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Deep brain stimulation of the nucleus basalis magnocellularis ameliorates autistic behavior in a rat model of autism via cholinergic modulation in the prefrontal cortex.
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Rusadze Khatuna Z, Burjanadze Maia A, Beselia Gela V, Chkhikvishvili Nino C, Chighladze Mariam R, Nozadze Barbare G, Naneishvili Temur L, Dashniani Manana G
Аннотация
OBJECTIVE: In the present study, we investigated whether deep brain stimulation (DBS) of the nucleus basalis magnocellularis (NBM) improves autism spectrum disorder (ASD)-related behavioral abnormalities in a valproic acid (VPA)-induced rat model of autism, consistent with changes in cholinergic markers in the medial prefrontal cortex (mPFC).
METHODS: On the 12.5th day of gestation, pregnant rats (n = 16) received a single intraperitoneal injection of 500 mg/kg sodium valproate dissolved in 0.9% saline, while others (n = 5) received saline alone. Male offspring were allowed to reach 3 months of age and then were randomly assigned to one of four experimental groups: Contr - prenatally saline injected, VPA - prenatally VPA-injected, VPA/I - VPA-injected with electrode implantation in the NBM, and VPA/S - VPA-injected with electrical stimulation. DBS was initiated in rats of the VPA/S group 10 days after surgery (two consecutive hours per day, every day for 2 weeks; DBS parameters: 60 Hz, 120 µs, and 50 µA).
RESULTS: The prenatally VPA-exposed rats demonstrate deficits in social behavior, increased locomotor activity, and reduced anxiety levels. Immunohistochemical evaluation shows a decrease in the number of acetylcholinesterase-immunoreactive neurons in the mPFC and choline acetyltransferase-immunoreactive neurons in the NBM. NBM-DBS improves VPA-induced autistic behavior and increases the number of acetylcholinesterase-immunoreactive neurons in the PFC.
CONCLUSION: The correlation between ASD-like behavior and cholinergic markers in the mPFC supports our hypothesis that NBM-DBS improves behavioral deficits by modulating cholinergic neurotransmission in the PFC in a rat model of autism.
METHODS: On the 12.5th day of gestation, pregnant rats (n = 16) received a single intraperitoneal injection of 500 mg/kg sodium valproate dissolved in 0.9% saline, while others (n = 5) received saline alone. Male offspring were allowed to reach 3 months of age and then were randomly assigned to one of four experimental groups: Contr - prenatally saline injected, VPA - prenatally VPA-injected, VPA/I - VPA-injected with electrode implantation in the NBM, and VPA/S - VPA-injected with electrical stimulation. DBS was initiated in rats of the VPA/S group 10 days after surgery (two consecutive hours per day, every day for 2 weeks; DBS parameters: 60 Hz, 120 µs, and 50 µA).
RESULTS: The prenatally VPA-exposed rats demonstrate deficits in social behavior, increased locomotor activity, and reduced anxiety levels. Immunohistochemical evaluation shows a decrease in the number of acetylcholinesterase-immunoreactive neurons in the mPFC and choline acetyltransferase-immunoreactive neurons in the NBM. NBM-DBS improves VPA-induced autistic behavior and increases the number of acetylcholinesterase-immunoreactive neurons in the PFC.
CONCLUSION: The correlation between ASD-like behavior and cholinergic markers in the mPFC supports our hypothesis that NBM-DBS improves behavioral deficits by modulating cholinergic neurotransmission in the PFC in a rat model of autism.