Histamin dan social recognition memory

Beberapa tes perilaku telah dikembangkan untuk mempelajari dan mengukur ingatan yang bermuatan emosional dan bagaimana hal ini dapat dipengaruhi oleh manipulasi farmakologis, diet, atau lingkungan. Beberapa teori dan penelitian mengungkapkan paradigma eksperimental yang digunakan dalam studi praklinis untuk mengungkap sirkuit otak yang terlibat dalam pengakuan dan menghafal rangsangan penting lingkungan tanpa nilai emosional yang kuat.

Peran modulatory dari sistem histaminergik otak dalam elaborasi memori pengakuan yang didasarkan pada penilaian kejadian sebelum kejadian, dan diyakini sebagai komponen penting dari memori deklaratif manusia. Banyak penelitian mengungkapkan peranan histamin pada gangguan memori deklaratif yang dijelaskan dalam beberapa gangguan afektif dan neuropsikiatri seperti ADHD, penyakit Alzheimer, dan gangguan neurokognitif utama.

Histamin dan social recognition memory

Seperti yang disebutkan sebelumnya, ingatan sosial mengacu pada kemampuan untuk mengingat identitas yang sejenis, yang mendasar bagi pembangunan hubungan sosial dan kelangsungan hidup. Neurotransmitter seperti noradrenalin, dopamin, dan asetilkolin  dan hormon seperti oksitosin  telah disarankan untuk memainkan peran kunci dalam diskriminasi sosial dan memori. Pekerjaan awal oleh Philippu dan rekannya menunjukkan bahwa histamin juga terlibat dalam jenis memori ini, karena peningkatan konsentrasi histamin di otak meningkatkan memori pengenalan jangka pendek, sedangkan menipisnya histamin neuron memiliki efek amnesik. Pengakuan sosial juga terganggu oleh penuaan; tikus dewasa mengenali remaja untuk jangka waktu yang lama, sedangkan tikus tua hampir tidak menyimpan informasi selama lebih dari 30 menit. Antagonis H3 ABT-239 yang tidak secara signifikan meningkatkan memori sosial pada tikus dewasa meningkatkan daya ingat pada tikus tua sejauh kinerja mereka sebanding dengan tikus dewasa, tanpa mengubah perilaku eksplorasi. Antagonis H3 lain yang baru-baru ini disintesis juga ditemukan untuk meningkatkan memori jangka pendek dalam model memori pengenalan sosial tikus. Menggunakan protokol yang mensyaratkan pemaparan ulang tikus dewasa ke remaja yang sama 90 menit setelah pertemuan pertama, Kraus dan rekannya menyarankan bahwa neurotransmisi neurotransmisi dalam nucleus accumbens memfasilitasi memori sosial jangka pendek tanpa mempengaruhi transmisi kolinergik dan glutamatergik (Kraus et al. , 2013). Dari catatan, salah satu komponen dari situs penyimpanan memori sosial tampaknya menjadi hippocampus ventral dan proyeksi ke cangkang nucleus accumbens.

Studi lain menggunakan protokol diskriminasi sosial untuk menunjukkan bahwa konsolidasi pengakuan dimediasi oleh reseptor H2 di kedua amigdala dan hippocampus dorsal, ketika tikus yang disuntik dengan antagonis H2 ranitidine menghabiskan waktu yang sama untuk mengeksplorasi novel dan remaja yang akrab, dan dimaprit agonis H2 membalikkan efek ini. Namun demikian, aktivasi reseptor H2 di korteks infralimbic tampaknya tidak berpartisipasi dalam konsolidasi memori pengenalan sosial. Kraus dan rekan sebelumnya melaporkan bahwa infus famotidine, antagonis H2 lain, tidak mempengaruhi efek fasilitator yang diinduksi thioperamide pada memori pengenalan (Kraus et al., 2013). Hasil yang tampaknya kontras ini dapat dikaitkan dengan perbedaan di situs injeksi. Famotidine diberikan ke dalam sistem ventrikel otak, sedangkan ranitidin diberikan langsung ke BLA atau CA1 dengan dosis yang sangat mirip; dengan demikian, dapat dibayangkan bahwa konsentrasi akhir famotidine dalam struktur spesifik ini tidak cukup untuk mencegah efek thioperamide.

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