Antagonism of N‐methylaspartate and synaptic responses of neurones in the rat ventrobasal thalamus by ketamine and MK‐801

Salt, Thomas E.; Wilson, David; Prasad, Sujata

doi:10.1111/j.1476-5381.1988.tb11546.x

Cited by 36 publications

(13 citation statements)

References 15 publications

(23 reference statements)

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“…Furthermore, we failed, by using a higher intraperitoneal dose (0.5%, 100 mg/kg) because of too much side effects, in observing the possible inhibitory effect on the spinal astrocytic activation. Intraperitoneal injection of ketamine majorly activate supraspinal sites, such as thalamus, cerebral cortex and descending inhibitory system in the midbrain, and then contribute to the analgesic effect (Kawamata et al 2000;Koizuka et al 2005;Salt et al 1988;Salt 1986;Thomson et al 1985), while leave the spinal astrocytes intact. But how does ketamine function on spinal astrocytes after intrathecal injection?…”

Section: Discussionmentioning

confidence: 99%

Inhibiting astrocytic activation: a novel analgesic mechanism of ketamine at the spinal level?

Mei

Wang

et al. 2009

Journal of Neurochemistry

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Although ketamine is widely used as an analgesic agent and has an anti‐allodynic effect on neuropathic pain, the underlying analgesic mechanisms are not fully explained by the modern ‘neuronal‐based’ theories. As emerging studies have focused on the critical role of spinal astrocytes in the pathological pain states, we have hypothesized that there exist some ‘astrocytes‐related’ mechanisms in the analgesic function of ketamine. In the present study, using the spinal nerve ligation (SNL) pain model, we investigated the anti‐nociceptive effects of intraperitoneal or intrathecal ketamine on SNL‐induced neuropathic pain response, meanwhile, we investigated the astrocytic activation after ketamine administration on SNL rats. Behavioral data showed that either intraperitoneal or intrathecal ketamine inhibited SNL‐induced allodynia, however, immunohistochemistry showed that SNL induced astrocytic activation was suppressed by intrathecal but not intraperitoneal ketamine. Using quantitative Western blot analysis, our report showed that intrathecal ketamine down‐regulated glial fibrillary acidic protein expression, suggesting inhibition of SNL‐induced astrocytic activation, which wasn’t influenced by intraperitoneal administration. We conclude that intraperitoneal ketamine could alleviate SNL‐induced neuropathic pain via the classical ‘neuronal‐based’ mechanisms, but in addition, ‘astrocytes‐related’ mechanisms were also important underlying the anti‐allodynic effect of intrathecal ketamine.

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Section: Discussionmentioning

confidence: 99%

Inhibiting astrocytic activation: a novel analgesic mechanism of ketamine at the spinal level?

Mei

Wang

et al. 2009

Journal of Neurochemistry

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“…Synapses are responsible for dynamic processes that regulate neuronal responsiveness and plasticity. Sensory-evoked TC responses include NMDAr-dependent component (Heynen and Bear, 2001;Salt et al, 1988). So, if ketamine decreases the amplitude of the sensory-evoked TC response, it is expected to reduce the LTP, at least of the TC neurotransmission (Heynen and Bear, 2001).…”

Section: Ketamine Disrupts Thalamocortical Ltpmentioning

confidence: 99%

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

Kulikova

Tolmacheva

Anderson

et al. 2012

Eur J of Neuroscience

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Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing Sofya P Kulikova (1,2)*, Elena A Tolmacheva (1,2)**, Paul Anderson (1,2,3), Julien Gaudias (1,2)***, Brendan E Adams (1,2)****, Thomas Zheng (1,2,3), and Didier Pinault (1,2)(1) INSERM U666, physiopathologie et psychopathologie cognitive de la schizophrénie, Strasbourg, France. Abstract:Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in cortex-related networks. However, the underlying anatomo-functional mechanisms remain elusive. Clinical and experimental evidence suggest that these deficits result from a hyporegulation of glutamate N-Methyl d-Aspartate receptors (NMDAr). Here we modeled these deficits in rats with ketamine, a non-competitive NMDAr antagonist and a translational psychotomimetic substance at subanesthetic doses. We tested the hypothesis that ketamine-induced sensory deficits involve an impairment of the ability of the thalamocortical (TC) system to discriminate the relevant information from the baseline activity. Furthermore we wanted to assess whether ketamine disrupts synaptic plasticity in TC systems. We conducted multisite network recordings in the rat somatosensory TC system, natural stimulation of the vibrissae and high-frequency electrical stimulation (HFS) of the thalamus.A single systemic injection of ketamine increased the amount of baseline GFO, reduced the amplitude of the sensory-evoked TC response and decreased the power of the sensoryevoked GFO. Furthermore, cortical application of ketamine elicited local and distant increases in baseline GFO. The ketamine effects were transient. Unexpectedly, HFS of the TC pathway had opposite actions. In conclusion, ketamine and thalamic HFS have opposite effects on the ability of the somatosensory TC system to discriminate the sensory-evoked response from the baseline GFO during information processing. Investigating the link between the state and function of the TC system may conceptually be a key strategy to design innovative therapies against neuropsychiatric disorders. 3The anatomofunctional mechanisms of sensory and cognitive deficits in schizophrenia are unknown. These deficits are commonly associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in corticocortical and thalamocortical (TC) circuits (Bokde et al., 2009;Clinton and Meador-Woodruff, 2004;de Haan W. et al., 2009;Friston, 2002;Herrmann and Demiralp, 2005;Light et al., 2006;Lisman, 2011;Meyer-Lindenberg, 2010;Pinault, 2011;Spencer et al., 2003;Uhlhaas and Singer, 2006). At least four types of GFO should be considered: 1) Spontaneously-occurring (baseline) GFO, which are dominant during desynchronized state of the electroencephalogram (Jasper, 1936;Sheer, 1975); 2) Sensory-evoked GFO, which are phase-locked to the stimulus onset (Pantev et al., 1991;Spencer et al., 2008b); 3) Steadystate GFO during r...

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“…Importantly, the corresponding NMDAR-related response is antagonized by the NMDAR antagonist ketamine or MK-801 [207], which significantly increases the power, and the synchrony, of ongoing GFO in the highly-distributed CT-TC systems [59,60,61,62]. Moreover, the CT pathway significantly contributes to thalamic GFO [59,208].…”

Section: Three Candidates For Preventive Tesmentioning

confidence: 99%

A Neurophysiological Perspective on a Preventive Treatment against Schizophrenia Using Transcranial Electric Stimulation of the Corticothalamic Pathway

Pinault

2017

Brain Sciences

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Schizophrenia patients are waiting for a treatment free of detrimental effects. Psychotic disorders are devastating mental illnesses associated with dysfunctional brain networks. Ongoing brain network gamma frequency (30–80 Hz) oscillations, naturally implicated in integrative function, are excessively amplified during hallucinations, in at-risk mental states for psychosis and first-episode psychosis. So, gamma oscillations represent a bioelectrical marker for cerebral network disorders with prognostic and therapeutic potential. They accompany sensorimotor and cognitive deficits already present in prodromal schizophrenia. Abnormally amplified gamma oscillations are reproduced in the corticothalamic systems of healthy humans and rodents after a single systemic administration, at a psychotomimetic dose, of the glutamate N-methyl-d-aspartate receptor antagonist ketamine. These translational ketamine models of prodromal schizophrenia are thus promising to work out a preventive noninvasive treatment against first-episode psychosis and chronic schizophrenia. In the present essay, transcranial electric stimulation (TES) is considered an appropriate preventive therapeutic modality because it can influence cognitive performance and neural oscillations. Here, I highlight clinical and experimental findings showing that, together, the corticothalamic pathway, the thalamus, and the glutamatergic synaptic transmission form an etiopathophysiological backbone for schizophrenia and represent a potential therapeutic target for preventive TES of dysfunctional brain networks in at-risk mental state patients against psychotic disorders.

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Antagonism of N‐methylaspartate and synaptic responses of neurones in the rat ventrobasal thalamus by ketamine and MK‐801

Cited by 36 publications

References 15 publications

Inhibiting astrocytic activation: a novel analgesic mechanism of ketamine at the spinal level?

Inhibiting astrocytic activation: a novel analgesic mechanism of ketamine at the spinal level?

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

A Neurophysiological Perspective on a Preventive Treatment against Schizophrenia Using Transcranial Electric Stimulation of the Corticothalamic Pathway

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