PubMed HealthSearch

PubMed · 420930

[Neuropathologic effects developing after administration of tetanus toxin to several rat brain structures].

Abstract

Neuropathological syndromes following local tetanus toxin (TT) injection into different rat brain structures were studied. As demonstrated, there arose specific neuropathological signs dissimilar to those developing with different TT localization, i.e. as a rule the action of TT in the given brain parts was local. Experiments carried out confirmed the theory of the generator mechanisms of the neuropathological syndromes according to which specific manifestations of the corresponding syndrome were due to the localization of a generator of pathologically-enhanced excitation in definite brain structures.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B A Konnikov, M B Rekhtman. 1979. [Neuropathologic effects developing after administration of tetanus toxin to several rat brain structures].. https://pubmed.ncbi.nlm.nih.gov/420930/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Effect of naloxone, haloperidol and propranolol on cyclic 3',5'-adenosine monophosphate content of rat amygdala.

Naloxone (0.4 mg/kg, i.p.) causes an increase of cyclic adenosine monophosphate levels in the amygdala, but not in the hippocampus, caudate, or hypothalamus, of rats. The effect is antagonized by haloperidol (0.5 mg/kg, i.p.) and by propranolol (0.5 mg/kg, i.p.). This is consistent with the hypothesis of a tonic inhibitory influence of endogenous opiates on central dopaminergic and beta-noradrenergic systems. Haloperidol had an effect of its own on amygdala cyclic adenosine monophosphate levels which was blocked by propranolol. This suggests the possibility of an antagonistic interaction between dopaminergic and beta-noradrenergic innervation on this structure.

Amygdala

Muscarinic cholinergic regulation of epileptic spiking in kindling.

Electroencephalographic monitoring of spontaneous interictal spiking (SIS) following kindling demonstrated that SIS occurs in both amygdalas and that it declines sharply during the days following kindling. Systemically administered muscarinic antagonists which pass the blood-brain barrier (atropine and scopolamine) activated interictal spiking in kindled rats but not in controls. Interictal spiking activated by atropine was reversed by physostigmine. Both physostigmine and choline, agents which increase brain ACh concentration by different mechanisms, caused a reduction in spontaneous (not drug activated) interictal spiking. The results of these pharmacologic studies indicate that the interaction of endogenous ACh with central muscarinic receptors is capable of suppressing SIS in kindled rats. Whether cholinergic suppression of SIS represents a convulsant or an anticonvulsant action is presently unclear.

Amygdala