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VM Sanders and AE Munson
The present study shows that positive and negative modulation of the immunoglobulin M antibody response in mouse spleen cells immunized with sheep erythrocytes can be achieved by selective activation of alpha adrenoceptor subtypes. Alpha-1 adrenoceptor activation by methoxamine produced a number of spleen cells secreting immunoglobulin M antibody which was enhanced 63% above control on day 4 after immunization and which returned to control levels on days 5 (peak day of control antibody response), 6 and 7. This response mimicked the previously reported response produced by norepinephrine in the presence of propranolol, but not by norepinephrine alone. Alpha-2 adrenoceptor activation by clonidine produced no change when compared to control on days 4, 6 or 7, but produced a 50% suppression on day 5. Activation of both adrenoceptor subtypes by phenylephrine produced a control response on day 4, a depressed response on day 5 and an elevated response on days 6 and 7 by 50 and 64% above control, respectively. All drug responses were concentration-dependent and the methoxamine and clonidine responses were antagonized by phentolamine. These results suggest that antibody responses can be modulated by alpha-1 adrenoceptor activation to produce an enhanced response 1 day sooner than the peak control response and by alpha-2 adrenoceptor activation to produce a depressed response at the time of the peak control response.
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