Acetylcholine produces stimulus-specific receptive field alterations in cat auditory cortex

Frequency receptive fields (RFs) were determined before and after pairing iontophorectic administration of acetylcholine (ACh) with a repeated single-frequency stimulus in the auditory cortex of barbiturate-anesthesized cats. In 58% of the cells, the paired ACh + tone treatment produced subsequent alterations of frequency RFs. In half of these cases, the RF modifications were highly specific to the frequency that had been paired with ACh. Atropine antagoized the frequency-effects of ACh, suggesting that they were mediated via muscarinic cholinergic receptors.     

TIDAL WAVES: Network mechanisms in the neuroendocrine control of prolactin release

Neuroendocrine tuberoinfundibular dopamine (TIDA) neurons tonically inhibit pituitary release of the hormone, prolactin. Through the powerful actions of prolactin in promoting lactation and maternal behaviour while suppressing sexual drive and fertility, TIDA neurons play a key role in reproduction. We summarize insights from recent in vitro studies into the membrane properties and network behaviour of TIDA neurons including the observations that TIDA neurons exhibit a robust oscillation that is synchronized between cells and depends on intact gap junction communication. Comparisons are made with phasic firing patterns in other neuronal populations. Modulators involved in the control of lactation – including serotonin, thyrotropin-releasing hormone and prolactin itself – have been shown to change the electrical behaviour of TIDA cells. We propose that TIDA discharge mode may play a central role in tuning the amount of dopamine delivered to the pituitary and hence circulating prolactin concentrations in different reproductive states and pathological conditions.     

Electrophysiological identification of a pathway from the septal area to the medial amygdala: sensitivity to estrogen and luteinizing hormone-releasing hormone

Medial amygdala neurons responsive to electrical stimulation of the medial septal area were electrophysiologically identified in ovariectomized, urethane-anesthetized female rats. Peristimulus time histograms were collected and used to define the orthodromic response. The action of iontophoretically applied luteinizing hormone-releasing hormone (LHRH) and an LHRH fragment, Ac-LHRH5-10, on the activity of orthodromically responsive neurons was tested. Of a total of 187 neurons recorded, 119 were identified as orthodromically responsive. Three types of orthodromic responses were observed: excitatory, inhibitory, and complex. Priming the animals with 5 micrograms estradiol benzoate (EB) 48 hr prior to recording had no effect on the overall number of neurons responding to septal area stimulation, but EB priming did significantly reduce the percentage of orthodromically excited neurons. The firing rate of the majority of amygdala neurons responsive to septal area stimulation was not affected by iontophoretically applied LHRH (59 of 76) or LHRH fragment (41 of 65). In some cases, application of LHRH (10 of 76) or Ac-LHRH5-10 (12 of 55) produced a change in neuronal firing that was similar in direction to the orthodromically evoked response. When applied during the collection of peristimulus time histograms, both peptides were also able to modulate the orthodromically evoked response (five of 18 cells tested with LHRH and three of 14 cells tested with Ac-LHRH5-10). The results demonstrate a large projection from the septal area to the amygdala, one component of which is altered by estrogen priming.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibitory action of adenosine on synaptic transmission in the hippocampus of the guinea pig in vitro

Thin hippocampal slices were prepared from guinea pig brains. the postsynaptic field potential elicited in the pyramidal cell layer of CA3 region by mossy fiber stimulation was reversibly inhibited by application of adenosine to the perfusion medium. Among purine and pyrimidine derivatives, only adenosine and adenine nucleotides depressed the field potential with similar dose-response curves at concentrations of 10(-5).10(-3) M. In order to elucidate the mechanism of the inhibitory action of these agents, the effects of adenosine and adenine nucleotides on membrane events in pyramidal neurons were studied using intracellular recording techniques. Application of adenosine and adenine nucleotides hyperpolarized membrane potential and markedly depressed the EPSPs (excitatory postsynaptic potentials) elicited in the pyramidal cell by granular cell activation. However the spike generating mechanism of the neuron was not interfered with and membrane conductance was not increased by adenosine and adenine nucleotides. 4-Aminopyridine counteracted the inhibitory action of adenosine. These findings indicate that the mechanism of the inhibitory action of adenosine and adenine nucleotides is different from that of conventional inhibitory neurotransmitters such as gamma-aminobutyric acid and suggest a presynaptic action of adenosine and adenine nucleotides.     

Sacral Nerve Stimulation for Treatment of Intractable Pain Associated with Cauda Equina Syndrome

Sacral nerve stimulation (SNS) is an effective treatment for bladder and bowel dysfunction, and also has a role in the treatment of chronic pelvic pain. We report two cases of intractable pain associated with cauda equina syndrome (CES) that were treated successfully by SNS. The first patient suffered from intractable pelvic pain with urinary incontinence and fecal incontinence after surgery for a herniated lumbar disc. The second patient underwent surgery for treatment of a burst fracture and developed intractable pelvic area pain, right leg pain, excessive urinary frequency, urinary incontinence, voiding difficulty and constipation one year after surgery. A SNS trial was performed on both patients. Both patients'' pain was significantly improved and urinary symptoms were much relieved. Neuromodulation of the sacral nerves is an effective treatment for idiopathic urinary frequency, urgency, and urge incontinence. Sacral neuromodulation has also been used to control various forms of pelvic pain. Although the mechanism of action of neuromodulation remains unexplained, numerous clinical success reports suggest that it is a therapy with efficacy and durability. From the results of our research, we believe that SNS can be a safe and effective option for the treatment of intractable pelvic pain with incomplete CES.     

Zinc release from Schaffer collaterals and its significance

On the basis of the evidence that approximately 45% of Schaffer collateral boutons are zinc-positive, zinc release from Schaffer collaterals and its action were examined in hippocampal slices. When zinc release from Schaffer collaterals was examined using ZnAF-2, a membrane-impermeable zinc indicator, ZnAF-2 signal in the stratum radiatum of the CA1 was increased by tetanic stimuli at 100 Hz for 1 s, suggesting that zinc is released from Schaffer collaterals in a calcium- and impulse-dependent manner. An in vivo microdialysis experiment indicated that the perfusion with 10 μM zinc significantly decreases extracellular glutamate concentration in the CA1. When tetanic stimuli at 100 Hz for 5 s were delivered to the dentate granule cells, the increase in calcium signal in the stratum radiatum of the CA1, as well as in the stratum lucidum of the CA3, was attenuated by addition of 10 μM zinc, while enhanced by addition of 1 mM CaEDTA, a membrane-impermeable zinc chelator. The increase in calcium signal in the CA1, in which Schaffer collateral synapses exist, during delivery of tetanic stimuli at 100 Hz for 1 s to the Schaffer collateral-commissural pathway was also significantly enhanced by addition of 1 mM CaEDTA. These results suggest that zinc released from Schaffer collaterals suppressively modulates presynaptic and postsynaptic calcium signaling in the CA1, followed by the suppression of glutamate release.