Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.64 (MPP)
 1,876 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of opioid receptors in long-term potentiation (LTP) of the medial (MPP) and lateral (LPP) divisions of the perforant path-granule cell projection was investigated in urethane anesthetized rats. A stimulating electrode was positioned in the dorsomedial or ventrolateral aspect of the angular bundle for selective activation of the MPP and LPP, respectively. A push-pull cannula served to focally perfuse artificial cerebrospinal fluid (ACSF) across the perforant path terminal zone, while perforant path evoked potentials were monitored in the dentate hilus. Robust LTP of the excitatory postsynaptic potential (EPSP) initial slope and population spike height was induced by high frequency stimulation (400 Hz, 8 bursts of 8 pulses) applied to the medial or lateral perforant path in rats perfused with standard medium. In the lateral perforant path, a putative proenkephalin system, LTP of the EPSP and population spike was blocked when ACSF containing 100 microM of the opioid receptor antagonist naloxone was present during the tetanus, while perfusion with 0.1 microM naloxone prevented EPSP potentiation but only reduced the magnitude of the population spike increase. Naloxone had no effect on LTP induction in the MPP. Importantly, 0.1 microM ICI 174,864, a selective antagonist of delta opioid receptors, blocked LTP of synaptic transmission in the LPP while leaving the population spike increase intact. The results indicate that LTP of synaptic transmission in the LPP requires activation of delta opioid receptors, while 'non-delta' opioid receptors may be involved in augmenting granule cell output. This opioid receptor-dependent LTP illustrates peptidergic regulation of synaptic plasticity in the hippocampus.
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PMID:Delta opioid receptor activation is required to induce LTP of synaptic transmission in the lateral perforant path in vivo. 166 45

In situ hybridization studies were performed to study the changes in proenkephalin mRNA levels in the neostriatum of rats with long-term (18 months) unilateral lesions of the nigrostriatal dopamine (DA) pathway induced by 1-methyl-4-phenylpyridinium ion (MPP+) and in animals bearing embryonic DA grafts implanted into the DA depleted striatum. In the ipsilateral striatum of MPP(+)-lesioned animals, there was a 2-fold increase in the levels of proenkephalin mRNA compared with those in the contralateral striatum of the same animals or the ipsilateral striatum of control animals. High resolution analysis using emulsion autoradiography showed that increase in proenkephalin gene expression in response to DA-denervation by MPP+ was due to an increase in the hybridization signal over individual expressing cells as well as to an increase in the number of labelled cells. In the DA-grafted striatum the levels of proenkephalin mRNA were significantly (P less than 0.01) reduced when compared with those in the MPP(+)-lesioned striatum due to both a decrease in the number of labelled cells as well as the hybridization density per individual cell. Moreover, when compared with the ipsilateral striatum of control animals, the levels of proenkephalin mRNA in the DA-grafted striatum was slightly lower due to a 20% decrease in the number of labelled cells rather than a decrease in the hybridization signal per individual cell. The results of this study are important in two respects. Firstly, they clearly show that the increase in proenkephalin gene expression in the striatum of rats with complete nigrostriatal DA lesions, can be maintained for many months after the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased proenkephalin mRNA levels in the rat neostriatum following lesion of the ipsilateral nigrostriatal dopamine pathway with 1-methyl-4-phenylpyridinium ion (MPP+): reversal by embryonic nigral dopamine grafts. 185 29