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Disinhibition in cat motor cortex by ammonia.
Journal of Neurophysiology
|March 1, 1975
Summary
Ammonia administration abolishes postsynaptic inhibition in cat motor cortex pyramidal tract cells. This disruption, by shifting the inhibitory postsynaptic potential reversal potential, impairs cortical functions reliant on inhibition.
Area of Science:
- Neuroscience
- Neurophysiology
- Motor Cortex Research
Background:
- Postsynaptic inhibition is crucial for regulating neuronal activity in the motor cortex.
- Understanding the effects of substances like ammonia on neuronal inhibition is vital for comprehending neurological function and dysfunction.
Purpose of the Study:
- To investigate the impact of systemically administered ammonium salts on postsynaptic inhibition in cat motor cortex pyramidal tract cells.
- To elucidate the specific mechanisms by which ammonia affects inhibitory postsynaptic potentials (IPSPs) and neuronal excitability.
Main Methods:
- Utilized extracellular and intracellular recordings in anesthetized cats.
- Administered ammonium salts intravenously to assess effects on antidromic action potentials and membrane potentials of pyramidal tract cells.
Main Results:
- Intravenous ammonia administration abolished both pyramidally and thalamically mediated inhibition of antidromic action potentials.
- Intracellular recordings showed the disappearance of hyperpolarizing IPSPs and the appearance of EPSPs.
- Neuronal resistance changes indicated intact inhibitory pathways, but the reversal potential for IPSPs (E(IPSP)) shifted to the resting membrane potential level.
Conclusions:
- Ammonia effectively disinhibits pyramidal tract cells by altering the E(IPSP), leading to impaired action potential generation and synaptic transmission.
- The findings suggest that ammonia significantly disrupts cortical functions that depend on intact postsynaptic inhibition, potentially leading to excitotoxicity or altered motor control.