Regional distribution of choline acetyltransferase and acetylcholinesterase within the amygdaloid complex and stria terminalis system
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Cited by (112)
Pathophysiology of nAChRs: Limbic circuits and related disorders
2023, Pharmacological ResearchAmygdala: Structure and Function
2015, The Rat Nervous System: Fourth EditionPathophysiological mechanisms underlying increased anxiety after soman exposure: Reduced GABAergic inhibition in the basolateral amygdala
2014, NeuroToxicologyCitation Excerpt :A number of modulatory systems are involved in regulating BLA excitability, mainly by affecting the excitability state of the principal cells and/or the GABAergic interneurons. The cholinergic input to the amygdala from the basal forebrain appears to be of major importance in this regard, as suggested by the remarkably dense cholinergic innervation of the BLA (Mesulam et al., 1992), its exceptionally high AChE activity (Ben-Ari et al., 1977; Prager et al., 2013, 2014), as well as the increase in anxiety-like behavior when the function of the basal forebrain is disrupted (Martinowich et al., 2012). The most well known behavioral evidence for the importance of the cholinergic system in the regulation of amygdalar function comes from the symptoms of Alzheimer's disease, where anxiety is prevalent (Espana et al., 2010; Ferretti et al., 2001).
The recovery of acetylcholinesterase activity and the progression of neuropathological and pathophysiological alterations in the rat basolateral amygdala after soman-induced status epilepticus: Relation to anxiety-like behavior
2014, NeuropharmacologyCitation Excerpt :At 14 days after soman exposure, AChE had returned to control levels in the hippocampus, piriform, and prelimbic cortex, while in the BLA it recovered to nearly basal levels in 7 days. The faster time course of recovery in the BLA may relate to the exceptionally dense cholinergic innervation of this region (Mesulam et al., 1992) – also reflected in the high basal level of AChE (Ben-Ari et al., 1977; Prager et al., 2013) – which could result in a more efficient recovery of the enzyme. The recovery of AChE is probably the result of de novo AChE synthesis rather than dephosphorylation of the inhibited AChE, as the inhibition of AChE by nerve agents is irreversible, and the state of irreversibility is reached very fast after exposure to soman (Sirin et al., 2012).
Acetylcholinesterase inhibition in the basolateral amygdala plays a key role in the induction of status epilepticus after soman exposure
2013, NeuroToxicologyCitation Excerpt :But it is also possible that the cholinergic system has a more significant role in the regulation of the excitability of the BLA, compared to the hippocampus and piriform cortex, and thus cholinergic hyperactivity in the BLA is more likely to produce hyperexcitability and seizures. The exceptionally dense cholinergic innervation of the BLA (Mesulam et al., 1992), its markedly high concentration of AChE (Ben-Ari et al., 1977 and present study), and the high expression of muscarinic receptors – which play a primary role in seizure initiation by nerve agents (Skovira et al., 2010) – on BLA pyramidal cells (McDonald and Mascagni, 2010), may be attesting to the prominent role that the cholinergic system plays in the regulation of the BLA excitability. Why AChE activity in the BLA of the no-SE rats was not significantly inhibited remains to be determined.
Presynaptic muscarinic M <inf>2</inf> receptors modulate glutamatergic transmission in the bed nucleus of the stria terminalis
2012, NeuropharmacologyCitation Excerpt :Stress has also been shown to increase ACh release in limbic structures (Fadda et al., 2000; Mark et al., 1996; Nail-Boucherie et al., 2000; Tajima et al., 1996), where it is thought to play a critical role in modulating cognition, attention, and synaptic plasticity (Hasselmo and Barkai, 1995; Ovsepian et al., 2004). Several markers for cholinergic terminals are expressed in the BNST, namely choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) (Ben-Ari et al., 1977; Gaspar et al., 1985; Prensa et al., 2003; Ruggiero et al., 1990; Woolf and Butcher, 1982), suggesting that local ACh release may play an important role in modulating the activity of neurons in this region. The response to ACh is mediated by activation of either muscarinic receptors (mAChR) or nicotinic receptors (nAChR), and high levels of muscarinic receptors have been detected in the BNST (Kobayashi et al., 1978; Kushida et al., 1995; Spencer et al., 1986; Wamsley et al., 1984).
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Present address: Department of Pharmacology, Harvard Medical School, Boston, Mass. 02115, U.S.A.