Decline of long-term potentiation (LTP) in the rat auditory cortex in vivo during postnatal life: Involvement of NR2B subunits

Hogsden, Jennifer L.; Dringenberg, Hans C.

doi:10.1016/j.brainres.2009.06.001

Cited by 29 publications

(34 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although previous studies have shown that excitability and neurotransmission in thalamocortical loops are susceptible to cholinergic modulation [46], [48], [66], there is still a lack of understanding on how synaptic plasticity in the MD-mPFC is affected by cholinergic-driven brain states. Here, our strategy of injecting PILO or NIC into the ventricle of anesthetized rats allowed us to achieve a global cholinergic activation that tried to mimic a physiological state of arousal or rapid-eye-movement (REM) sleep, which are endogenously regulated by ascending projections from the brainstem, basal forebrain, and septum [29], [30].…”

Section: Discussionmentioning

confidence: 99%

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

et al. 2012

View full text Add to dashboard Cite

The mediodorsal nucleus of the thalamus (MD) is a rich source of afferents to the medial prefrontal cortex (mPFC). Dysfunctions in the thalamo-prefrontal connections can impair networks implicated in working memory, some of which are affected in Alzheimer disease and schizophrenia. Considering the importance of the cholinergic system to cortical functioning, our study aimed to investigate the effects of global cholinergic activation of the brain on MD-mPFC synaptic plasticity by measuring the dynamics of long-term potentiation (LTP) and depression (LTD) in vivo. Therefore, rats received intraventricular injections either of the muscarinic agonist pilocarpine (PILO; 40 nmol/µL), the nicotinic agonist nicotine (NIC; 320 nmol/µL), or vehicle. The injections were administered prior to either thalamic high-frequency (HFS) or low-frequency stimulation (LFS). Test pulses were applied to MD for 30 min during baseline and 240 min after HFS or LFS, while field postsynaptic potentials were recorded in the mPFC. The transient oscillatory effects of PILO and NIC were monitored through recording of thalamic and cortical local field potentials. Our results show that HFS did not affect mPFC responses in vehicle-injected rats, but induced a delayed-onset LTP with distinct effects when applied following PILO or NIC. Conversely, LFS induced a stable LTD in control subjects, but was unable to induce LTD when applied after PILO or NIC. Taken together, our findings show distinct modulatory effects of each cholinergic brain activation on MD-mPFC plasticity following HFS and LFS. The LTP-inducing action and long-lasting suppression of cortical LTD induced by PILO and NIC might implicate differential modulation of thalamo-prefrontal functions under low and high input drive.

show abstract

Section: Discussionmentioning

confidence: 99%

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

et al. 2012

View full text Add to dashboard Cite

show abstract

“…This TC critical period corresponds to a time when silent synapses are present and long-term synaptic plasticity can be induced at TC inputs to L4 (Crair and Malenka, 1995; Daw et al, 2007b; Feldman et al, 1998; Isaac et al, 1997; Kidd and Isaac, 1999). Nevertheless, in contrast to the observations on the slice preparation studies, there is growing evidence to show the potential contribution of changes of TC inputs to adult brain plasticity detected in vivo (Cooke and Bear, 2010; Hogsden and Dringenberg, 2009; Lee and Ebner, 1992). In the present study the MEMRI and slice electrophysiology data demonstrate that changes in TC inputs to L4 make a major contribution to experience dependent plasticity in the mature brain past the end of the TC critical period.…”

Section: Discussionmentioning

confidence: 80%

Thalamocortical Inputs Show Post-Critical-Period Plasticity

Chung

Chen

et al. 2012

Neuron

View full text Add to dashboard Cite

Summary Experience-dependent plasticity in the adult brain has clinical potential for functional rehabilitation following central and peripheral nerve injuries. Here, plasticity induced by unilateral infraorbital (IO) nerve resection in four week-old rats was mapped using MRI and synaptic mechanisms were elucidated by slice electrophysiology. Functional MRI demonstrates a cortical potentiation compared to thalamus two weeks after IO nerve resection. Tracing thalamocortical (TC) projections with manganese-enhanced MRI revealed circuit changes in the spared layer 4 (L4) barrel cortex. Brain slice electrophysiology revealed TC input strengthening onto L4 stellate cells due to an increase in postsynaptic strength and the number of functional synapses. This work shows that the TC input is a site for robust plasticity after the end of the previously defined critical period for this input. Thus, TC inputs may represent a major site for adult plasticity in contrast to the consensus that adult plasticity mainly occurs at cortico-cortical connections.

show abstract

“…Electrophysiological assessments were carried out at the end of the treatment period (rat age of about 90–95 days) and followed previously established procedures [21, 22]. Rats were anesthetized using urethane (Sigma-Aldrich, Oakville, ON, Canada; 1.5 g/kg, given as three intraperitoneal (i.p.)…”

Section: Methodsmentioning

confidence: 99%

“…Stimulation trains were repeated every 10 s for a total of four trains. This induction protocol has previously been shown to elicit reliable LTP in the thalamocortical auditory system in vivo [21, 22]. After the TBS delivery, fPSPs were recorded for 60 min (every 30 s), followed by a second TBS episode (same as above) and a final 60 min of fPSP recordings.…”

Section: Methodsmentioning

confidence: 99%

“…LTP in this projection system shows a sharp, age-dependent decline over postnatal life, with high levels of LTP present during the first 5-6 weeks of postnatal life, but only modest levels after postnatal day (PD) 100 [21]. Here, we tested whether chronic fluoxetine treatment of adult rats would restore LTP to levels normally seen only in juveniles, similar to the effects reported for plasticity in V1 of adult rodents [10].…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

Chronic Fluoxetine Treatment Suppresses Plasticity (Long-Term Potentiation) in the Mature Rodent Primary Auditory CortexIn Vivo

2014

Self Cite

View full text Add to dashboard Cite

Several recent studies have provided evidence that chronic treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine can facilitate synaptic plasticity (e.g., ocular dominance shifts) in the adult central nervous system. Here, we assessed whether fluoxetine enhances long-term potentiation (LTP) in the thalamocortical auditory system of mature rats, a developmentally regulated form of plasticity that shows a characteristic decline during postnatal life. Adult rats were chronically treated with fluoxetine (administered in the drinking water, 0.2 mg/mL, four weeks of treatment). Electrophysiological assessments were conducted using an anesthetized (urethane) in vivo preparation, with LTP of field potentials in the primary auditory cortex (A1) induced by theta-burst stimulation of the medial geniculate nucleus. We find that, compared to water-treated control animals, fluoxetine-treated rats did not express higher levels of LTP and, in fact, exhibited reduced levels of potentiation at presumed intracortical A1 synapses. Bioactivity of fluoxetine was confirmed by a reduction of weight gain and fluid intake during the four-week treatment period. We conclude that chronic fluoxetine treatment fails to enhance LTP in the mature rodent thalamocortical auditory system, results that bring into question the notion that SSRIs act as general facilitators of synaptic plasticity in the mammalian forebrain.

show abstract

Decline of long-term potentiation (LTP) in the rat auditory cortex in vivo during postnatal life: Involvement of NR2B subunits

Cited by 29 publications

References 55 publications

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

Thalamocortical Inputs Show Post-Critical-Period Plasticity

Chronic Fluoxetine Treatment Suppresses Plasticity (Long-Term Potentiation) in the Mature Rodent Primary Auditory CortexIn Vivo

Contact Info

Product

Resources

About