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Effect of acetylcholine receptors on the pain-related electrical activities in the hippocampal CA3 region of morphine-addicted rats.

Li GZ, Liu ZH, Wei X, Zhao P, Yang CX, Xu MY - Iran J Basic Med Sci (2015)

Bottom Line: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN.The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect.Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Liaocheng People's Hospital, 67 Dongchang Xi Road, Liaocheng 252000, China.

ABSTRACT

Objectives: To determine the effect of acetylcholine (ACh), pilocarpine, and atropine on pain evoked responses of pain excited neurons (PEN) and pain inhibited neurons (PIN) in hippocampal CA3 region of morphine addicted rats.

Materials and methods: Female Wistar rats, weighing between 230-260 g were used in this study. Morphine addicted rats were generated by subcutaneous injection of increasing concentrations of morphine hydrochloride for six days. Trains of electrical impulses applied to the sciatic nerve were used as noxious stimulation and the evoked electrical activities of PEN or PIN in hippocampal CA3 area were recorded using extracellular electrophysiological recording techniques in hippocampal slices. The effect of acetylcholine receptor stimulation by ACh, the muscarinic agonist pilocarpine, and the muscarinic antagonist atropine on the pain evoked responses of pain related electrical activities was analyzed in hippocampal CA3 area of morphine addicted rats.

Results: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN. The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect. The peak activity of cholinergic modulators was 2 to 4 min later in morphine addicted rats compared to peak activity previously observed in normal rats.

Conclusion: ACh dependent modulation of noxious stimulation exists in hippocampal CA3 area of morphine addicted rats. Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

No MeSH data available.


Related in: MedlinePlus

Effects of intra-CA3 injection of different substances on the evoked discharges of PINs in the CA3 of morphine-addicted rats Morphine-dependent rats were injected with (A) saline (1 µl), (B) ACh (2 μg/1 µl), (C) atropine (0.5 μg/1 μl); and (D) pilocarpine (2 μg/1 μl). ↑, Stimulus artifact; ▲, injection substance; X, before injection; 0, 8, 12, 20, 30, time after injection (min)
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Figure 3: Effects of intra-CA3 injection of different substances on the evoked discharges of PINs in the CA3 of morphine-addicted rats Morphine-dependent rats were injected with (A) saline (1 µl), (B) ACh (2 μg/1 µl), (C) atropine (0.5 μg/1 μl); and (D) pilocarpine (2 μg/1 μl). ↑, Stimulus artifact; ▲, injection substance; X, before injection; 0, 8, 12, 20, 30, time after injection (min)

Mentions: In the control group, the noxious stimulation increased the discharge frequency of PENs while decreasing the frequency of PINs. The average NIV of PENs was 3.15±0.15 Hz, and the latency was 0.26±0.03 sec. The NIV of PENs and the latency showed no significant differences 0-30 min after the intra-CA3 administration of saline compared to values before injection (Figure 2A). The average NIV of PINs was –4.01±0.57 Hz and the average ID of PINs was 0.31±0.04 sec. Zero to 30 min after the intra-CA3 administration of saline, the NIV of PINs and the ID showed no significant differences compared to values before injection (Figure 3A). Administration of saline as a control treatment produced no significant change in the electrical activity of PENs and PINs (Figure 2A and Figure 3A).


Effect of acetylcholine receptors on the pain-related electrical activities in the hippocampal CA3 region of morphine-addicted rats.

Li GZ, Liu ZH, Wei X, Zhao P, Yang CX, Xu MY - Iran J Basic Med Sci (2015)

Effects of intra-CA3 injection of different substances on the evoked discharges of PINs in the CA3 of morphine-addicted rats Morphine-dependent rats were injected with (A) saline (1 µl), (B) ACh (2 μg/1 µl), (C) atropine (0.5 μg/1 μl); and (D) pilocarpine (2 μg/1 μl). ↑, Stimulus artifact; ▲, injection substance; X, before injection; 0, 8, 12, 20, 30, time after injection (min)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556759&req=5

Figure 3: Effects of intra-CA3 injection of different substances on the evoked discharges of PINs in the CA3 of morphine-addicted rats Morphine-dependent rats were injected with (A) saline (1 µl), (B) ACh (2 μg/1 µl), (C) atropine (0.5 μg/1 μl); and (D) pilocarpine (2 μg/1 μl). ↑, Stimulus artifact; ▲, injection substance; X, before injection; 0, 8, 12, 20, 30, time after injection (min)
Mentions: In the control group, the noxious stimulation increased the discharge frequency of PENs while decreasing the frequency of PINs. The average NIV of PENs was 3.15±0.15 Hz, and the latency was 0.26±0.03 sec. The NIV of PENs and the latency showed no significant differences 0-30 min after the intra-CA3 administration of saline compared to values before injection (Figure 2A). The average NIV of PINs was –4.01±0.57 Hz and the average ID of PINs was 0.31±0.04 sec. Zero to 30 min after the intra-CA3 administration of saline, the NIV of PINs and the ID showed no significant differences compared to values before injection (Figure 3A). Administration of saline as a control treatment produced no significant change in the electrical activity of PENs and PINs (Figure 2A and Figure 3A).

Bottom Line: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN.The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect.Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Liaocheng People's Hospital, 67 Dongchang Xi Road, Liaocheng 252000, China.

ABSTRACT

Objectives: To determine the effect of acetylcholine (ACh), pilocarpine, and atropine on pain evoked responses of pain excited neurons (PEN) and pain inhibited neurons (PIN) in hippocampal CA3 region of morphine addicted rats.

Materials and methods: Female Wistar rats, weighing between 230-260 g were used in this study. Morphine addicted rats were generated by subcutaneous injection of increasing concentrations of morphine hydrochloride for six days. Trains of electrical impulses applied to the sciatic nerve were used as noxious stimulation and the evoked electrical activities of PEN or PIN in hippocampal CA3 area were recorded using extracellular electrophysiological recording techniques in hippocampal slices. The effect of acetylcholine receptor stimulation by ACh, the muscarinic agonist pilocarpine, and the muscarinic antagonist atropine on the pain evoked responses of pain related electrical activities was analyzed in hippocampal CA3 area of morphine addicted rats.

Results: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN. The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect. The peak activity of cholinergic modulators was 2 to 4 min later in morphine addicted rats compared to peak activity previously observed in normal rats.

Conclusion: ACh dependent modulation of noxious stimulation exists in hippocampal CA3 area of morphine addicted rats. Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

No MeSH data available.


Related in: MedlinePlus