Biomedical subjects

D F MacFabe

Publications and source records attributed to D F MacFabe.

3 recordsLinked to original sources

PubMed1987

Electrical activity of the cingulate cortex. II. Cholinergic modulation.

The role of the cholinergic innervation in the modulation of cingulate electrical activity was studied by means of pharmacological manipulations and brain lesions. In the normal rat, an irregular slow activity (ISA) accompanied with EEG-spikes was recorded in the cingulate cortex during immobility as compared to walking. Atropine sulfate, but not atropine methyl nitrate, increased ISA and the frequency of cingulate EEG-spikes. Pilocarpine suppressed ISA and EEG-spikes during immobility, and induced a slow (4-7 Hz) theta rhythm. Unilateral or bilateral lesions of the substantia innominata and ventral globus pallidus area using kainic acid did not significantly change the cingulate EEG or its relation to behavior. Large electrolytic lesions of the medial septal nuclei and vertical limbs of the diagonal band generally decreased or abolished all theta activity in the cingulate cortex and the hippocampus. However, in 5 rats the cingulate theta rhythm increased while the hippocampal theta disappeared after a medial septal lesion. The large, postlesion cingulate theta, accompanied by sharp EEG-spikes during its negative phase, is an unequivocal demonstration of the existence of a theta rhythm in the cingulate cortex, independent of the hippocampal rhythm. Cholinergic afferents from the medial septum and diagonal band nuclei are inferred to be responsible for the behavioral suppression of cingulate EEG-spikes and ISA, and partially for the generation of a local cingulate theta rhythm. However, an atropine-resistant pathway and a theta-suppressing pathway, possibly coming from the medial septum or the hippocampus, may also be important in cingulate theta generation.

Acetylcholinesterase↗

PubMed1985

Topographical projection of cholinergic neurons in the basal forebrain to the cingulate cortex in the rat.

The cholinergic innervation of the rat's posterior cingulate cortex (Brodmann's area 29) was studied using acetylcholinesterase (AChE) histochemistry. Electrolytic lesion of the ipsilateral medial septum and diagonal band region (MS-DB) reduced the diffuse AChE staining in layers I, II, III and V of the cingulate cortex. Kainic acid lesion of the ipsilateral globus pallidus and substantia innominata area (GP-SI) abolished the dense band of AChE stain in layer IV, with small reductions of AChE stain in other layers. The results indicate that the medial cholinergic pathway from MS-DB terminates diffusely in layers I, II, III and V while the lateral cholinergic pathway from the GP-SI predominantly ends in layer IV of the posterior cingulate cortex.

Acetylcholinesterase↗

PubMed1984

Cholinergic activation of the electrocorticogram: role of the substantia innominata and effects of atropine and quinuclidinyl benzilate.

Systemic injection of quinuclidinyl benzilate partially abolished low voltage fast activity (LVFA) in the neocortex of waking rats, resulting in the appearance of large irregular slow waves during Type 2 behaviors (e.g. immobility, sniffing without head movement, face washing). These slow waves did not occur during Type 1 behavior (e.g. walking, head movement). Atropine sulfate produced a similar effect but it was less potent by a factor of about 12. Injection of kainic acid into the substantia innominata: (a) destroyed local cells which contain acetylcholinesterase (AChE) and reduced AChE staining in the ipsilateral neocortex; and (b) produced large slow waves in the ipsilateral neocortex during Type 2 behavior but not during Type 1 behavior. These slow waves were abolished by systemic injection of pilocarpine. Kainic acid injection into the thalamus produced extensive local cell loss but failed to produce slow waves in the neocortex. The data suggest that the LVFA which is normally present in the neocortex during waking Type 2 behavior is dependent on a cholinergic input to the neocortex from the substantia innominata. The relevance of these findings to Alzheimer's disease is discussed.

Animals↗