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Muscarinic acetylcholine (ACh) receptors are a type of G protein-coupled receptors (GPCRs) found in the membranes of various cells, including those in the heart. They play a crucial role in modulating the response of the heart to the neurotransmitter acetylcholine. Step 1: Activation of the muscarinic ACh receptor When acetylcholine is released from the nerve terminals, it binds to the muscarinic ACh receptors on the cell membranes of the heart. This binding leads to a conformational change in the receptor that subsequently activates the G protein. Step 2: Activation of the G protein The activated G protein, known as Gi, downregulates the activity of adenylate cyclase, an enzyme involved in the production of cyclic adenosine monophosphate (cAMP). Step 3: Decreased cAMP production The downregulation of adenylate cyclase results in decreased cAMP production. cAMP is a secondary messenger involved in multiple intracellular signaling pathways. Step 4: Inhibition of calcium channels The decrease in cAMP levels leads to the decreased activation of protein kinase A (PKA), which in turn inhibits the opening of L-type calcium channels in the cardiac cells. Step 5: Decreased heart rate and force of contraction The inhibition of L-type calcium channels reduces the influx of calcium ions into the cardiac cells. This reduces the strength and rate of contraction of the heart muscle, thereby leading to inhibition of the heart's activity.

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system (CNS) that helps in maintaining the balance between excitation and inhibition. GABA receptors are found on the neuronal cell membranes and are responsible for mediating the inhibitory effects of GABA. Step 1: GABA binding to the GABA receptors GABA binds to specific GABA receptors on the postsynaptic neuron. Step 2: Activation of GABA receptors Two types of GABA receptors exist: GABA-A and GABA-B. GABA-A receptors are ionotropic, meaning they are directly linked to ion channels, while GABA-B receptors are metabotropic, functioning through G proteins. Step 3: Inhibition through GABA-A receptors When GABA binds to GABA-A receptors, it causes the opening of chloride ion channels. This results in the influx of negative chloride ions into the neuron, leading to hyperpolarization of the membrane potential. Hyperpolarization makes it more difficult for the neuron to reach the action potential threshold, thus inhibiting neuronal firing. Step 4: Inhibition through GABA-B receptors Binding of GABA to GABA-B receptors leads to the activation of G proteins. These proteins, in turn, can either indirectly open potassium channels, resulting in the efflux of positive potassium ions and hyperpolarization, or inhibit calcium channels, limiting the influx of positive calcium ions. Both of these actions result in a decrease in neuronal excitability and inhibition of neural activity. In summary, inhibitory effects are produced by muscarinic ACh receptors in the heart through the downregulation of cAMP production and inhibition of calcium channels, leading to a decreased heart rate and force of contraction. In CNS neurons, GABA receptors mediate inhibition by inducing hyperpolarization, primarily via the opening of chloride or potassium ion channels and inhibition of calcium channels.