Functional state of the cerebral cortex and mesencephalic reticular formation in the course of traumatic shock

1981 ◽  
Vol 91 (3) ◽  
pp. 300-303
Author(s):  
S. P. Matua
Keyword(s):  
Cerebral Cortex ◽  
Reticular Formation ◽  
Functional State ◽  
Mesencephalic Reticular Formation ◽  
Traumatic Shock

scholarly journals Ouabain Induced Seizures: Site of Production and Response to Anticonvulsants

1978 ◽  
Vol 5 (4) ◽  
pp. 405-411 ◽  
Author(s):  
Duncan L.W. Davidson ◽  
Yasuo Tsukada ◽  
André Barbeau
Keyword(s):  
Cerebral Cortex ◽  
Reticular Formation ◽  
Dorsal Hippocampus ◽  
Mesencephalic Reticular Formation ◽  
Cerebellar Nuclei ◽  
Inhibitory Effect ◽  
Transport Mechanisms ◽  
Limbic Seizures ◽  
Temporal Lobe Seizures ◽  
Low Volume

SUMMARY:Ouabain, an inhibitor of Na+-K+-ATP'ase, has been administered intraventricularly to rats to study the effect of impairment of membrane transport mechanisms on the genesis of seizures. Running and leaping seizures occur rapidly after injection oj ouabain in a low volume (10μl) when the maximal uptake of ouabain (39.8%) is in the hippocampus. Generalized clonic-lonic seizures are induced by higher volume injections (50μl) associated with wider distribution of ouabain, including the cerebellum and brainstem.Ouabain was injected into cerebral cortex, caudate nucleus, dorsal hippocampus, fastigeal nucleus, ventrolateral mesencephalic reticular formation and cerebellar cortex. The cerebellar injections produced both running and leaping and generalized clonic-lonic seizures. It is suggested that this results from decreased inhibitory effect of vermal and paravermal Purkinje cells on intra-cerebellar nuclei, which alters cerebellar influence on the reticular formation and the limbic system.Diphenylhydantoin, phenobarbitone, phenacemide, carbamezepine and clonazepam but not ethosuximide are effective against generalized clonic-lonic seizures, suggesting that this is a model for “grand mat” but not “petit mal” seizure mechanisms. It is furthermore suggested that running and leaping are subcortical, probably limbic, seizures that are most relevant as a model for temporal lobe seizures.

Neurotransmitter modulation of VIP release from cat cerebral cortex

1986 ◽  
Vol 250 (1) ◽  
pp. R104-R111
Author(s):  
J. Y. Wang ◽  
T. L. Yaksh ◽  
G. J. Harty ◽  
V. L. Go
Keyword(s):  
Cerebral Cortex ◽  
Reticular Formation ◽  
Mesencephalic Reticular Formation ◽  
Inhibitory Effect ◽  
Gamma Aminobutyric Acid ◽  
Opiate Antagonists ◽  
Cholinergic Agents ◽  
Opioid Receptor Agonists ◽  
Cat Cerebral Cortex

The cortical release of vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) in vivo was examined by superfusion of the pial surface of the cerebral cortex of the cat. The modulation of cortical VIP release by several neurotransmitters [gamma-aminobutyric acid (GABA), opioids, norepinephrine, acetylcholine, and glutamate] normally present in the cerebral cortex was studied by administering respective agonists and antagonists for their receptors. Although GABA and opiate agonists did not influence the resting release of VIP-LI, GABA antagonists (picrotoxin and bicuculline) and opiate antagonists (naloxone and naltrexone) significantly elevated the resting release. The evoked release from cortex of VIP-LI (by electrical stimulation of the cortex or mesencephalic reticular formation) was suppressed by GABA and mu- but not delta-, kappa-, or sigma-opioid receptor agonists. Glutamate and kainic acid increased the resting release of VIP-LI from the cerebral cortex. Noradrenergic (alpha 2 but not alpha 1) displayed an inhibitory effect on the evoked release of cortical VIP-LI release. Resting VIP-LI release was enhanced by cholinergic agents (carbachol). The facilitatory effects of mesencephalic reticular formation stimulation on VIP-LI release were demonstrated by atropine. These observations suggest characteristic interactions reflecting the circuitry modulating the activity of cortical VIP-releasing neurons.

scholarly journals A central mesencephalic reticular formation projection to the Edinger–Westphal nuclei

2015 ◽  
Vol 221 (8) ◽  
pp. 4073-4089 ◽  
Author(s):  
Paul J. May ◽  
Susan Warren ◽  
Martin O. Bohlen ◽  
Miriam Barnerssoi ◽  
Anja K. E. Horn
Keyword(s):  
Reticular Formation ◽  
Mesencephalic Reticular Formation ◽  
Central Mesencephalic Reticular Formation
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