Limbic thalamus and state-dependent behavior: The paraventricular nucleus of the thalamic midline as a node in circadian timing and sleep/wake-regulatory networks

Colavito, Valeria; Tesoriero, Chiara; Wirtu, Amenu T.; Grassi-Zucconi, Gigliola; Bentivoglio, Marina

doi:10.1016/j.neubiorev.2014.11.021

Cited by 89 publications

(78 citation statements)

References 238 publications

(321 reference statements)

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“…Peak melatonin concentration in nocturnal periods [16] may contribute to decreased seizure occurrence in the early morning period (0:00-4:00). The hypothalamic suprachiasmatic nucleus (SCN) is the regulatory center of several physiological and behavioral circadian rhythms [17]. Suprachiasmatic nucleus periodicity and neuronal interactions have been hypothesized to play a role in the afternoon seizure occurrence peak [9].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Gender and age influence in daytime and nighttime seizure occurrence in epilepsy associated with mesial temporal sclerosis

Passarelli

Castro

2015

Epilepsy & Behavior

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Section: Discussionmentioning

confidence: 99%

“…Suprachiasmatic nucleus periodicity and neuronal interactions have been hypothesized to play a role in the afternoon seizure occurrence peak [9]. The SCN displays dense connectivity with the amygdala [17], and the SCN shows greater neuronal activity in daytime hours [16].…”

Section: Discussionmentioning

confidence: 99%

Gender and age influence in daytime and nighttime seizure occurrence in epilepsy associated with mesial temporal sclerosis

Passarelli

Castro

2015

Epilepsy & Behavior

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“…These neurons are activated upon exposure to cocaine or cocaine-associated cues (Brown et al, 1992;Franklin and Druhan, 2000;Matzeu et al, 2015), and disrupting the normal function of these neurons prevents cocaine priminginduced drug reinstatement, sensitization to cocaine, and expression of cocaine-conditioned placed preference (Young and Deutch, 1998;James et al, 2010;Browning et al, 2014). These addiction-related effects are thought to be mediated partially by PVT projections to the limbic system, particularly to the NAc and medial prefrontal cortex (mPFC) (Colavito et al, 2015). Notably, a portion of PVT neurons is highly branched, simultaneously projecting to both the NAc and mPFC (Schenk et al, 1991;Otake and Nakamura, 1998).…”

Section: The Pvt-to-nac Projectionmentioning

confidence: 99%

“…If cocaine-induced generation of silent synapses and the subsequent unsilencing of these synapses are indeed a synaptogensis process, this leads to a quantitative increase in the number of synapses, thus strengthening PVT to NAc transmission. The PVT is often regarded as an 'interface' that receives arousal-provoking stimuli signals, including visceral, reward, circadian, and sensory signals, and sends output signals to the NAc that regulate sensorimotor responses and motivated behaviors (Kelley et al, 2005;Parsons et al, 2007;Colavito et al, 2015). An overall strengthening of the PVT-to-NAc projection may thus increase and bias the responsiveness of the NAc to corresponding internal and external stimuli, contributing to the sensitized state of the animal after drug withdrawal.…”

Section: Circuitry Consequencesmentioning

confidence: 99%

Cocaine-Induced Synaptic Alterations in Thalamus to Nucleus Accumbens Projection

Neumann

Wang

Yan

et al. 2016

Neuropsychopharmacol

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Exposure to cocaine induces addiction-associated behaviors partially through remodeling neurocircuits in the nucleus accumbens (NAc). The paraventricular nucleus of thalamus (PVT), which projects to the NAc monosynaptically, is activated by cocaine exposure and has been implicated in several cocaine-induced emotional and motivational states. Here we show that disrupting synaptic transmission of select PVT neurons with tetanus toxin activated via retrograde trans-synaptic transport of cre from NAc efferents decreased cocaine selfadministration in rats. This projection underwent complex adaptations after self-administration of cocaine (0.75 mg/kg/infusion; 2 h/d × 5 d, 1 d overnight training). Specifically, 1d after cocaine self-administration, we observed increased levels of AMPA receptor (AMPAR)-silent glutamatergic synapses in this projection, accompanied by a decreased ratio of AMPAR-to-NMDA receptor (NMDAR)-mediated EPSCs. Furthermore, the decay kinetics of NMDAR EPSCs was significantly prolonged, suggesting insertion of new GluN2B-containing NMDARs to PVT-to-NAc synapses. After 45-d withdrawal, silent synapses within this projection returned to the basal levels, accompanied by a return of the AMPAR/NMDAR ratio and NMDAR decay kinetics to the basal levels. In amygdala and infralimbic prefrontal cortical projections to the NAc, a portion of cocaine-generated silent synapses becomes unsilenced by recruiting calcium-permeable AMPARs (CP-AMPARs) after drug withdrawal. However, the sensitivity of PVT-to-NAc synapses to CP-AMPAR-selective antagonists was not changed after withdrawal, suggesting that CP-AMPAR trafficking is not involved in the evolution of cocaine-generated silent synapses within this projection. Meanwhile, the release probability of PVT-to-NAc synapses was increased after short-and long-term cocaine withdrawal. These results reveal complex and profound alterations at PVT-to-NAc synapses after cocaine exposure and withdrawal.

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“…Studies in rodents have shown that PVT is activated by a variety of physical and psychological stressors including restraint 114, 115 , foot shock 116 , sleep deprivation 117 , and forced swim 118, 119 . In turn, PVT activity has been shown to modulate neuroendocrine 120, 121 , autonomic 114, 122 and behavioral responses to stress 123 . Together, these studies suggest that recruitment of PVT during the establishment of long-term fear memories may serve to coordinate adaptive responses to stress.…”

Section: Introductionmentioning

confidence: 99%

Retrieving fear memories, as time goes by…

Monte

Quirk

et al. 2016

Mol Psychiatry

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Fear conditioning researches have led to a comprehensive picture of the neuronal circuit underlying the formation of fear memories. In contrast, knowledge about the retrieval of fear memories is much more limited. This disparity may stem from the fact that fear memories are not rigid, but reorganize over time. To bring clarity and raise awareness on the time-dependent dynamics of retrieval circuits, we review current evidence on the neuronal circuitry participating in fear memory retrieval at both early and late time points after conditioning. We focus on the temporal recruitment of the paraventricular nucleus of the thalamus, and its BDNFergic efferents to the central nucleus of the amygdala, for the retrieval and maintenance of fear memories. Finally, we speculate as to why retrieval circuits change across time, and the functional benefits of recruiting structures such as the paraventricular nucleus into the retrieval circuit.

show abstract

Limbic thalamus and state-dependent behavior: The paraventricular nucleus of the thalamic midline as a node in circadian timing and sleep/wake-regulatory networks

Cited by 89 publications

References 238 publications

Gender and age influence in daytime and nighttime seizure occurrence in epilepsy associated with mesial temporal sclerosis

Gender and age influence in daytime and nighttime seizure occurrence in epilepsy associated with mesial temporal sclerosis

Cocaine-Induced Synaptic Alterations in Thalamus to Nucleus Accumbens Projection

Retrieving fear memories, as time goes by…

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