Dorsal hippocampus field CA1 pyramidal cell responses to a persistent vs an acute nociceptive stimulus and their septal modulation

Khanna, Sanjay

doi:10.1016/s0306-4522(96)00456-3

Cited by 63 publications

(69 citation statements)

References 47 publications

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“…the temporoammonic path, in determining hippocampal function [41,53] Then what is the relationship between the two perforant path pathways to pain? Given the electrophysiological results from Khanna's group [56][57][58] , it might be logically predicted that formalin-induced pyramidal cell excitation is dependent on the excitatory input from the EC, implicating a possible link between EC and pain processing in the HF (see below). Nonetheless, the exact route by which peripheral noxious information enters the HF via the EC is still unclear, but here we try to propose two possibilities.…”

Section: Entorhinal Cortex As a Main Station Relaying Pain Sig-mentioning

confidence: 99%

“…In the discussion, the authors explained the finding by saying "One could hypothesize that the responses of SHNs to noxious peripheral stimulation are due to the input coming from locus coeruleus, raphe nuclei, and/or other brainstem structures." In addition, several studies from Khanna's group have shown a modulatory effect of this sepo-hippocampal pathway on hippocampal neuronal responses to formalin-evoked pain [56][57][58]75] . A systemic description of the cholinergic modulation of pain processing in the HF, either behaviorally or electrophysiologically, will be presented below.…”

Section: Septo-hippocampal Pathway An Alternative Pathwaymentioning

confidence: 99%

“…Furthermore, this depression of neuronal transmission was found to be dependent on the hippocampal EEG state of the animal [150] . To further characterize this phenomenon, Khanna and Sinclair [75] reported that: (1) sal hippocampal CA1 pyramidal cell responses to a persistent (formalin pain) versus an acute nociceptive stimulus [56] .…”

Section: Influences Of Cholinergic Input On Pain-evoked Responsesmentioning

confidence: 99%

“…Lastly, the septohippocampal cholinergic input, though might enhance the excitement of CA1 pyramidal cells (via disinhibition) at the cell body region [148,149] , evokes a presynaptic inhibition of excitatory synaptic transmission across the apical dendrites of these neurons and increases the inhibitory GABAergic tonus impinging upon them [157] . Based on these considerations, Khanna [56] [57] . Collectively, these results provide further support to the idea that formalin-induced theta activation, pyramidal cell suppression and 'signal-to-noise' processing are all influenced, at least partially, by a common network involving CA1 perisomatic inhibitory interneurons modulated by MS-VLDBB cholinergic inputs.…”

Section: Modulation Of Formalin-induced Nociceptive Processing In Thementioning

confidence: 99%

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Roles of the hippocampal formation in pain information processing

2009

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Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

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Section: Entorhinal Cortex As a Main Station Relaying Pain Sig-mentioning

confidence: 99%

Section: Septo-hippocampal Pathway An Alternative Pathwaymentioning

confidence: 99%

Section: Influences Of Cholinergic Input On Pain-evoked Responsesmentioning

confidence: 99%

Section: Modulation Of Formalin-induced Nociceptive Processing In Thementioning

confidence: 99%

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Roles of the hippocampal formation in pain information processing

2009

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“…Recently a study by Dutta et al indicates that the medial septal glutamate receptors play an important role in the modulation of immune responses [8]. There are significant numbers of studies suggesting a probable role of septal nuclei in modulation of pain [9][10][11][12][13][14][15][16][17][18]. While the nature of neurochemical transmission involved in the septal nuclei which causes modulation of pain have not been explored previously.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Pain by Naloxone and a Possible Role of Neurotransmitters with Selective Lesion of Septal Nuclei

Somade¹,

Brid²

2015

J Spine

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Septum occupies a strategic position in limbic system and has been implicated in variety of behaviors. Present study was designed to evaluate the role of medial septum in modulation of pain and explore the role of neurotransmitters.The present study was divided in two parts in first part the tail flick latencies were observed in rats with septal lesions and compared with sham operated ones. While in the second part, the effect of intraseptal injections of neurotransmitters and naloxone on tail flick latencies ofcannulated rats was recorded after intraseptal lesions.It was observed that the septal lesions decrease pain threshold. The interaseptal injection of Acetylcholine (5 µg to 20 µg) and Naloxone (5 µg to 20 µg) increases pain threshold. While the Interaseptal injection of Noradrenaline and Scopolamine decreases pain threshold.The findings of the present study suggest that septum may be involved in modulation of pain. The neurotransmitters like Acetylcholine, Noradrenaline and opioid peptides may have an individual or collective role to play in the observed pain modulation.

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Effects of glial glutamate transporter activator in formalin‐induced pain behaviour in mice

Alotaibi

Rahman

2018

European Journal of Pain

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Background Nociceptive pain remains a prevalent clinical problem and often poorly responsive to the currently available analgesics. Previous studies have shown that astroglial glutamate transporter‐1 (GLT‐1) in the hippocampus and anterior cingulate cortex (ACC) is critically involved in pain processing and modulation. However, the role of astroglial GLT‐1 in nociceptive pain involving the hippocampus and ACC remains unknown. We investigated the role of 3‐[[(2‐Methylphenyl) methyl]thio]‐6‐(2‐pyridinyl)‐pyridazine (LDN‐212320), a GLT‐1 activator, in nociceptive pain model and hippocampal‐dependent behavioural tasks in mice. Methods We evaluated the effects of LDN‐212320 in formalin‐induced nociceptive pain model. In addition, formalin‐induced impaired hippocampal‐dependent behaviours were measured using Y‐maze and object recognition test. Furthermore, GLT‐1 expression and extracellular signal‐regulated kinase phosphorylation (pERK1/2) were measured in the hippocampus and ACC using Western blot analysis and immunohistochemistry. Results The LDN‐212320 (10 or 20 mg/kg, i.p) significantly attenuated formalin‐evoked nociceptive behaviour. The antinociceptive effects of LDN‐212320 were reversed by systemic administration of DHK (10 mg/kg, i.p), a GLT‐1 antagonist. Moreover, LDN‐212320 (10 or 20 mg/kg, i.p) significantly reversed formalin‐induced impaired hippocampal‐dependent behaviour. In addition, LDN‐212320 (10 or 20 mg/kg, i.p) increased GLT‐1 expressions in the hippocampus and ACC. On the other hand, LDN‐212320 (20 mg/kg, i.p) significantly reduced formalin induced‐ERK phosphorylation, a marker of nociception, in the hippocampus and ACC. Conclusion These results suggest that the GLT‐1 activator LDN‐212320 prevents nociceptive pain by upregulating astroglial GLT‐1 expression in the hippocampus and ACC. Therefore, GLT‐1 activator could be a novel drug candidate for nociceptive pain. Significance The present study provides new insights and evaluates the role of GLT‐1 activator in the modulation of nociceptive pain involving hippocampus and ACC. Here, we provide evidence that GLT‐1 activator could be a potential therapeutic utility for the treatment of nociceptive pain.

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Dorsal hippocampus field CA1 pyramidal cell responses to a persistent vs an acute nociceptive stimulus and their septal modulation

Cited by 63 publications

References 47 publications

Roles of the hippocampal formation in pain information processing

Roles of the hippocampal formation in pain information processing

Modulation of Pain by Naloxone and a Possible Role of Neurotransmitters with Selective Lesion of Septal Nuclei

Effects of glial glutamate transporter activator in formalin‐induced pain behaviour in mice

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