaries of layer III of the piriform cortex. These are the same layers in which neurons express Fos within 30-45 minutes following soman administration; (3) between 1 and 4 hours, resting (ramified) microglia in the piriform cortex and the hippocampus alter their morphology to resemble active microglia. From 4-8 hours, active microglia undergo morphological changes characteristic of reactive microglia that resemble macrophages. Taken together, these observations indicate that astrocytes and microglia in brain regions susceptible to soman become rapidly "reactive" in response to seizures. The highly specific anatomical codistribution of reactive glia and Fos-expressing neurons suggests that intensely active neurons provide local signals that trigger reactive changes in neighboring glia.

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“…Autoradiographic studies yielded conflicting results. The areas of diffusion ranged from less than 1P0 mm up to several millimetres (Harrison, 1961;Wolfson & Brown, 1983;Millan, Patel, Mello & Meldrum, 1986) and appeared to depend critically on the kind of drug injected, the volume of injection, the speed of injection, and the time in which the cannula was left in place after end of injection. The present study uses a technique of injection which minimizes the area of diffusion.…”

Section: Specificity Of Local Injectionsmentioning

confidence: 99%

Excitatory amino acid receptor‐mediated transmission of somatosensory evoked potentials in the rat thalamus.

Klockgether

1987

The Journal of Physiology

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SUMMARY1. To examine the role of excitatory amino acid receptors in the rat ventrobasal thalamic nucleus (v.b.t.n.) for the transmission of cortical somatosensory evoked potentials (s.e.p.s), potentials were recorded from the somatosensory cortex of barbiturate-anaesthetized and of unanaesthetized awake rats. The effects of microapplications of the selective N-methyl-D-aspartate (NMDA) antagonist (-)-2-amino-7-phosphono-heptanoate ((-)AP7) and the broad-spectrum excitatory amino acid antagonist 1-(p-chlorobenzoyl)-piperazine-2,3-dicarboxylate (pCB-PzDA) into the thalamus on the amplitudes and latencies of cortical potentials were measured.2. To define the receptor specificity of local microinjections of (-)AP7 and pCB-PzDA electroencephalogram (e.e.g.) recordings were made from the immediate vicinity of the injection cannula within the thalamus. (-)AP7 selectively antagonized epileptic discharges induced by NMDA, but not those by kainate, whereas pCB-PzDA antagonized epileptic discharges induced by both.3. In both anaesthetized and unanaesthetized rats, microapplications of pCB-PzDA into the thalamus suppressed transmission of cortical potentials as indicated by a decrease of their amplitudes and an increase of their peak latencies.Further experiments in anaesthetized rats showed that pCB-PzDA exerted its effects in a dose-dependent and site-specific way. 4. In both anaesthetized and unanaesthetized rats, microapplications of (-)AP7 into the ventrobasal thalamus did not affect cortical potentials.5. These results are consistent with the assumption that an excitatory amino acid serves as transmitter at thalamic synapses mediating transmission of cortical potentials, and that this transmitter interacts preferentially with non-NMDA receptors.

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Focal injection of 2-amino-7-phosphonoheptanoic acid into prepiriform cortex protects against pilocarpine-induced limbic seizures in rats

Cited by 61 publications

References 6 publications

Validation of a method for localised microinjection of drugs into thalamic subregions in rats for epilepsy pharmacological studies

Validation of a method for localised microinjection of drugs into thalamic subregions in rats for epilepsy pharmacological studies

Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

Excitatory amino acid receptor‐mediated transmission of somatosensory evoked potentials in the rat thalamus.

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