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Agen pelepas dopamin

Artikel ini bukan mengenai antagonis reseptor dopamin.

Amfetamin, sebuah NDRA dan salah satu DRA yang paling terkenal.
4-Metilaminoreks (4-MAR), isomer cis-nya merupakan salah satu NDRA yang paling selektif terhadap dopamin.

Agen pelepas dopamin (dopamine releasing agent, disingkat DRA) adalah jenis obat yang menginduksi pelepasan dopamin dalam tubuh dan/atau otak.[1][2][3][4]

Saat ini belum diketahui adanya DRA selektif.[5][6][7] Namun, DRA non-selektif termasuk agen pelepas norepinefrin–dopamin (NDRA) seperti amfetamin dan metamfetamin, agen pelepas serotonin–norepinefrin–dopamin (SNDRA) seperti MDMA dan mefedrona, dan agen pelepas serotonin–dopamin (SDRA) seperti 5-kloro-αMT dan BK-NM-AMT, telah diketahui.[8][9][10][7]

Jenis obat yang terkait erat dengannya adalah penghambat penyerapan kembali dopamin (DRI). Berbeda dengan kasus DRA, banyak DRI selektif yang telah diketahui. Contoh DRI selektif meliputi amineptin, modafinil, dan vanokserinel.[11][12][13]

Selektivitas

Saat ini belum diketahui adanya DRA selektif dan kuat.[5][6][7] Kurangnya DRA selektif yang diketahui berkaitan dengan fakta bahwa sangat sulit untuk memisahkan afinitas transporter dopamin (DAT) dari afinitas transporter norepinefrin (NET) dan mempertahankan kemampuan pelepasan pada saat yang sama. Meskipun telah dilakukan evaluasi terhadap lebih dari 350 senyawa, dilaporkan pada tahun 2007 bahwa hampir tidak mungkin untuk memisahkan pelepasan norepinefrin dan dopamin.[6] Hingga tahun 2014, masih belum ada DRA selektif yang teridentifikasi, meskipun sekitar 1.400 senyawa telah disaring.[7][3] Demikian pula, meskipun agen pelepas norepinefrin (NRA) yang cukup selektif telah diketahui (misalnya preferensi ~10 hingga 20 kali lipat pelepasan norepinefrin dibandingkan dopamin),[8][9][14][15] belum ada NRA yang sangat selektif yang teridentifikasi.[7] Meskipun belum ada DRA selektif yang teridentifikasi, SDRA selektif, meskipun dengan agonisme reseptor serotonin bersamaan, telah dijelaskan pada tahun 2014.[10] SDRA tanpa agonisme reseptor serotonin yang diketahui seperti BK-NM-AMT telah dijelaskan pada tahun 2019.[16][17][18]

Meskipun saat ini belum diketahui adanya agen pelepas dopamin selektif, banyak agen pelepas dopamin non-selektif (agen pelepas norepinefrin–dopamin atau NDRA) dan serotonin, norepinefrin, dan dopamin (agen pelepas serotonin–norepinefrin–dopamin atau SNDRA) yang diketahui. Contoh NDRA utama termasuk psikostimulan amfetamin dan metamfetamin, sedangkan contoh SNDRA adalah entaktogen metilenadioksimetamfetamina (MDMA).[8][9] Obat-obatan ini sering digunakan untuk tujuan rekreasi dan ditemukan sebagai obat-obatan terlarang. DRA, termasuk NDRA dan secara teoritis juga DRA selektif, memiliki kegunaan medis dalam pengobatan gangguan pemusatan perhatian dan hiperaktivitas (ADHD).[19] SDRA, misalnya 5-kloro-αMT, kurang umum dan tidak selektif untuk pelepasan dopamin, tetapi juga telah dikembangkan.[10][20] Triptamina seperti 5-kloro-αMT adalah satu-satunya kerangka pelepasan yang diketahui secara konsisten melepaskan dopamin lebih kuat daripada norepinefrin.[16]

Penggunaan terapeutik

DRA selektif mungkin memiliki efek klinis yang berbeda dalam pengobatan gangguan pemusatan perhatian dan hiperaktivitas (ADHD) dibandingkan dengan NDRA seperti amfetamin dan penghambat penyerapan kembali norepinefrin–dopamin (NDRI) seperti metilfenidat yang saat ini digunakan.[19] Misalnya, mereka mungkin telah meningkatkan selektivitas terapeutik dengan mengurangi atau menghilangkan efek samping kardiovaskular dan simpatomimetik dari NDRA.[21]

Contoh

Amfetamin seperti dekstroamfetamin dan dekstrometamfetamin adalah NDRA yang cukup seimbang tetapi melepaskan norepinefrin sekitar 2 hingga 3 kali lebih kuat daripada dopamin.[8][9][15][22] Namun, penelitian lain menemukan bahwa dekstroamfetamin dan dekstrometamfetamin kurang lebih setara atau sedikit lebih menguntungkan dopamin dalam hal pelepasan norepinefrin versus dopamin.[1][23] Sejumlah NDRA yang berpotensi lebih seimbang termasuk levometkatinona (l-MC),[15] 3-kloroamfetamin (3-CA, PAL-304),[1][24] 3-klorometkatinona (3-CMC, klofedrona, PAL-434),[25] dan 2-fenilmorfolina (2-PM, PAL-632)[26] diketahui, dan semuanya tampak kurang lebih sama kuatnya dalam menginduksi pelepasan dopamin versus norepinefrin. Beberapa NDRA termasuk cis-4-metilaminoreks (cis-4-MAR),[27][28] 3-klorofenmetrazina (3-CPM, PAL-594),[29][26] dan naftilmetrazina (PAL-704),[26] tampaknya melepaskan dopamin sekitar 2 hingga 3 kali lebih kuat daripada norepinefrin, dan karenanya mungkin termasuk di antara NDRA yang paling selektif terhadap dopamin yang diketahui.

Pemolina, yang secara struktural terkait dengan aminoreks, adalah stimulan yang digunakan untuk mengobati ADHD yang dikatakan bertindak sebagai DRI dan DRA selektif, tetapi dikatakan hanya merangsang pelepasan dopamin secara lemah.[30][31][32] Terdapat beberapa bukti in vitro, meskipun beragam, bahwa antidepresan dan DRI yang agak selektif yakni amineptin, selain menghambat penyerapan kembali dopamin, juga dapat secara selektif menginduksi pelepasan dopamin presinaptik tanpa memengaruhi pelepasan norepinefrin atau serotonin.[33][34][35] Namun, amineptin lebih besar daripada batas ukuran struktural kecil yang diketahui dari agen pelepas monoamina,[3] menunjukkan bahwa mungkin sebenarnya bukan DRA.

Meskipun belum ada DRA selektif yang pasti yang telah dijelaskan, salah satu pengecualian yang mungkin adalah 2-fluorometkatinona (2-FMC). 2-FMC memiliki EC50 untuk pelepasan dopamin sebesar 48,7 nM tetapi hanya menginduksi 85% pelepasan norepinefrin pada konsentrasi 10 μM. Sebagai perbandingan, nilai EC50 dari NDRA metkatinona adalah 49,9 nM untuk pelepasan dopamin; dan 22,4 nM untuk pelepasan norepinefrin; dan menginduksi 100% pelepasan norepinefrin pada konsentrasi 10 μM. Oleh karena itu, dibandingkan dengan metkatinona, 2-FMC tampaknya relatif lebih selektif atau efektif untuk menginduksi pelepasan dopamin dibandingkan pelepasan norepinefrin.[16][1] Bagaimanapun, nilai EC50 dari 2-FMC untuk induksi pelepasan norepinefrin tampaknya tidak tersedia.[16] Selain itu, dalam kasus lain, obat terkait 3-metoksimetkatinona (3-MeOMC) hanya melepaskan 68% norepinefrin pada konsentrasi 10 μM, namun nilai EC50 obat tersebut sebesar 111 nM untuk induksi pelepasan norepinefrin telah diberikan dalam publikasi lain.[36][37]

Mekanisme kerja

Artikel utama: Agen pelepas monoamina § Mekanisme kerja

Lihat juga

Referensi

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