Depression Treatment: Transmitter Release From Cochlear Hair Cells Is Phase Locked to Cyclic Stimuli of Different Intensities and Frequencies.

Transmitter release from cochlear hair cells is phase locked to cyclic stimuli of different intensities and frequencies.

Filed under: Depression Treatment

J Neurosci. 2012 Nov 21; 32(47): 17025-36
Goutman JD

The auditory system processes time and intensity through separate brainstem pathways to derive spatial location as well as other salient features of sound. The independent coding of time and intensity begins in the cochlea, where afferent neurons can fire action potentials at constant phase throughout a wide range of stimulus intensities. We have investigated time and intensity coding by simultaneous presynaptic and postsynaptic recording at the hair cell-afferent synapse from rats. Trains of depolarizing steps to the hair cell were used to elicit postsynaptic currents that occurred at constant phase for a range of membrane potentials over which release probability varied significantly. To probe the underlying mechanisms, release was examined using single steps to various command voltages. As expected for vesicular release, first synaptic events occurred earlier as presynaptic calcium influx grew larger. However, synaptic depression produced smaller responses with longer first latencies. Thus, during repetitive hair cell stimulation, as the hair cell is more strongly depolarized, increased calcium channel gating hurries transmitter release, but the resulting vesicular depletion produces a compensatory slowing. Quantitative simulation of ribbon function shows that these two factors varied reciprocally with hair cell depolarization (stimulus intensity) to produce constant synaptic phase. Finally, we propose that the observed rapid vesicle replenishment would help maintain the vesicle pool, which in turn would equilibrate with the stimulus intensity (and therefore the number of open Ca(2+) channels), so that for trains of different levels the average phase will be conserved.
HubMed – depression

 

Chronic Intermittent Hypoxia Depresses Afferent Neurotransmission in NTS Neurons by a Reduction in the Number of Active Synapses.

Filed under: Depression Treatment

J Neurosci. 2012 Nov 21; 32(47): 16736-46
Almado CE, Machado BH, Leão RM

Long-term synaptic plasticity has been recently described in brainstem areas associated to visceral afferent sensory integration. Chronic intermittent hypoxia (CIH), an animal model for studying obstructive sleep apnea in humans, depresses the afferent neurotransmission in nucleus tractus solitarii (NTS) neurons, which affect respiratory and autonomic regulation. Here we identified the synaptic mechanisms of CIH-induced depression of the afferent neurotransmission in NTS neurons in juvenile rats. We verified that CIH reduced the amplitude of both NMDA and non-NMDA glutamatergic excitatory currents (eEPSCs) evoked by tractus solitarii stimulation (TS-eEPSC) of second-order neurons in the NTS. No changes were observed in release probability, evidenced by absence of any CIH-elicited effects on short-term depression and failures in EPSCs evoked in low calcium. CIH also produced no changes in TS-eEPSC quantal size, since the amplitudes of both low calcium-evoked EPSCs and asynchronous TS-eEPSCs (evoked in the presence of Sr(2+)) were unchanged. Using single TS afferent fiber stimulation in slices from control and CIH rats we clearly show that CIH reduced the quantal content of the TS-eEPSCs without affecting the quantal size or release probability, suggesting a reduction in the number of active synapses as the mechanism of CIH induced TS-eEPSC depression. In accordance with this concept, the input-output relationship of stimulus intensity and TS-eEPSC amplitude shows an early saturation in CIH animals. These findings open new perspectives for a better understanding of the mechanisms underlying the synaptic plasticity in the brainstem sensory neurons under challenges such as those produced by CIH in experimental and pathological conditions.
HubMed – depression

 

The border-land of epilepsy–Revisited.

Filed under: Depression Treatment

Neurology. 2012 Nov 21;
Barkley GL

In his 1907 book, The Border-land of Epilepsy, William R. Gowers(1) wrote in the Preface that he “kept a special list of all cases which seemed to be in the border-land of epilepsy- near it, but not of it… when these cases were collected and classified, their comparison and study revealed a large number of unfamiliar facts and many instructive lessons, throwing light on the nature of the affections, and on their relation to epilepsy, and on questions of practical diagnosis.” Depression, or at least depressed moods in people with epilepsy, was not on Gowers’ list but should now be added to the border-lands as it is near it, but not of it too. Epilepsy specialists often recognize the connection between depression and epilepsy, as depression is more common in their selected population with the most intractable epilepsy; yet the magnitude of the problem of depression in epilepsy is probably not as well-recognized by general neurologists and primary care physicians.
HubMed – depression

 


 

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