Although the sympathetic nervous system (SNS) plays a major role in mediating the peripheral stress response, due consideration is not usually given to the effects of prolonged stress on the SNS. The present study examined changes in neurotransmission in the SNS after exposure of mice (BALB/c) to stressful housing conditions. Focal extracellular recording of excitatory junction currents (EJCs) was used as a relative measure of neurotransmitter release from different regions of large surface areas of the mouse vas deferens. Mice were either group housed (control), isolation housed (social deprivation), group housed in a room containing rats (rat odor stress), or isolation housed in a room containing rats (concurrent stress). Social deprivation and concurrent stressors induced an increase of 30 and 335% in EJC amplitude, respectively. The success rate of recording EJCs from sets of varicosities in the concurrent stressor group was greater compared with all other groups. The present study has shown that some common animal housing conditions act as stressors and induce significant changes in sympathetic neurotransmission.

Contraction of the smooth muscle in the mouse vas deferens is elicited by sympathetic nerves releasing at least two neurotransmitters, adenosine triphosphate (ATP) and noradrenaline (NA). Several studies have indicated the presence of regional variation in the purinergic and noradrenergic contributions to sympathetic nerve-evoked contractions in rodent vasa deferentia. We examined the relative contribution of ATP and NA to neurotransmission and contraction at the prostatic and epididymal ends of the mouse vas deferens. The success rate of recording excitatory junction currents (EJCs, extracellular indication of ATP release) from varicosities at the prostatic end of the vas deferens was eight times greater than for varicosities located at the epididymal end. Both regions of the vas deferens responded similarly to focal application of NA and ATP. Furthermore, the relative density and distribution of P2X(1)-receptor mRNA and anti-P2X(1) immunostaining did not differ between the two regions. Our results suggest that most varicosities located at the epididymal end of the vas deferens are releasing an insufficient amount of ATP to evoke detectable EJCs.

ATP released by sympathetic varicosities of the mouse vas deferens binds to P2X receptors which activate fast, ligand-gated channels, resulting in depolarisation of smooth muscle cells. We examined the development of fast neuromuscular transmission at surface longitudinal smooth muscle fibres of the mouse vas deferens. Sympathetic varicosities were visualised using DiOC(2)(5)-fluorescence to aid in positioning loose patch electrodes over small sets of sympathetic varicosities to record the nerve terminal impulse (NTI) and excitatory junction currents (EJCs) evoked during nerve stimulation. At the earliest age at which EJCs could be detected, 21 days postnatal (PN), most recording sites rarely showed a detectable EJC over 100 trials, even though NTIs were recorded without failure. The extent of such intermittence in transmitter release progressively declined between 21 and 42 days PN. In addition, the mean amplitude of spontaneous EJCs (SEJCs) and EJCs increased by 2- and 2.4-fold, respectively, between 21 and 42 days PN. The rise time of EJCs varied widely at each age but declined with development (e.g., 7-14 ms at 28 days PN, 3-12 ms at 42 days PN). All EJCs were abolished by suramin (100 microM). Fast rise time EJCs were rapidly abolished by alpha,beta-methylene ATP (20 microM) while some (34%) of the slower rise time EJCs were resistant to rapid desensitisation of this kind. P2X(1) and P2X(2) mRNAs were detected by reverse transcription and polymerase chain reaction (RT-PCR) to determine whether levels of expression of the receptor subunits might explain the increased EJC amplitude. Between 10 and 42 days PN no marked change was observed in the P2X(2) receptor mRNA or beta-actin mRNA (control). In contrast, the intensity of the RT-PCR band for P2X(1) receptor showed a progressive approximately 4.3-fold developmental increase relative to the P2X(2) band. These observations suggest that both prejunctional and postjunctional mechanisms cause the maturation of fast purinergic junctional transmission at the longitudinal muscle of the mouse vas deferens between 21 and 42 days PN.

ATP released by sympathetic varicosities of the mouse vas deferens binds to P2X receptors which activate fast, ligand‐gated channels, resulting in depolarisation of smooth muscle cells. We examined the development of fast neuromuscular transmission at surface longitudinal smooth muscle fibres of the mouse vas deferens. Sympathetic varicosities were visualised using DiOC2(5)‐fluorescence to aid in positioning loose patch electrodes over small sets of sympathetic varicosities to record the nerve terminal impulse (NTI) and excitatory junction currents (EJCs) evoked during nerve stimulation. At the earliest age at which EJCs could be detected, 21 days postnatal (PN), most recording sites rarely showed a detectable EJC over 100 trials, even though NTIs were recorded without failure. The extent of such intermittence in transmitter release progressively declined between 21 and 42 days PN. In addition, the mean amplitude of spontaneous EJCs (SEJCs) and EJCs increased by 2‐ and 2.4‐fold, respectively, between 21 and 42 days PN. The rise time of EJCs varied widely at each age but declined with development (e.g., 7–14 ms at 28 days PN, 3–12 ms at 42 days PN). All EJCs were abolished by suramin (100 μM). Fast rise time EJCs were rapidly abolished by α,β‐methylene ATP (20 μM) while some (34%) of the slower rise time EJCs were resistant to rapid desensitisation of this kind. P2X1 and P2X2 mRNAs were detected by reverse transcription and polymerase chain reaction (RT‐PCR) to determine whether levels of expression of the receptor subunits might explain the increased EJC amplitude. Between 10 and 42 days PN no marked change was observed in the P2X2 receptor mRNA or β‐actin mRNA (control). In contrast, the intensity of the RT‐PCR band for P2X1 receptor showed a progressive ∼4.3‐fold developmental increase relative to the P2X2 band. These observations suggest that both prejunctional and postjunctional mechanisms cause the maturation of fast purinergic junctional transmission at the longitudinal muscle of the mouse vas deferens between 21 and 42 days PN. Synapse 37:283–291, 2000. © 2000 Wiley‐Liss, Inc.

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