Compromised GABAergic inhibition contributes to tumor-associated epilepsy

Tumor-associated epilepsy.

Tumor-associated epilepsy is an important contributor to morbidity in patients with brain tumors. Proposed pathophysiological mechanisms to explain these effects range from neuronal and glial dysfunction to deranged vascular homeostasis, to ionic and pH changes. Perilesional tissue alterations play a vital role in the generation of tumor-associated seizures. Clinical studies have determined tha...

Tumor Associated Epilepsy

Aberrant hippocampal neurogenesis contributes to epilepsy and associated cognitive decline

Acute seizures after a severe brain insult can often lead to epilepsy and cognitive impairment. Aberrant hippocampal neurogenesis follows the insult but the role of adult-generated neurons in the development of chronic seizures or associated cognitive deficits remains to be determined. Here we show that the ablation of adult neurogenesis before pilocarpine-induced acute seizures in mice leads t...

Glutamate and tumor-associated epilepsy

For many patients an unexplained seizure is among the earliest symptoms of a growing primary brain tumor. These tumors originate from glial cells or their progenitors in the brain and are often referred to as glioma. In approximately 30% of patients seizures recur spontaneously giving rise to tumor associated epilepsy [1]. While these fits are generally well controlled by antiepileptic medicati...

Presynaptic GABAergic inhibition regulated by BDNF contributes to neuropathic pain induction

The gate control theory proposes the importance of both pre- and post-synaptic inhibition in processing pain signal in the spinal cord. However, although postsynaptic disinhibition caused by brain-derived neurotrophic factor (BDNF) has been proved as a crucial mechanism underlying neuropathic pain, the function of presynaptic inhibition in acute and neuropathic pain remains elusive. Here we sho...