Hemmungsimpuls

Hemmungsimpuls, literally “inhibition impulse,” is a neural signal that reduces the activity of a neuron, neuronal network, or muscle. It contrasts with excitatory impulses that promote action potentials. In the nervous system, hemmungsimpulses are typically chemical signals transmitted at synapses, most commonly through inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine. Their activation makes the generation of action potentials less likely by diminishing neuronal excitability.

Mechanisms of inhibition occur mainly as postsynaptic or presynaptic processes. Postsynaptic inhibition hyperpolarizes the target neuron by opening ion channels that allow chloride or potassium currents, often via GABA-A or glycine receptors, while GABA-B receptors can reduce excitability through second messenger systems. Presynaptic inhibition reduces neurotransmitter release from the presynaptic terminal, for example by limiting calcium influx at the synapse, thereby dampening the signal transmitted to the postsynaptic cell.

Functions of hemmungsimpuls include shaping neural processing, maintaining network stability, and refining motor control and sensory discrimination. In the spinal cord, inhibitory interneurons provide recurrent and intersegmental inhibition that modulates reflexes and muscle tone. In cortical circuits, inhibition helps contrast signals and prevent runaway excitation, contributing to attention and information processing.

Clinical relevance exists where inhibitory signaling is altered. Reduced inhibition is associated with conditions such as epilepsy and hyperexcitability, while excessive inhibition can contribute to sedation or motor suppression. Pharmacological agents that enhance GABAergic inhibition, such as benzodiazepines or baclofen, are commonly used to treat related disorders.