Cholinergic plasticity in the hippocampus

Abstract

Tests were made for use-dependent plasticity in the cholinergic projections to hippocampus. Transient infusion of the cholinergic agonist carbachol into hippocampal slices induced rhythmic activity that persisted for hours after washout. Comparable effects were obtained with physostigmine, a drug that blocks acetylcholine breakdown and thereby enhances cholinergic transmission. It thus seems that activation of cholinergic synapses induces lasting changes in hippocampal physiology. Two lines of evidence indicated that cholinergic synapses are also the sites at which the plasticity is expressed. First, the induction and expression of the rhythms were not blocked by the N-methyl-D-aspartate receptor antagonist D-2-amino-5-phosphonovaleric acid, indicating that a long-term potentiation effect between pyramidal cells was not involved. Second, a muscarinic antagonist (atropine) completely abolished stable rhythmic activity after agonist washout. This result indicates that endogenous cholinergic activity is responsible for the persistence of rhythmic oscillations. These experiments suggest that short periods of intense cholinergic activity induce lasting changes in cholinergic synapses and thus extend such forms of plasticity to beyond the glutamatergic system.

Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer β-amyloid peptide in rodent

“…40), a recent study suggested that cholinergic neurons may also have similar plasticity. Colgin et al (25) showed that endogenous activity of cholinergic pathways in the hippocampus (probably within the field CA3) could induce electrophysiological responses that resembled LTP following brief periods of intense activity. Therefore, the role of cholinergic neurons in learning and memory may involve direct effects besides a modulatory role via glutamatergic synapses.…”

“…Studies were performed on transverse slices of rat brain (male Sprague-Dawley-Harlan, 10-25 days old, n ϭ 6). Standard procedures for preparing and maintaining hippocampal slices (350 m) in artificial CSF (ACSF) were used (25,26). Slices were allowed to recover for at least 1 h, transferred to a submerged recording chamber, and continuously perfused at 2 ml͞min in media (30-32°C).…”

Selective septohippocampal – but not forebrain amygdalar – cholinergic dysfunction in diencephalic amnesia

“…However, to answer that question we must also understand the molecular mechanisms responsible for the Cholinergic activation in the hippocampus triggers rhythmic activity that can persist for hours and such rhythmic activity is related to both learning and neural plasticity [11]. Furthermore, our recent data demonstrated that when the hippocampal ACh levels are increased in the hippocampus by direct application of physostigmine, the behavioral impairment in spontaneous alternation in PTD rats is eliminated (unpublished data).…”

The Role of Acetylcholine in Cocaine Addiction

“…Hippocampal ACh is theorized to facilitate the encoding of new information by simultaneously suppressing excitatory synaptic transmission and enhancing long-term potentiation, while leaving excitatory feed-forward synapses relatively unaffected (Hasselmo et al, 2002). ACh also modulates synaptic plasticity within the hippocampus (Colgin et al, 2003) and long-term potentiation is drastically reduced in genetically engineered mice lacking the mACh M 2 receptor (Seeger et al, 2004).…”