Noxious stimuli produce prolonged changes in the CA1 region of the rat hippocampus

Khanna, Sanjay; Sinclair, John G.

doi:10.1016/0304-3959(89)90047-x

Cited by 62 publications

(39 citation statements)

References 25 publications

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“…Overall, all of these four studies provide converging evidence that painful stimulation can indeed elicit electrophysiological changes in the septum and HF, the response pattern of which partially relies on the cholinergic inputs. 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: 91%

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: Influences Of Cholinergic Input On Pain-evoked Responsesmentioning

confidence: 91%

Roles of the hippocampal formation in pain information processing

2009

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“…For example, Sacchetti et al demonstrated that shock, alone, did not affect baseline excitability in the hippocampus, in vitro, either soon after shock delivery or 7 days later. Numerous other studies on the hippocampus, in vitro and in vivo, have shown that stress or corticosterone can block LTP without increasing baseline excitability (Foy et al, 1987;Khanna and Sinclair, 1989;Diamond et al, 1990;Khanna and Sinclair, 1992;Shors and Dryver, 1994;Diamond et al, 1994;Hesen and Joels, 1996a;Garcia et al, 1997;Xu et al, 1997;Khanna, 1997;Shors et al, 1997b;Bramham et al, 1998;Garcia et al, 1998b;Mesches et al, 1999;Diamond et al, 1999a;Alfarez et al, 2002;Yamada et al, 2003;Joels et al, 2003;Kim et al, 2005). This issue was revisited recently by Kim et al, (2005), who noted that stress blocked the induction of LTP, but did not increase baseline synaptic transmission in CA1, as indicated by an absence of stress effects on inputoutput (I/O) functions (p. 1538).…”

Section: Does Stress Generate An Endogenous Form Of Ltp?mentioning

confidence: 99%

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

et al. 2005

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ABSTRACT:This speculative review serves two purposes. First, it as an extension of the ideas we developed in a previous review (Diamond et al., Hippocampus, 2004;14:281-291), and second, it is a rebuttal to Abraham's (Hippocampus, 2004;14:675-676) critique of that review. We had speculated on the functional significance of the finding that post-training LTP induction produces retrograde amnesia. We noted the similarities between the findings that strong tetanizing stimulation can produce LTP and retrograde amnesia, and that a strong emotional experience can produce a long-lasting memory and retrograde amnesia, as well. The commonalities between LTP induction and emotional learning provided the basis of our hypothesis that an emotional experience generates endogenous LTD/depotentiation, which reverses synaptic plasticity formed during previous learning experiences, and endogenous LTP, which underlies the storage of new information. Abraham raised several concerns with our review, including the criticism that our speculation ''falters because there is no evidence that stress causes LTD or depotentiation,'' and that research on stress and hippocampus has ''failed to report any LTP-like changes.'' Abraham's points are well-taken because stress, in isolation, does not appear to generate long-lasting changes in baseline measures of hippocampal excitability. Here, within the context of a reply to Abraham's critique, we have provided a review of the literature on the influence of stress, novelty, fear conditioning, and the retrieval of emotional memories on cognitive and physiological measures of hippocampal functioning. An emphasis of this review is our hypothesis that endogenous forms of depotentiation, LTD and LTP are generated only when arousing experiences occur in conjunction with memory-related activation of the hippocampus and amygdala. We conclude with speculation that interactions among the different forms of endogenous plasticity underlie a form of competition by synapses and memories for access to retrieval resources. V V C 2005 Wiley-Liss, Inc.

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“…Therefore, the hippocampus was investigated since it is replete with α 2 -adrenergic receptors (Scheinin et al, 1994) that inhibit NE release (Kiss et al, 1995). The hippocampus is also involved in processing painful stimuli and regulating mood states (Delgado, 1954;Dutar et al, 1985;Khanna and Sinclair, 1989;McEwen, 2001;McKenna and Melzack, 1992). Furthermore, tricyclic antidepressant drugs (desipramine, amitriptyline, zimelidine) elicit neuroplastic changes in the regulation of NE release from the hippocampus following i.p.…”

Section: Introductionmentioning

confidence: 99%

Antinociception mediated by α2-adrenergic activation involves increasing tumor necrosis factor α (TNFα) expression and restoring TNFα and α2-adrenergic inhibition of norepinephrine release

et al. 2007

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The central component that establishes chronic pain from peripheral nerve injury is associated with increased tumor necrosis factor-α (TNFα) production in the brain. This study examined TNFα and its reciprocally permissive role with α 2 -adrenergic activation during peak and progressive decline of thermal hyperalgesia in sciatic nerve chronic constriction injury (CCI). Accumulation of TNFα mRNA (in situ hybridization) increases in the hippocampus and locus coeruleus during the onset of neuropathic pain and persists as hyperalgesia abates. Activation of α 2 -adrenergic receptors in control rats decreases TNFα mRNA accumulation in these brain regions. In contrast, during hyperalgesia, α 2 -adrenergic activation enhances TNFα mRNA accumulation. Whether this enhanced TNFα production is associated with changes in the regulation of norepinephrine (NE) release was tested. Hippocampal slices were electrically depolarized to evaluate α 2 -adrenergic and TNFα regulation of NE release. While inhibition of NE release by TNFα is maximal during peak hyperalgesia, it subsequently transforms to facilitate NE release. In addition, α 2 -adrenergic receptor activation with clonidine (0.2 mg/kg, i.p.) in CCI rats experiencing hyperalgesia restores TNFα and α 2 -adrenergic inhibition of NE release. While TNFα directs the development of hyperalgesia, it also directs its resolution. Transformed sensitivity to α 2 -adrenergic agonists during hyperalgesia demonstrates a mechanism for therapy.

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Noxious stimuli produce prolonged changes in the CA1 region of the rat hippocampus

Cited by 62 publications

References 25 publications

Roles of the hippocampal formation in pain information processing

Roles of the hippocampal formation in pain information processing

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

Antinociception mediated by α2-adrenergic activation involves increasing tumor necrosis factor α (TNFα) expression and restoring TNFα and α2-adrenergic inhibition of norepinephrine release

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