Differential projections from the mediodorsal and centrolateral thalamic nuclei to the frontal cortex in rats

Wang, Chia–Chuan; Shyu, Bai-Chuang

doi:10.1016/j.brainres.2003.10.006

Cited by 78 publications

(61 citation statements)

References 54 publications

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“…The ACC primarily receives extensive projections from the mediodorsal thalamic nucleus and broadly connects with relevant regions of the descending modulation system, including PAG [4,19] . Recent functional imaging data provide evidence that the rostral ACC is a crucial cortical area for placebo analgesia and that this type of endogenous pain control depends on the enhanced functional connectivity of the rostral ACC with subcortical brain structures that are crucial for conditioned learning and descending inhibition of nociception [20] .…”

Section: Involvement Of Acc In Nociceptive Modulationmentioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary (SΙ) and secondary somatosensory (SΠ) cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.

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Section: Involvement Of Acc In Nociceptive Modulationmentioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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“…Layer II/III of the PFC was examined because preliminary data indicated a greater impact of PCP on synapses in this layer, and because layer II/III is critical for cognitive function, being the origin and termination of profuse corticocortical connections (Fuster, 1997). In addition, the mediodorsal thalamus, a region implicated in the pathology of schizophrenia (Cronenwett and Csernansky, 2010), projects heavily to layer III of PFC (Wang and Shyu, 2004), and virtually all of the inputs from mediodorsal thalamus to layer III of rat PFC make asymmetric synapses on dendritic spines (Rotaru et al, 2005). As the loss of dendritic spine synapses in the PFC may contribute in part to the PCP-induced cognitive dysfunction and decreased prefrontal cellular activity observed in the rat model (Jentsch and Roth, 1999), we have examined the time course of the loss of asymmetric spine synapses on pyramidal neurons in layer II/III, and the relationship of synapse loss to the cognitive deficits observed following PCP treatment.…”

Section: Introductionmentioning

confidence: 99%

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

Elsworth

Morrow

Hajszán

et al. 2011

Neuropsychopharmacol

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Enduring cognitive deficits exist in schizophrenic patients, long-term abusers of phencyclidine (PCP), as well as in animal PCP models of schizophrenia. It has been suggested that cognitive performance and memory processes are coupled with remodeling of pyramidal dendritic spine synapses in prefrontal cortex (PFC), and that reduced spine density and number of spine synapses in the medial PFC of PCP-treated rats may potentially underlie, at least partially, the cognitive dysfunction previously observed in this animal model. The present data show that the decrease in number of asymmetric (excitatory) spine synapses in layer II/III of PFC, previously noted at 1-week post PCP treatment also occurs, to a lesser degree, in layer V. The decrease in the number of spine synapses in layer II/III was sustained and persisted for at least 4 weeks, paralleling the observed cognitive deficits. Both acute and chronic treatment with the atypical antipsychotic drug, olanzapine, starting at 1 week after PCP treatment at doses that restore cognitive function, reversed the asymmetric spine synapse loss in PFC of PCP-treated rats. Olanzapine had no significant effect on spine synapse number in saline-treated controls. These studies demonstrate that the effect of PCP on asymmetric spine synapse number in PFC lasts at least 4 weeks in this model. This spine synapse loss in PFC is reversed by acute treatment with olanzapine, and this reversal is maintained by chronic oral treatment, paralleling the time course of the restoration of the dopamine deficit, and normalization of cognitive function produced by olanzapine.

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“…Previous anatomical studies have revealed that the ACC area has different projecting fibers and cell types within different layers [3][4][5][6] . Additionally, the inter-layer connections have also been well investigated [32,33] .…”

Section: Discussionmentioning

confidence: 99%

“…with ad libitum water and rat chow. The experimental proceother brain structures [3][4][5] . Especially, several lines of evidence from animals to human studies have suggested that the ACC serves as an important limbic structure for the central process of pain [6,7] .…”

Section: Introductionmentioning

confidence: 99%

长串与短串θ节律刺激在大鼠前扣带回皮质脑片诱导长时程增强效应的不同作用: 平面微电极阵列记录技术

2009

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Objective There is substantial evidence supporting the notion that the anterior cingulate cortex (ACC) is an important limbic structure involved in multiple brain functions such as sensory perception, motor conflict monitoring, memory, emotion and cognition. It has been shown that long term potentiation (LTP) is an important synaptic model of neural plasticity in the ACC, however, little is known about the spatiotemporal properties of ACC at network level. The present study was designed to see the LTP induction effects across different layers of the ACC by using different conditioning stimuli (CS) protocols. Methods A unique multi-electrode array recording technique was used in the acutely-dissociated ACC slices of rats. Long and short train theta burst stimulation (TBS) paradigms were applied in layer V-VI as the CS and the LTP induction effects were compared across different layers of the ACC. Briefly, both long and short train TBS are composed of bursts (4 pulses at 100 Hz) with a 200 ms interval, however, the former (TBS1) was with 10 trains and the latter (TBS2) was with 5 trains.After test stimulation at layer V-VI in the ACC, network field potentials (FPs) could be simultaneously recorded across all layers of the ACC. Results The waveforms of FPs were different across different layers. Namely, positive-going waveforms were recorded in layer I and negative-going waveforms were recorded in layers V-VI, in contrast, complex waveforms were localized mainly in layers II-III. Following application of two CS protocols, the induction rate of LTP was significantly different between TBS1 and TBS2 regardless of the spatial properties. TBS1 had more than 60% success, while TBS2 was less than 25% in induction of LTP. Moreover, both the 2 CS protocols could induce LTP in layers II-III and layers V-VI without layer-related difference. However, no LTP was inducible in layer I. Conclusion The present findings indicate that stimulation protocols may, at least in part, account for a large portion of variations among previous LTP studies, and hence highlight the importance of selecting the best LTP induction protocol when designing such experiments. Moreover, the present results demonstrate the prominent superiority of multi-electrode array recording in revealing the network properties of synaptic activities in the ACC, especially in comparing the spatiotemporal characteristics between different layers of this structure.

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Differential projections from the mediodorsal and centrolateral thalamic nuclei to the frontal cortex in rats

Cited by 78 publications

References 54 publications

Cerebral cortex modulation of pain

Cerebral cortex modulation of pain

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

长串与短串θ节律刺激在大鼠前扣带回皮质脑片诱导长时程增强效应的不同作用: 平面微电极阵列记录技术

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