Long-term potentiation in the in vitro perirhinal cortex displays associative properties

Bilkey, David K.

doi:10.1016/0006-8993(96)00789-5

Cited by 49 publications

(39 citation statements)

References 12 publications

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“…Glutamate receptors are involved in the induction of synaptic plasticity in different brain regions (Bliss and Collingridge, 1993;Bear and Abraham, 1996;Bilkey, 1996;McCaffery et al, 1999;Ziakopoulos et al, 1999;Cho et al, 2000), but it is unclear how other neurotransmitter systems modulate synaptic plasticity in the CNS. We now demonstrate that pharmacological activation of acetylcholine receptors induces LTD in the mPFC.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Stimulus intensity was adjusted to induce Ϸ50% of the maximal synaptic response. LTP was induced by a 100-Hz theta-burst stimulation (TBS), consisting of four sets of stimulations delivered 15 s apart, each one consisting of 10 bursts of five pulses at 100 Hz with interburst intervals of 150 ms (28). Two weaker TBSs were also used, including (i) 25-Hz TBS, differing only in the frequency at which the five pulses were delivered, and (ii) a 100-Hz TBS, consisting of two sets of stimulations at 100 Hz instead of four sets [TBS-100 Hz (two sets)].…”

Section: Methodsmentioning

confidence: 99%

Induction of long-term potentiation and depression is reflected by corresponding changes in secretion of endogenous brain-derived neurotrophic factor

Aicardi

Argilli

Cappello

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

222

158

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Neurotrophins play an important role in modulating activitydependent neuronal plasticity. In particular, threshold levels of brain-derived neurotrophic factor (BDNF) are required to induce long-term potentiation (LTP) in acute hippocampal slices. Conversely, the administration of exogenous BDNF prevents the induction of long-term depression (LTD) in the visual cortex. A long-standing missing link in the analysis of this modulatory role of BDNF was the determination of the time-course of endogenous BDNF secretion in the same organotypic preparation in which LTP and LTD are elicited. Here, we fulfilled this requirement in slices of perirhinal cortex. Classical theta-burst stimulation patterns evoking LTP lasting >180 min elicited a large increase in BDNF secretion that persisted 5-12 min beyond the stimulation period. Weaker theta-burst stimulation patterns leading only to the initial phase of LTP (Ϸ35 min) were accompanied by a smaller increase in BDNF secretion lasting <1 min. Sequestration of BDNF by TrkB-IgG receptor bodies prevented LTP. Low-frequency stimulations leading to LTD were accompanied by reductions in BDNF secretion that never lasted beyond the duration of the stimulation. N eurotrophins, in particular brain-derived neurotrophic factor (BDNF), play an important modulatory role in activitydependent neuronal plasticity (1-5). The physiological relevance of this action is based on the observation that BDNF differentially modulates activity-dependent changes in synaptic strength, as reflected by long-term potentiation (LTP) and long-term depression (LTD), which are cellular paradigms for learning and memory (6). Hippocampal LTP is strongly impaired in both BDNF (7-9) and TrkB (10, 11) knock-out mice. Conversely, LTD in the visual cortex is facilitated by blocking anti-BDNF Abs or TrkB-IgG receptor bodies (12). It is of particular interest that in the hippocampus of BDNF knock-out mice (7) the extent of LTP reduction is the same in both homozygote and heterozygote animals, indicating that a minimal, critical concentration of BDNF has to be available to fulfill its modulatory functions. LTP could be rescued by adenoviral-mediated (re)expression of BDNF in the CA1 region (8) or administration of exogenous BDNF (9). Relatively detailed studies have been performed on the regulation of BDNF synthesis (13-17) and secretion (18)(19)(20)(21)(22)(23)(24)(25)(26)(27). The studies concerned with the regulation of BDNF secretion have been conducted in reductionistic systems, such as synaptosomes (18) and dissociated neuronal cultures in which BDNF secretion was evoked by high potassium depolarization or exogenous neurotransmitter administration (19-24). Recent studies using primary cultures of hippocampal neurons were designed specifically to investigate the relationship between electrical stimulation parameters and BDNF secretion. However, to reach this goal either the overexpression of BDNF (25, 26) or long stimulation periods in nontranduced cultures (27) were necessary to permit the determination of BDNF secret...

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“…For example, 100 Hz high frequency stimulation (HFS) in layers II/III neurons of the perirhinal cortex in vitro produces NMDA receptor-dependent long-term potentiation (LTP) in the same layers (Bilkey, 1996) and, tetanic and theta-burst stimulation at 100 Hz in layers II/III can also induce NMDA receptor-dependent LTP in layer I neurons (Ziakopoulos et al, 1999). LTP in the perirhinal cortex is associated with an increase in BDNF secretion in the first 5-12 post-stimulation and this LTP can be blocked by inhibiting the BDNF receptor TrkB (Aicardi et al, 2004).…”

Section: Synaptic Plasticity In the Perirhinal Cortexmentioning

confidence: 99%

The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

Kealy

Commins

2011

Progress in Neurobiology

105

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Long-term potentiation in the in vitro perirhinal cortex displays associative properties

Cited by 49 publications

References 12 publications

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

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

Induction of long-term potentiation and depression is reflected by corresponding changes in secretion of endogenous brain-derived neurotrophic factor

The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

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