Cellular effects of swim stress in the dorsal raphe nucleus.
ABSTRACT Swim stress regulates forebrain 5-hydroxytryptamine (5-HT) release in a complex manner and its effects are initiated in the serotonergic dorsal raphe nucleus (DRN). The purpose of this study was to examine the effects of swim stress on the physiology of DRN neurons in conjunction with 5-HT immunohistochemistry. Basic membrane properties, 5-HT(1A) and 5-HT(1B) receptor-mediated responses and glutamatergic excitatory postsynaptic currents (EPSCs) were measured using whole-cell patch clamp techniques. Rats were forced to swim for 15min and 24h later DRN brain slices were prepared for electrophysiology. Swim stress altered the resting membrane potential, input resistance and action potential duration of DRN neurons in a neurochemical-specific manner. Swim stress selectively elevated glutamate EPSC frequency in 5-HT DRN neurons. Swim stress non-selectively reduced EPSC amplitude in all DRN cells. Swim stress elevated the 5-HT(1B) receptor-mediated inhibition of glutamatergic synaptic activity that selectively targeted 5-HT cells. Non-5-HT DRN neurons appeared to be particularly responsive to the effects of a milder handling stress. Handling elevated EPSC frequency, reduced EPSC decay time and enhanced a 5-HT(1B) receptor-mediated inhibition of mEPSC frequency selectively in non-5-HT DRN cells. These results indicate that swim stress has both direct, i.e., changes in membrane characteristics, and indirect effects, i.e., via glutamatergic afferents, on DRN neurons. These results also indicate that there are distinct local glutamatergic afferents to neurochemically specific populations of DRN neurons, and furthermore that these distinct afferents are differentially regulated by swim stress. These cellular changes may contribute to the complex effects of swim stress on 5-HT neurotransmission and/or the behavioral changes underlying the forced swimming test model of depression.
Article: Activation of 5-HT1B receptors suppresses low but not high frequency synaptic transmission in the rat subicular cortex in vitro.[show abstract] [hide abstract]
ABSTRACT: We have shown previously that activation of 5-HT1B serotonin receptors mediates suppression of the amplitude of evoked potentials in the subiculum . Here we show that after application of 5-HT (10 microM), excitatory postsynaptic potentials of subicular neurons have reduced amplitudes with no change in membrane potential, input resistance and presynaptic fiber volleys. These results suggest that activation of 5-HT1B receptors reduces the release of glutamate from incoming fibers originating from CA1 pyramidal cells. In presence of 5-HT (10 microM), theta patterned stimulation still induced LTP, similar to that observed in control slices. Application of similar concentrations of 5-HT during double pulse stimulation (interval 10-15 ms) reduced the response to the first pulse (repetition interval 30 s), but the response to the second pulse of the pair was unaffected. We propose that 5-HT1B receptor activity suppresses subicular transmission at low but not at high frequencies.Brain Research 06/1996; 721(1-2):59-65. · 2.73 Impact Factor