Binding of girisopam (a 2,3-benzodiazepine derivative) to the substantia nigra is prevented by lesioning of the striatonigral pathway.

The binding sites of girisopam, a homophthalazine (2,3-benzodiazepine)-derivate have a specific distribution pattern restricted to the striato-pallido-nigral system of the rat brain. Following kainic acid lesions in the caudate-putamen or the ventral striatum (nucleus accumbens, olfactory tubercle), as well as after surgical transection of the striatonigral pathway, [3H]girisopam binding sites were reduced or completely eliminated from the substantia nigra and the entopeduncular nucleus. Kainic acid lesions of the globus pallidus failed to act on girisopam binding sites in the substantia nigra. Surgical transections or 6-hydroxydopamine lesions of the striatonigral pathway, as well as intranigral kainic acid injections did not influence binding sites in the striatum or the pallidum. These findings indicate that girisopam in the striatum to be postsynaptic on striatonigral projecting neurons. Girisopam in the striatum seems is present in striatonigral projecting neurons. The binding sites are transported from the striatum (mainly from the caudate-putamen, partly from the ventral striatum) to the substantia nigra and the entopeduncular nucleus. The exact identity of these striatonigral fibres bearing homopthalazines is uncertain.