Epileptogenesis<i>In Vivo</i>Enhances the Sensitivity of Inhibitory Presynaptic Metabotropic Glutamate Receptors in Basolateral Amygdala Neurons<i>In Vitro</i>

Neugebauer, Volker; Keele, N. Bradley; Shinnick‐Gallagher, Patricia

doi:10.1523/jneurosci.17-03-00983.1997

Cited by 85 publications

(51 citation statements)

References 62 publications

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“…Synaptic plasticity in the amygdala, particularly the lateral and basolateral nuclei (LA and BLA), is involved in a variety of behavioral modifications and disorders, including models of epilepsy, drug addiction, conditioned fear, and associative learning (Rainnie et al, 1992;McKernan and Shinnick-Gallagher, 1997;Neugebauer et al, 1997a;Davis, 1998;Huang and Kandel, 1998;Post et al, 1998;Maren, 1999;LeDoux, 2000;Lin et al, 2000Lin et al, , 2001Rolls, 2000;Bauer et al, 2001;Blair et al, 2001). The role of the amygdala in persistent and chronic pain is not clear.…”

Section: Discussionmentioning

confidence: 99%

“…Brain slices containing the CeA were obtained as previously described (Neugebauer et al 1997a) (see Fig. 1).…”

Section: Electrophysiologymentioning

confidence: 99%

“…Synaptic plasticity in the amygdala has been shown to underlie a number of long-term behavioral modifications in the kindling model of epilepsy, chronic cocaine model of drug addiction, and models of conditioned fear and associative learning [lateral amygdala (LA)-BLA: LeDoux et al, 1990;Rainnie et al, 1992;McKernan and Shinnick-Gallagher, 1997;Neugebauer et al, 1997a;Wang and Gean, 1999;Lin et al, 2000Blair et al, 2001;Lin et al, 2001] (CeA: Neugebauer et al, 2000;Nader et al, 2001). To test whether the arthritic pain behavior is associated with synaptic plasticity in the "nociceptive amygdala" (Bourgeais et al, 2001;Neugebauer and Li, 2002), we performed whole-cell patch-clamp recordings of membrane properties and synaptic transmission in CeA neurons recorded in brain slices obtained from control (normal and sham) rats and arthritic rats.…”

Section: Synaptic Plasticity and Altered Membrane Properties In Cea Nmentioning

confidence: 99%

“…The role of mGluRs in the brain, however, in prolonged, and chronic pain states are for the most part unknown. Accumulating evidence suggests a role of mGluRs in the amygdala in synaptic plasticity associated with behavioral modifications (Holmes et al, 1996;Neugebauer et al, 1997aNeugebauer et al, ,b, 2000Masugi et al, 1999;Keele et al, 2000;Lin et al, 2000). Thus, it is conceivable that mGluRs also contribute to pain-related synaptic plasticity in the amygdala.…”

Section: Synaptic Plasticity and Altered Membrane Properties In Cea Nmentioning

confidence: 99%

“…The amygdala exhibits a high degree of plasticity in models of tetanic, pharmacologically induced, and behavioral long-term modification of synaptic transmission (McKernan and ShinnickGallagher, 1997;Neugebauer et al, 1997aNeugebauer et al, , 2000Maren, 1999;Wang and Gean, 1999;LeDoux, 2000;Martin et al, 2000;Bauer et al, 2001;Blair et al, 2001;Lin et al, 2001). Such neuroplasticity is believed to be involved in associative learning and in certain neurological and psychiatric disorders.…”

Section: Introductionmentioning

confidence: 99%

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Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

et al. 2003

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Pain has a strong emotional-affective dimension, and the amygdala plays a key role in emotionality. Mechanisms of pain-related changes in the amygdala were studied at the cellular and molecular levels in a model of arthritis pain. The influence of the arthritic condition induced in vivo on synaptic transmission and group I metabotropic glutamate receptor (mGluR1 and mGluR5) function was examined in vitro using whole-cell voltage-clamp recordings of neurons in the central nucleus of the amygdala (CeA). G-protein-coupled mGluRs are implicated in various forms of neuroplasticity as well as in neurological and psychiatric disorders. Synaptic transmission was evoked by electrical stimulation of afferents from the basolateral amygdala (BLA) and the pontine parabrachial (PB) area in brain slices from control (untreated or saline-injected) rats and from arthritic rats. This study shows enhanced synaptic transmission of nociceptivespecific inputs (PB3 CeA synapse) and polymodal sensory inputs (BLA3 CeA synapse) in the arthritis model. CeA neurons from arthritic rats also developed increased excitability compared with control CeA neurons. Synaptic plasticity in the CeA was accompanied by increased presynaptic mGluR1 function and upregulation of mGluR1 and mGluR5. A selective mGluR1 antagonist reduced transmission in CeA neurons from arthritic animals but not in control neurons, and increased levels of mGluR1 and mGluR5 protein were measured in the CeA of arthritic rats compared with controls. Our results show that plastic changes in the amygdala in an arthritis model that produces prolonged pain involve a critical switch of presynaptic mGluR1 expression and function.

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Section: Discussionmentioning

confidence: 99%

“…Brain slices containing the CeA were obtained as previously described (Neugebauer et al 1997a) (see Fig. 1).…”

Section: Electrophysiologymentioning

confidence: 99%

Section: Synaptic Plasticity and Altered Membrane Properties In Cea Nmentioning

confidence: 99%

Section: Synaptic Plasticity and Altered Membrane Properties In Cea Nmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

et al. 2003

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Kindled seizures increase metabotropic glutamate receptor expression and function in the rat supraoptic nucleus

1998

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The spread of experimentally kindled seizures in rats results in sustained increases in plasma vasopressin (VP) and VP mRNA in the supraoptic nucleus (SON). These increases provide an excellent example of the pathological plasticity that can develop in normal cells exposed to recurrent seizure activity. To test whether this plasticity might be due in part to changes in metabotropic glutamate receptors (mGluRs), we examined mGluR mRNA expression in the SON 1 month after stage 5 amygdala kindling. Three mGluR subtypes were detected by in situ hybridization in the SON in the following relative levels: mGluR3 > mGluR1 > mGluR7. Both mGluR1 and mGluR3 mRNAs were significantly increased in the SON (+28-61%) and cortex (+27-42%) after kindling. Immunoreactivity for mGluR1 but not mGluR2/3 was significantly increased in vivo in the SON. Receptor protein expression and intracellular calcium accumulation in response to the mGluR agonist, 1S,3R ACPD, were evaluated after in vitro "kindling" of neuroendocrine cells by Mg2+ deprivation. Increased immunoreactivity for mGluR1 and mGluR2/3 was seen in all cultures 3 days after a brief exposure to Mg2+-free medium. 1S,3R 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) induced rapid peak responses and gradual accumulations of intracellular Ca2+ in neurons. Both responses were increased in the "kindled" cells. Increases in the expression of functional mGluR1 and perhaps mGluR3 receptors may contribute to the development of long-lasting plastic changes associated with seizure activity.

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Up-regulation of the metabotropic glutamate receptor mGluR4 in hippocampal neurons with reduced seizure vulnerability

et al. 2000

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Selective hippocampal cell loss and altered neurotransmitter receptor expression have been proposed as pathogenic mechanisms in the development of chronic mesial temporal lobe epilepsy (TLE). Studies in animal models point to metabotropic glutamate receptors (mGluRs) as modulators of hippocampal epileptogenesis. In addition, mGluRs may constitute specific targets for the development of novel anticonvulsive drugs. As mGluR4 represents an inhibitory class III mGluR associated with the reduction of intracellular cyclic AMP levels and calcium influx, we have analyzed the regional and cellular expression of mGluR4 in surgical hippocampal specimens obtained from patients with TLE by using immunohistochemistry and in situ hybridization. Although the hippocampi of control specimens (n = 11) were almost devoid of mGluR4 immunolabeling, all TLE specimens (n = 35) showed a striking up‐regulation of mGluR4 immunoreactivity, in particular within the dentate gyrus. Immunoelectron microscopy localized the receptor protein to the periphery of presynaptic and postsynaptic membranes. In situ hybridization revealed increased transcript levels of mGluR4 in dentate granule cells and residual CA4 neurons of TLE specimens compared with controls. Our results suggest a potential role of mGluR4 in counteracting excitatory hippocampal activity and in modulating seizure‐associated vulnerability of hippocampal neurons. These data may also provide a basis for pharmacological studies of mGluR4 agonists as potential novel drugs in the treatment of TLE. Ann Neurol 2000; 47:26–35

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EpileptogenesisIn VivoEnhances the Sensitivity of Inhibitory Presynaptic Metabotropic Glutamate Receptors in Basolateral Amygdala NeuronsIn Vitro

Cited by 85 publications

References 62 publications

Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

Kindled seizures increase metabotropic glutamate receptor expression and function in the rat supraoptic nucleus

Up-regulation of the metabotropic glutamate receptor mGluR4 in hippocampal neurons with reduced seizure vulnerability

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