Effect of anticholinergic drug on long-term potentiation in rat hippocampal slices

Hirotsu, Ichiro; Hori, Nobuaki; Katsuda, Nobuo; Ishihara, Takafumi

doi:10.1016/0006-8993(89)90561-1

Cited by 102 publications

(29 citation statements)

References 19 publications

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“…Several in vitro studies have demonstrated a cholinergic enhancement of hippocampal LTP using cholinergic agonists or AChE inhibitors [21,23,83]. In anesthetized rats, hippocampal LTP facilitated by tetanic stimulation of the MS was blocked by systemic administration of cholinergic antagonists [24,25] and MS tetanus delivered longer than 5 min before hippocampal LTP induction will not potentiate hippocampal responses [25].…”

Section: Septohippocampal Cholinergic Modulation Of Ltpmentioning

confidence: 99%

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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Section: Septohippocampal Cholinergic Modulation Of Ltpmentioning

confidence: 99%

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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“…22 Scopolamine also suppressed potentiation of the population spike in CA1. 19,21 In a different study, however, scopolamine had no effect on LTP induction in CA1 but suppressed LTP in CA3. 37 Finally, effects of cholinergic antagonists on LTP induction were different according to tetanic stimulation patterns.…”

mentioning

confidence: 93%

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat

et al. 2000

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“…Pharmacological activation of mAChRs facilitates induction of long-term potentiation (LTP) in various brain regions (Blitzer et al, 1990;Burgard and Sarvey, 1990;Bröcher et al, 1992;Patil et al, 1998) and, under some circumstances, produces a lasting enhancement of synaptic transmission in hippocampus (Ito et al, 1988;Segal, 1994, 1996;Kojima and Onodera, 1998). Blockade of acetylcholine receptors can also block induction of LTP (Hirotsu et al, 1989;Katsuki et al, 1992;Kobayashi et al, 1997;Hess and Donoghue, 1999). Furthermore, mAChR activation facilitates (Kirkwood et al, 1999) or induces LTD in visual cortex (McCoy and McMahon, 2007) and induces LTD in perirhinal cortex (Massey et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Induction of Activity-Dependent LTD Requires Muscarinic Receptor Activation in Medial Prefrontal Cortex

Caruana¹,

Warburton²,

Bashir³

2011

J. Neurosci.

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The medial prefrontal cortex (mPFC) forms part of a neural circuit involved in the formation of lasting associations between objects and places. Cholinergic inputs from the basal forebrain innervate the mPFC and may modulate synaptic processes required for the formation of object-in-place memories. To investigate whether acetylcholine regulates synaptic function in the rat mPFC, whole-cell voltage-clamp recordings were made from pyramidal neurons in layer V. Bath application of the cholinergic agonist carbachol caused a potent and long-term depression (LTD) of synaptic responses that was blocked by the muscarinic receptor antagonist scopolamine and was mimicked, in part, by the M 1 receptor agonists McN-A-343 or AF102B. Furthermore, inhibition of PKC blocked carbachol-mediated LTD. We next determined the requirements for activity-dependent LTD in the prefrontal cortex. Synaptic stimulation that was subthreshold for producing LTD did, however, result in LTD when acetylcholine levels were enhanced by inhibition of acetylcholinesterase or when delivered in the presence of the M 1 -selective positive allosteric modulator BQCA. Increasing the levels of synaptic stimulation resulted in M 1 receptor-dependent LTD without the need for pharmacological manipulation of acetylcholine levels. These results show that synaptic stimulation of muscarinic receptors alone can be critical for plastic changes in excitatory synaptic transmission in the mPFC. In turn, these muscarinic mediated events may be important in the formation of object-in-place memories. A loss of basal forebrain cholinergic neurons is a classic hallmark of Alzheimer's dementia and our results provide a potential explanation for the loss of memory associated with the disease.

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Effect of anticholinergic drug on long-term potentiation in rat hippocampal slices

Cited by 102 publications

References 19 publications

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat

Induction of Activity-Dependent LTD Requires Muscarinic Receptor Activation in Medial Prefrontal Cortex

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