<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16(2)</volume><submitter>Goericke-Pesch S</submitter><pubmed_abstract>Following the downregulation of testicular endocrine and germinative function by slow-release gonadotropin-releasing hormone (GnRH)-agonist implants, testicular functions are quickly restored after implant removal. As an intact blood-testis barrier (BTB) is crucial for normal spermatogenesis and its integrity is FSH- and androgen-dependent, alterations in the BTB gene and protein expressions during downregulation and subsequent restart seem inevitable. We investigated &lt;i>occludin&lt;/i> (&lt;i>OCLN&lt;/i>), &lt;i>claudin&lt;/i> (&lt;i>CLDN&lt;/i>) &lt;i>3&lt;/i>, &lt;i>5&lt;/i>, &lt;i>11,&lt;/i> and &lt;i>connexin&lt;/i> (&lt;i>CX&lt;/i>) &lt;i>43&lt;/i> mRNA-, and CLDN11 and CX43 protein expressions during GnRH implant-induced downregulation (W0) and restart of spermatogenesis after implant removal (week, W, 3-12). Untreated juvenile (JG) and a</pubmed_abstract><journal>Animals : an open access journal from MDPI</journal><pagination>254</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12837560</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Testicular Gap (&lt;i>CX43&lt;/i>) and Tight Junction (&lt;i>OCLN&lt;/i>, &lt;i>CLDN3&lt;/i>, &lt;i>5&lt;/i> and &lt;i>11&lt;/i>) Components in the Dog Are Affected by GnRH-Mediated Downregulation.</pubmed_title><pmcid>PMC12837560</pmcid><pubmed_authors>Frimodt Ronnow A</pubmed_authors><pubmed_authors>Korber H</pubmed_authors><pubmed_authors>Wallrabenstein S</pubmed_authors><pubmed_authors>Langeheine M</pubmed_authors><pubmed_authors>Goericke-Pesch S</pubmed_authors><pubmed_authors>Packeiser EM</pubmed_authors><pubmed_authors>Fietz D</pubmed_authors><pubmed_authors>Rohrs L</pubmed_authors><pubmed_authors>Brehm R</pubmed_authors><pubmed_authors>Wehrend A</pubmed_authors><pubmed_authors>Hoffmann B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Testicular Gap (&lt;i>CX43&lt;/i>) and Tight Junction (&lt;i>OCLN&lt;/i>, &lt;i>CLDN3&lt;/i>, &lt;i>5&lt;/i> and &lt;i>11&lt;/i>) Components in the Dog Are Affected by GnRH-Mediated Downregulation.</name><description>Following the downregulation of testicular endocrine and germinative function by slow-release gonadotropin-releasing hormone (GnRH)-agonist implants, testicular functions are quickly restored after implant removal. As an intact blood-testis barrier (BTB) is crucial for normal spermatogenesis and its integrity is FSH- and androgen-dependent, alterations in the BTB gene and protein expressions during downregulation and subsequent restart seem inevitable. We investigated &lt;i>occludin&lt;/i> (&lt;i>OCLN&lt;/i>), &lt;i>claudin&lt;/i> (&lt;i>CLDN&lt;/i>) &lt;i>3&lt;/i>, &lt;i>5&lt;/i>, &lt;i>11,&lt;/i> and &lt;i>connexin&lt;/i> (&lt;i>CX&lt;/i>) &lt;i>43&lt;/i> mRNA-, and CLDN11 and CX43 protein expressions during GnRH implant-induced downregulation (W0) and restart of spermatogenesis after implant removal (week, W, 3-12). Untreated juvenile (JG) and a</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-06-12T03:16:56.931Z</modification><creation>2026-06-12T03:11:26.354Z</creation></dates><accession>S-EPMC12837560</accession><cross_references><pubmed>41594443</pubmed><doi>10.3390/ani16020254</doi></cross_references></HashMap>